**Right Chambers Quantification in Clinical Practice: Echocardiography Compared with Cardiac Magnetic Resonance Imaging**

Lucia Agoston-Coldea and Silvia Lupu

Additional information is available at the end of the chapter

http://dx.doi.org/10.5772/55832

#### **1. Introduction**

The right ventricle (RV) has its own particular morphology and functions, which are different when compared to the left ventricle (LV). In clinical practice, the right heart chambers are often overlooked, as most physicians tend to focus more on LV and left atrium (LA) morphology and functions. However, cardiac pathology is often associated with right chambers impair‐ ment, which can occur as a primary pathophysiological response to elevated pressure in the pulmonary arterial circulation associated with primary pulmonary artery hypertension [1-2], in pulmonary diseases associated with pulmonary venous or arterial hypertension [3-4], pulmonary embolism [5], but also in congenital heart disease [6]. Most often, RV dysfunction is triggered by left chamber impairment [7-9].

Right cardiac imaging is quite challenging, as there are few validated and reproducible parameters that can be employed for an accurate right atrium (RA) and RV morphology and function assessment. However, some imaging techniques are available for this purpose. Nowadays, cardiac magnetic resonance imaging (MRI) is the golden standard for right chambers evaluation [10], due to its unlimited imaging planes, higher image resolution, and the ability to calculate volumes using three-dimensional (3D) measurements. Regrettably, this type of evaluation is not available in many centres and rather expensive, requiring high quality equipment and highly trained examiners.

Although cardiac MRI is the preferred method [11], echocardiography remains a valuable alternative, as it is widely available, non-invasive, and less expensive and can be performed in all patients oblivious of associated pathology or the presence of metallic devices such as pacemakers, implanted cardioverter defibrillators, cochlear implants or drug infusion pumps.

© 2013 Agoston-Coldea and Lupu; licensee InTech. This is a paper distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Some studies seem to suggest that the risk usually associated with cardiac MRI in patients with pace makers and defibrillators is overestimated and that examination using magnetic fields up to 1.5 Tesla can be safe [12-13]. However, performing such an examination is not without risk and should be attempted in selected patients, with several precautions including complete resuscitation facilities and in the presence of an electrophysiologist [14]. All in all, cardiac MRI requires many precautions, in such cases, whereas echocardiography is without risk and easier to perform. Despite its major advantages, echocardiography has its limitations, mainly due to the particular morphology of the RV. The thin, trabeculated right free wall and the anterior position in the chest render RV assessment difficult [15]. Moreover, endocardial border tracing is strenuous due to the presence of trabeculations, which can be a source of error when attempting to obtain precise dimension assessment. These downfalls are limited when realtime 3D echocardiography is used, although, for the time being, end-systolic and end-diastolic RV volumes seem to be underestimated when compared to cardiac MRI measurements [16]. Some studies have shown, however, that, in spite of the difference in volume measurements, the correlation between 3D echocardiography and MRI assessment of the right ventricle ejection fraction (RVEF) is quite strong [17]. All in all, echocardiography can be very useful, provided that a complex standard protocol is followed.

mechanic activity which consists of inward, longitudinal and circumferential traction; the systolic function is mainly determined by the longitudinal contraction which causes the shortening of the ventricle, with equal contribution from the interventricular septum and the free wall [24]. Several factors contribute to RV global function, namely the preload, afterload and contractility. The preload is dependant on the volume status, the tricuspid valve gradient and the venous return from the vena cava. The afterload is determined by the resistance opposed by the pulmonary valve, the pulsatile flow reflected from the main pulmonary artery, the impedance of the proximal pulmonary artery and arterioles [25]. Pulmonary vascular resistance may not, therefore, be used to assess RV total afterload, particularly in patients with pulmonary hypertension [25]. Due to its thin free wall and high compliance, the RV can easily adapt to increased preload by dilatation, which can be well tolerated for a long time, although it eventually leads to RV failure. By contrast, elevated afterload is poorly tolerated from an early stage, as the RV has little capacity for compensatory hypertrophy, which is quickly followed by increased stiffness and chamber dilatation [3]. In clinical practice, changes in preload and afterload alter RV contraction. Other factors that may impair RV systolic function include abnormal variations of the heart rate, pharmacological agents, or ventricular interde‐ pendence [25]. Ventricular interdependence refers to the fact that the shape, size and compli‐ ance of one ventricle may influence the shape, size or pressures in the other ventricle, an

**Figure 1.** Segmental anatomy of right ventricle in correlation with segmental coronary vascularisation. Adapted from Rudski et al. [23]. RV=right ventricle; RVOT= right ventricular outflow tract; RA=right atrium; RCA=right coronary ar‐

Lateral wall of the RV Inferior wall of the RV Anterior wall of the RV Marginal branch of the RCA

LV

http://dx.doi.org/10.5772/55832

Ao

Posterior descending of the RCA Conus branch of the RCA Left anterior descending artery

LA

Imaging

13

RA

RV

essential concept for understanding the pathophysiology of RV dysfunction [9].

**3. Assessment of right chambers morphology and systolic function**

Echocardiography can help with qualitative morphological examination by 2D and 3D echocardiography. Although 2D echocardiography is widely applied in everyday clinical practice for the morphological and functional assessment of cardiac chambers and valves, 3D echocardiography is more accurate in assessing chamber volumes, mass and functions and

**3.1. Echocardiography**

RV

RA

LV

LA

tery; PA=pulmonary artery; LV=left ventricle; LA=left atrium.

Ao

LA LV

LA RA RVOT

PA

RA

LV

RA

LA

RV

Right Chambers Quantification in Clinical Practice: Echocardiography Compared with Cardiac Magnetic Resonance

RV

RVOT

PA

RV

LV

RV

#### **2. Anatomy and physiology of the right ventricle**

The RV has an anterior position in the chest and lies immediately behind the sternum. It has a triangular or crescent shape and three distinct regions with different embryological origin and electrophysiological properties. The three regions include: 1) the inlet component, 2) the apical trabecular component and 3) the outlet component [18]. The inlet component extends from the tricuspid valve insertion to the level of the papillary muscle, surrounding and supporting the tricuspid valve and the subvalvular apparatus. The trabecular component extends from the papillary muscles level to the apex and contains coarse trabeculations. The inlet and trabecular components have a common embryological origin and form a morpho‐ logical and functional structure called sinus. The sinus is the pivot structure for RV contraction. The outlet component, also called the infundibulum, conus or the RV outflow tract (RVOT) has its distinct embryological origin and is functionally different from the sinus. This compo‐ nent has a smooth surface and a minute contribution to RV output volume, and is the last cardiac structure to be activated, at end systole [19]. This region is particularly important in patients with congenital heart disease [20] and arrhythmias such as the idiopathic outflow tachycardia [21], as well as for the diagnosis of arrhythmogenic right ventricle dysplasia (ARVD), for which the left parasternal long-axis view is usually preferred [22]. All in all, each region of the RV (Figure 1) is essential in patients with cardiopulmonary disorders and should be analysed in correlation with segmental coronary vascularisation [18, 23].

RV physiology is closely linked to its anatomical properties. The thin, trabeculated free wall is adapted to the low pressures in the pulmonary circulation, its dynamics being very different from that of the LV. RV contraction is generated by the progression of a peristaltic wave which begins at the inlet and moves towards the infundibulum. RV depolarization triggers the

Right Chambers Quantification in Clinical Practice: Echocardiography Compared with Cardiac Magnetic Resonance Imaging http://dx.doi.org/10.5772/55832 13

**Figure 1.** Segmental anatomy of right ventricle in correlation with segmental coronary vascularisation. Adapted from Rudski et al. [23]. RV=right ventricle; RVOT= right ventricular outflow tract; RA=right atrium; RCA=right coronary ar‐ tery; PA=pulmonary artery; LV=left ventricle; LA=left atrium.

mechanic activity which consists of inward, longitudinal and circumferential traction; the systolic function is mainly determined by the longitudinal contraction which causes the shortening of the ventricle, with equal contribution from the interventricular septum and the free wall [24]. Several factors contribute to RV global function, namely the preload, afterload and contractility. The preload is dependant on the volume status, the tricuspid valve gradient and the venous return from the vena cava. The afterload is determined by the resistance opposed by the pulmonary valve, the pulsatile flow reflected from the main pulmonary artery, the impedance of the proximal pulmonary artery and arterioles [25]. Pulmonary vascular resistance may not, therefore, be used to assess RV total afterload, particularly in patients with pulmonary hypertension [25]. Due to its thin free wall and high compliance, the RV can easily adapt to increased preload by dilatation, which can be well tolerated for a long time, although it eventually leads to RV failure. By contrast, elevated afterload is poorly tolerated from an early stage, as the RV has little capacity for compensatory hypertrophy, which is quickly followed by increased stiffness and chamber dilatation [3]. In clinical practice, changes in preload and afterload alter RV contraction. Other factors that may impair RV systolic function include abnormal variations of the heart rate, pharmacological agents, or ventricular interde‐ pendence [25]. Ventricular interdependence refers to the fact that the shape, size and compli‐ ance of one ventricle may influence the shape, size or pressures in the other ventricle, an essential concept for understanding the pathophysiology of RV dysfunction [9].

#### **3. Assessment of right chambers morphology and systolic function**

#### **3.1. Echocardiography**

Some studies seem to suggest that the risk usually associated with cardiac MRI in patients with pace makers and defibrillators is overestimated and that examination using magnetic fields up to 1.5 Tesla can be safe [12-13]. However, performing such an examination is not without risk and should be attempted in selected patients, with several precautions including complete resuscitation facilities and in the presence of an electrophysiologist [14]. All in all, cardiac MRI requires many precautions, in such cases, whereas echocardiography is without risk and easier to perform. Despite its major advantages, echocardiography has its limitations, mainly due to the particular morphology of the RV. The thin, trabeculated right free wall and the anterior position in the chest render RV assessment difficult [15]. Moreover, endocardial border tracing is strenuous due to the presence of trabeculations, which can be a source of error when attempting to obtain precise dimension assessment. These downfalls are limited when realtime 3D echocardiography is used, although, for the time being, end-systolic and end-diastolic RV volumes seem to be underestimated when compared to cardiac MRI measurements [16]. Some studies have shown, however, that, in spite of the difference in volume measurements, the correlation between 3D echocardiography and MRI assessment of the right ventricle ejection fraction (RVEF) is quite strong [17]. All in all, echocardiography can be very useful,

The RV has an anterior position in the chest and lies immediately behind the sternum. It has a triangular or crescent shape and three distinct regions with different embryological origin and electrophysiological properties. The three regions include: 1) the inlet component, 2) the apical trabecular component and 3) the outlet component [18]. The inlet component extends from the tricuspid valve insertion to the level of the papillary muscle, surrounding and supporting the tricuspid valve and the subvalvular apparatus. The trabecular component extends from the papillary muscles level to the apex and contains coarse trabeculations. The inlet and trabecular components have a common embryological origin and form a morpho‐ logical and functional structure called sinus. The sinus is the pivot structure for RV contraction. The outlet component, also called the infundibulum, conus or the RV outflow tract (RVOT) has its distinct embryological origin and is functionally different from the sinus. This compo‐ nent has a smooth surface and a minute contribution to RV output volume, and is the last cardiac structure to be activated, at end systole [19]. This region is particularly important in patients with congenital heart disease [20] and arrhythmias such as the idiopathic outflow tachycardia [21], as well as for the diagnosis of arrhythmogenic right ventricle dysplasia (ARVD), for which the left parasternal long-axis view is usually preferred [22]. All in all, each region of the RV (Figure 1) is essential in patients with cardiopulmonary disorders and should

provided that a complex standard protocol is followed.

12 Hot Topics in Echocardiography

**2. Anatomy and physiology of the right ventricle**

be analysed in correlation with segmental coronary vascularisation [18, 23].

RV physiology is closely linked to its anatomical properties. The thin, trabeculated free wall is adapted to the low pressures in the pulmonary circulation, its dynamics being very different from that of the LV. RV contraction is generated by the progression of a peristaltic wave which begins at the inlet and moves towards the infundibulum. RV depolarization triggers the Echocardiography can help with qualitative morphological examination by 2D and 3D echocardiography. Although 2D echocardiography is widely applied in everyday clinical practice for the morphological and functional assessment of cardiac chambers and valves, 3D echocardiography is more accurate in assessing chamber volumes, mass and functions and provides a superior view of the valves. 2D echocardiography of the right chambers may provide diameter, area and volume measurements, which should be indexed to body surface, and allows the assessment of the systolic pulmonary artery pressure (sPAP) using the tricuspid regurgitation flow and inferior vena cava (IVC) diameter and its variations during the respiratory cycle. Newer techniques, such as tissue Doppler and strain-rate imaging, provide valuable data on the systolic and diastolic functions of the RV.

#### *3.1.1. Right ventricle*

A complete evaluation of RV structure should include the study of RV volume, shape and internal architecture, RV hypertrophy and mass, tissue characterization, assessment for potential masses [8], and regional wall motion abnormalities [26]. Normally, the RV has a crescent shape when viewed from the parasternal short-axis incidence; when the RV is submitted to pressure and volume overload, the crescent shape changes to a D shape, with subsequent septal flattening, leading to impaired LV filling and decreased output. Septal movement analysis can help distinguish between RV volume and pressure overload; in the case of volume overload, septal flattening only occurs during the diastole, whereas, in the presence of pressure overload, it is persistent throughout the entire cardiac cycle [27-28]. This phenomenon is quantitatively analyzed by deriving the eccentricity index, calculated as the RV anteroposterior over the RV septolateral diameter ratio (which may be measured at endsystole or end-diastole); a value>1 suggests RV overload and was shown to be positively correlated with pulmonary artery hypertension [29].

**a.** Acquisition and measurements:

Although qualitative assessment of the RV has its virtues, quantitative assessment provides more accurate and interpretable data. Morphology assessment may include diameter, area and volume measurements. RV morphology should be assessed by 2D using several acoustic windows such as the parasternal long-axis view (which allows RV anterior wall visualisation), the parasternal short-axis view (to assess the infundibulum and some of the RV anterior wall), the left parasternal RV inflow window (for the anterior, lateral and inferior RV walls, depend‐ ing on the section level), the subcostal view (for the lateral wall and the infundibulum), the apical 4-chamber view, and apical 5-chamber view (for assessment of the RV lateral wall) [26] (Figure 2). Usually, the RV is best measured at end-diastole using the 4-chamber apical view. From this window, three dimensions can be derived: the basal diameter (the largest diameter in the basal third of the RV, usually just below the tricuspid annulus); the medial diameter (measured at the level of the LV papillary muscles); the longitudinal diameter (measured from the RV apex to the tricuspid annulus plane). RV free wall thickness is best measured from the subcostal view at the end of the diastole, using either 2D or M-mode imaging techniques; oblivious of the preferred method, measurements should exclude trabeculations, the papillary muscle, and the pericardium. RV volume and function may also be assessed by 3D trans‐ thoracic echocardiography using apical and subcostal views. Usually, four-beat images are necessary to include the entire RV, although newer techniques allow a good evaluation using a single beat, at the expense of temporal and spatial resolution [26].

5

Imaging

15

http://dx.doi.org/10.5772/55832

Parasternal long-axis view

Parasternal short-axis view

Apical 4-chamber view

Subcostal view

**Figure 2.** Echocardiography 2D views for right ventricle chamber.

**b.** Qualitative values:

as well as RVEF and RV mass are calculated using Simpson's rule.

Images are available for off-line analysis, allowing accurate endocardial contours delineation and RV volumes measurement from sequential long axis planes. End-diastolic measurements are taken at the peak of the R wave of QRS complexes, while end-systolic volumes are measured in the first frame before opening of the tricuspid valve [26]. Furthermore, trabecu‐ lations are included in the blood pool. The end-diastolic, end-systolic RV and stroke volume,

Right Chambers Quantification in Clinical Practice: Echocardiography Compared with Cardiac Magnetic Resonance

An empirical comparison of LV and RV dimensions allows RV description as (Table 1): normal (when the RV has smaller dimensions when compared to the LV, with RV apex more basal than the LV apex); mildly dilated (when the RV is enlarged, but still smaller than the LV);

Right Chambers Quantification in Clinical Practice: Echocardiography Compared with Cardiac Magnetic Resonance Imaging http://dx.doi.org/10.5772/55832 15

**Figure 2.** Echocardiography 2D views for right ventricle chamber.

5 Images are available for off-line analysis, allowing accurate endocardial contours delineation and RV volumes measurement from sequential long axis planes. End-diastolic measurements are taken at the peak of the R wave of QRS complexes, while end-systolic volumes are measured in the first frame before opening of the tricuspid valve [26]. Furthermore, trabecu‐ lations are included in the blood pool. The end-diastolic, end-systolic RV and stroke volume, as well as RVEF and RV mass are calculated using Simpson's rule.

**b.** Qualitative values:

provides a superior view of the valves. 2D echocardiography of the right chambers may provide diameter, area and volume measurements, which should be indexed to body surface, and allows the assessment of the systolic pulmonary artery pressure (sPAP) using the tricuspid regurgitation flow and inferior vena cava (IVC) diameter and its variations during the respiratory cycle. Newer techniques, such as tissue Doppler and strain-rate imaging, provide

A complete evaluation of RV structure should include the study of RV volume, shape and internal architecture, RV hypertrophy and mass, tissue characterization, assessment for potential masses [8], and regional wall motion abnormalities [26]. Normally, the RV has a crescent shape when viewed from the parasternal short-axis incidence; when the RV is submitted to pressure and volume overload, the crescent shape changes to a D shape, with subsequent septal flattening, leading to impaired LV filling and decreased output. Septal movement analysis can help distinguish between RV volume and pressure overload; in the case of volume overload, septal flattening only occurs during the diastole, whereas, in the presence of pressure overload, it is persistent throughout the entire cardiac cycle [27-28]. This phenomenon is quantitatively analyzed by deriving the eccentricity index, calculated as the RV anteroposterior over the RV septolateral diameter ratio (which may be measured at endsystole or end-diastole); a value>1 suggests RV overload and was shown to be positively

Although qualitative assessment of the RV has its virtues, quantitative assessment provides more accurate and interpretable data. Morphology assessment may include diameter, area and volume measurements. RV morphology should be assessed by 2D using several acoustic windows such as the parasternal long-axis view (which allows RV anterior wall visualisation), the parasternal short-axis view (to assess the infundibulum and some of the RV anterior wall), the left parasternal RV inflow window (for the anterior, lateral and inferior RV walls, depend‐ ing on the section level), the subcostal view (for the lateral wall and the infundibulum), the apical 4-chamber view, and apical 5-chamber view (for assessment of the RV lateral wall) [26] (Figure 2). Usually, the RV is best measured at end-diastole using the 4-chamber apical view. From this window, three dimensions can be derived: the basal diameter (the largest diameter in the basal third of the RV, usually just below the tricuspid annulus); the medial diameter (measured at the level of the LV papillary muscles); the longitudinal diameter (measured from the RV apex to the tricuspid annulus plane). RV free wall thickness is best measured from the subcostal view at the end of the diastole, using either 2D or M-mode imaging techniques; oblivious of the preferred method, measurements should exclude trabeculations, the papillary muscle, and the pericardium. RV volume and function may also be assessed by 3D trans‐ thoracic echocardiography using apical and subcostal views. Usually, four-beat images are necessary to include the entire RV, although newer techniques allow a good evaluation using

valuable data on the systolic and diastolic functions of the RV.

correlated with pulmonary artery hypertension [29].

a single beat, at the expense of temporal and spatial resolution [26].

**a.** Acquisition and measurements:

*3.1.1. Right ventricle*

14 Hot Topics in Echocardiography

An empirical comparison of LV and RV dimensions allows RV description as (Table 1): normal (when the RV has smaller dimensions when compared to the LV, with RV apex more basal than the LV apex); mildly dilated (when the RV is enlarged, but still smaller than the LV); moderately dilated (when the RV and LV dimensions are equal); severely dilated (when the RV is larger than the LV) [30]. However, normal values have been established for quantitative assessment: a basal diameter >42 mm, a median diameter >35 mm and a longitudinal diameter >86 mm indicate RV dilatation. The parasternal short-axis view of the great vessels allows RVOT measurement at the level of the pulmonary valve insertion (the distal diameter) for which a value of >27 mm signifies RV dilatation. Proximal RVOT diameter can be measured from either the long or the short-axis parasternal views, with a normal maximum value of 33 mm. However, the former is usually preferred, as it is more reproducible [23]. RV areas are measured at end-diastole and end-systole, with the following normal values: RV end-diastole area 20.1 ± 4 cm2 and RV end-systole area 10.9 ± 2.9 cm2 [26, 30]. RV volumes may be calculated by using either the Simpson method or the area-length method and normal values range between 63-103 mL for end-diastolic volumes and 22-56 mL for end-systolic volume [31]. However, these 2D echocardiography measurements were proved to be inaccurate by comparison with 3D echocardiography and cardiac MRI derived volumes. Normal thickness ranges from 3 to 5 mm [23], and any value surpassing 5 mm suggests RV hypertrophy, which is usually a response to pressure overload, in the absence of associated pathology, such as infiltrative or hypertrophic cardiomyopathies [23].

The lack of accuracy in assessing RV volumes by 2D echocardiography is mainly determined by the complex RV geometry and the heavily trabeculated inner wall contour. Real 3D echocardiography overcomes these limitations and provides a superior evaluation of ventric‐ ular volume, mass and function, as well as a more complete view of the valves [26]. Moreover, 3D echocardiography was proved to be a reliable noninvasive modality of directing the bioptome to the desired site of biopsy within the RV. In one study, 3D echocardiography provided accurate anatomic details and was proved to allow sufficient pulmonary valve visualization in 68% of the patients and an excellent RVOT visualisation in 40% [32]. Normal medium values of RV end-diastolic and end-systolic volumes were established at 49 ± 10 and 16 ± 6 mL/m2 respectively, with a mean RVEF of 67 ± 8% [33]. Another study provided normal reference ranges of indexed volumes: 38.6 to 92.2 mL/m2 for RV end-diastolic volume, 7.8 to

Right Chambers Quantification in Clinical Practice: Echocardiography Compared with Cardiac Magnetic Resonance

for stroke volume in women and higher

for end-

Imaging

17

http://dx.doi.org/10.5772/55832

for RV end-diastolic volume, 14.2 to 48.4 mL/m2

for stroke volume [34].

The structural assessment of the RV provides information concerning the pressure and volume loading conditions which may lead to functional impairment. The RV gradually adapts to pressure overload by hypertrophy and interventricular septal flattening, with systolic function impairment, RV and tricuspid annulus enlargement and aggravated tricuspid regurgitation, which trigger RV diastolic dysfunction. Therefore, RV morphology should be assessed periodically in patients with acute or chronic respiratory pathology and valvulopathies with the purpose of identifying early anomalies which might be corrected by a proper therapeutic approach. Until recently, the eccentricity index was based on measurements made from the parasternal short-axis view, at the level of papillary muscles. However, one recent study shows that these measurements were less accurate than those made at the apical level, which was superior in terms of correlation with aggravated pulmonary hypertension [35], right chamber dilatation and RV systolic dysfunction [36]. In addition to that, ultrasound imaging techniques may identify regional morphologic abnormalities that occur in ARVD, provided the area of dysplasia is large enough. The diagnosis of ARVD is likely in the presence of significant local wall aneurysm (major diagnostic criterion), trabeculation disarray, increased thickness of the moderator band, with hyperechogenic appearance and RVOT dilatation [37]. However, despite the advantages, the diagnosis of ARVD by imaging techniques cannot rely on echo‐

The RA has its own complex pathology, as it responds to both RV volume and pressure overload. In addition to that, RA enlargement was documented in patients with atrial ar‐ rhythmias such as atrial fibrillation by both 2D and 3D echocardiography; moreover, it has been proven that RA remodelling occurs in atrial fibrillation and regresses if sinus rhythm is restored and maintained after radiofrequency catheter ablation [38]. However, RA dilatation

is most often encountered in patients with elevated pulmonary hypertension.

for end-systolic volume, 22.5 to 42.9 mL/m2

50.6 mL/m2

values in men: 47.0 to 100 mL/m2

**c.** Clinical Application

cardiography alone.

*3.1.2. Right atrium*

systolic volume, and 23.0 to 52.6 mL/m2


**Table 1.** Reference limits and partition values of right ventricular size

The lack of accuracy in assessing RV volumes by 2D echocardiography is mainly determined by the complex RV geometry and the heavily trabeculated inner wall contour. Real 3D echocardiography overcomes these limitations and provides a superior evaluation of ventric‐ ular volume, mass and function, as well as a more complete view of the valves [26]. Moreover, 3D echocardiography was proved to be a reliable noninvasive modality of directing the bioptome to the desired site of biopsy within the RV. In one study, 3D echocardiography provided accurate anatomic details and was proved to allow sufficient pulmonary valve visualization in 68% of the patients and an excellent RVOT visualisation in 40% [32]. Normal medium values of RV end-diastolic and end-systolic volumes were established at 49 ± 10 and 16 ± 6 mL/m2 respectively, with a mean RVEF of 67 ± 8% [33]. Another study provided normal reference ranges of indexed volumes: 38.6 to 92.2 mL/m2 for RV end-diastolic volume, 7.8 to 50.6 mL/m2 for end-systolic volume, 22.5 to 42.9 mL/m2 for stroke volume in women and higher values in men: 47.0 to 100 mL/m2 for RV end-diastolic volume, 14.2 to 48.4 mL/m2 for endsystolic volume, and 23.0 to 52.6 mL/m2 for stroke volume [34].

#### **c.** Clinical Application

moderately dilated (when the RV and LV dimensions are equal); severely dilated (when the RV is larger than the LV) [30]. However, normal values have been established for quantitative assessment: a basal diameter >42 mm, a median diameter >35 mm and a longitudinal diameter >86 mm indicate RV dilatation. The parasternal short-axis view of the great vessels allows RVOT measurement at the level of the pulmonary valve insertion (the distal diameter) for which a value of >27 mm signifies RV dilatation. Proximal RVOT diameter can be measured from either the long or the short-axis parasternal views, with a normal maximum value of 33 mm. However, the former is usually preferred, as it is more reproducible [23]. RV areas are measured at end-diastole and end-systole, with the following normal values: RV end-diastole

by using either the Simpson method or the area-length method and normal values range between 63-103 mL for end-diastolic volumes and 22-56 mL for end-systolic volume [31]. However, these 2D echocardiography measurements were proved to be inaccurate by comparison with 3D echocardiography and cardiac MRI derived volumes. Normal thickness ranges from 3 to 5 mm [23], and any value surpassing 5 mm suggests RV hypertrophy, which is usually a response to pressure overload, in the absence of associated pathology, such as

> **Mildly dilated**

Basal RV diameter (RVD1), mm 20-28 29-33 34-38 "/>39 Mid-RV diameter (RVD2), mm 27-33 34-37 38-41 "/>42 Base-to-apex length (RVL), mm 71-79 80-85 86-91 "/>92

RV diastolic area, cm2 11-28 29-32 33-37 "/>38 RV systolic area, cm2 7.5-16 17-19 20-22 "/>23

**Moderately**

25-29 30-32 33-35 "/>36

17-23 24-27 28-31 "/>32

**dilated Severely dilated**

and RV end-systole area 10.9 ± 2.9 cm2 [26, 30]. RV volumes may be calculated

area 20.1 ± 4 cm2

16 Hot Topics in Echocardiography

**2D echocardiography**

RV dimensions

RVOT diameters

proximal) mm

distal), mm

RV volume

RV area

Above aortic valve, (RVOT

Above pulmonic valve (RVOT

RV diastolic volume, mL 63–103 RV systolic volume, mL 22–56

**Table 1.** Reference limits and partition values of right ventricular size

infiltrative or hypertrophic cardiomyopathies [23].

**Reference values**

The structural assessment of the RV provides information concerning the pressure and volume loading conditions which may lead to functional impairment. The RV gradually adapts to pressure overload by hypertrophy and interventricular septal flattening, with systolic function impairment, RV and tricuspid annulus enlargement and aggravated tricuspid regurgitation, which trigger RV diastolic dysfunction. Therefore, RV morphology should be assessed periodically in patients with acute or chronic respiratory pathology and valvulopathies with the purpose of identifying early anomalies which might be corrected by a proper therapeutic approach. Until recently, the eccentricity index was based on measurements made from the parasternal short-axis view, at the level of papillary muscles. However, one recent study shows that these measurements were less accurate than those made at the apical level, which was superior in terms of correlation with aggravated pulmonary hypertension [35], right chamber dilatation and RV systolic dysfunction [36]. In addition to that, ultrasound imaging techniques may identify regional morphologic abnormalities that occur in ARVD, provided the area of dysplasia is large enough. The diagnosis of ARVD is likely in the presence of significant local wall aneurysm (major diagnostic criterion), trabeculation disarray, increased thickness of the moderator band, with hyperechogenic appearance and RVOT dilatation [37]. However, despite the advantages, the diagnosis of ARVD by imaging techniques cannot rely on echo‐ cardiography alone.

#### *3.1.2. Right atrium*

The RA has its own complex pathology, as it responds to both RV volume and pressure overload. In addition to that, RA enlargement was documented in patients with atrial ar‐ rhythmias such as atrial fibrillation by both 2D and 3D echocardiography; moreover, it has been proven that RA remodelling occurs in atrial fibrillation and regresses if sinus rhythm is restored and maintained after radiofrequency catheter ablation [38]. However, RA dilatation is most often encountered in patients with elevated pulmonary hypertension.

#### **a.** Acquisition and measurements:

The RA is most often visualized from the apical 4-chamber view or the subcostal view [23, 26, 39]. However, due to the fact that standardized data concerning RA assessment is scarce, current evaluation includes exclusively RA minimum and maximum diameter and RA area estimation. All these measurements are made by planimetry from the apical 4-chamber view, at the end of the ventricular systole, when the atrium volume is largest (Figure 3). 3D echo‐ cardiography, although time consuming, may also be employed to calculate RA volume, with the advantage of more accurate endocardial border tracing at end-systole. To this purpose, two orthogonal planes (two-plane), four equiangular planes (four-plane), and eight equian‐ gular planes (eight-plane) may be used [40]. All the collected data can be analyzed on and offline, with cropping and threshold processing. The final result depends on the accurate and complementary use of these processing tools [41].

In 3D echocardiography, RA volumes are calculated using the following formula: 0.85 (D2

**RA 3D echocardiography Men Women** RAEF, % 46-74 48-83 RAVI max, mL/m2 18-50 17-41 RAVI min, mL/m2 7-22 5-18

**Table 3.** Reference limits and partition values for right atrium 3D dimensions

**c.** Clinical Application

disease, and heart failure.

**a.** Acquisition and measurements:

**b.** Qualitative values:

*3.1.3. Inferior vena cava*

where D is the area in the four-chamber view and L the vertical long-axis [42]. Images should be taken from three different beats and the loops and tracings from the first examination should be available during the second and third examination to improve accuracy (Table 3) [42].

Right Chambers Quantification in Clinical Practice: Echocardiography Compared with Cardiac Magnetic Resonance

Real-time 3D echocardiography is believed to be a more reproducible and robust method for atrial volume measurements than 2D echocardiography [42], particularly in the presence of pathological conditions such as pulmonary disorders, congenital heart disease, valvular

Right chamber and pulmonary artery pressure assessment also relies on inferior vena cava (IVC) diameter measurement and the study of its variation during the respiratory cycle. In normal subjects, the IVC collapses, reducing its diameter with more than 50% after a sniff [43]; during a spontaneous, normal breathing cycle, changes in pleural pressure occur, which influence RA pressure; while inbreathing, the intrathoracic pressure becomes lower, allowing a more significant venous return and a decrease in IVC diameter. Respiratory variations are

The subcostal 4-chamber view is used to measure the IVC at end-expiration, proximal to the emergence of the hepatic veins, which is usually located at 0.5 to 3 cm of the IVC-RA ostium. Maximum and minimum diameters should be measured perpendicular to the long axis of the

Current guidelines [23] established an upper reference limit of 21 mm for IVC diameter. For an IVC diameter ≤21 mm and an inbreathe variation of >50%, the RA pressure is estimated at 3 mmHg (range 0 – 5 mmHg). If IVC diameter is >21 mm, and the inbreathe collapse is lower than 50%, the RA pressure is estimated at 15 mmHg (range, 10 – 20 mmHg). However, some cases do not fit this paradigm; in that situation, if IVC >21 mm and significant collapse (>50%) occurs after a sniff, or if IVC ≤21 mm, but there is scarcely any inbreathe diameter variation or none at all, RA pressure is estimated at 8 mmHg (Table 4). Other authors [44] have previously

abolished in case of cardiac tamponade or severe right heart failure [43].

IVC. Measurements may be facilitated by using M-mode (Figure 4).

)/L,

19

Imaging

http://dx.doi.org/10.5772/55832

**Figure 3.** Echocardiography 2D views for right atrium.

**b.** Qualitative values:

The maximal short-axis distance is measured at mid level, with an upper reference limit of 44 mm. The maximal long axis distance is measured from the center of the tricuspid annular plane to the center of the RA superior wall, describing a straight line parallel to the interatrial septum; the threshold for the maximal normal value has been established at 53 mm [23] (Table 2). RA area provides a more accurate assessment, but it is more time-consuming and, thusly, avoided by most physicians. The upper reference limit has been established at 18 cm2 or at 9 cm2 /m2 . The normal RA volume indexed to body surface area is 34 mL/m2 for men and 27 mL/m2 for women [26, 36].


**Table 2.** Reference limits and partition values for right atrium 2D dimensions

In 3D echocardiography, RA volumes are calculated using the following formula: 0.85 (D2 )/L, where D is the area in the four-chamber view and L the vertical long-axis [42]. Images should be taken from three different beats and the loops and tracings from the first examination should be available during the second and third examination to improve accuracy (Table 3) [42].


**Table 3.** Reference limits and partition values for right atrium 3D dimensions

#### **c.** Clinical Application

**a.** Acquisition and measurements:

18 Hot Topics in Echocardiography

complementary use of these processing tools [41].

**Figure 3.** Echocardiography 2D views for right atrium.

**2D echocardiography Reference**

**Table 2.** Reference limits and partition values for right atrium 2D dimensions

**b.** Qualitative values:

women [26, 36].

RA dimensions

The RA is most often visualized from the apical 4-chamber view or the subcostal view [23, 26, 39]. However, due to the fact that standardized data concerning RA assessment is scarce, current evaluation includes exclusively RA minimum and maximum diameter and RA area estimation. All these measurements are made by planimetry from the apical 4-chamber view, at the end of the ventricular systole, when the atrium volume is largest (Figure 3). 3D echo‐ cardiography, although time consuming, may also be employed to calculate RA volume, with the advantage of more accurate endocardial border tracing at end-systole. To this purpose, two orthogonal planes (two-plane), four equiangular planes (four-plane), and eight equian‐ gular planes (eight-plane) may be used [40]. All the collected data can be analyzed on and offline, with cropping and threshold processing. The final result depends on the accurate and

The maximal short-axis distance is measured at mid level, with an upper reference limit of 44 mm. The maximal long axis distance is measured from the center of the tricuspid annular plane to the center of the RA superior wall, describing a straight line parallel to the interatrial septum; the threshold for the maximal normal value has been established at 53 mm [23] (Table 2). RA area provides a more accurate assessment, but it is more time-consuming and, thusly, avoided

The normal RA volume indexed to body surface area is 34 mL/m2 for men and 27 mL/m2

**values**

RA minor-axis dimension, mm 29-45 46-49 50-54 "/>55 RA minor-axis dimension/BSA, mm/m2 17-25 26-28 29-31 "/>22

**Mildly dilated** **Moderately dilated**

or at 9 cm2

**Severely dilated**

/m2 .

for

by most physicians. The upper reference limit has been established at 18 cm2

Real-time 3D echocardiography is believed to be a more reproducible and robust method for atrial volume measurements than 2D echocardiography [42], particularly in the presence of pathological conditions such as pulmonary disorders, congenital heart disease, valvular disease, and heart failure.

#### *3.1.3. Inferior vena cava*

Right chamber and pulmonary artery pressure assessment also relies on inferior vena cava (IVC) diameter measurement and the study of its variation during the respiratory cycle. In normal subjects, the IVC collapses, reducing its diameter with more than 50% after a sniff [43]; during a spontaneous, normal breathing cycle, changes in pleural pressure occur, which influence RA pressure; while inbreathing, the intrathoracic pressure becomes lower, allowing a more significant venous return and a decrease in IVC diameter. Respiratory variations are abolished in case of cardiac tamponade or severe right heart failure [43].

**a.** Acquisition and measurements:

The subcostal 4-chamber view is used to measure the IVC at end-expiration, proximal to the emergence of the hepatic veins, which is usually located at 0.5 to 3 cm of the IVC-RA ostium. Maximum and minimum diameters should be measured perpendicular to the long axis of the IVC. Measurements may be facilitated by using M-mode (Figure 4).

**b.** Qualitative values:

Current guidelines [23] established an upper reference limit of 21 mm for IVC diameter. For an IVC diameter ≤21 mm and an inbreathe variation of >50%, the RA pressure is estimated at 3 mmHg (range 0 – 5 mmHg). If IVC diameter is >21 mm, and the inbreathe collapse is lower than 50%, the RA pressure is estimated at 15 mmHg (range, 10 – 20 mmHg). However, some cases do not fit this paradigm; in that situation, if IVC >21 mm and significant collapse (>50%) occurs after a sniff, or if IVC ≤21 mm, but there is scarcely any inbreathe diameter variation or none at all, RA pressure is estimated at 8 mmHg (Table 4). Other authors [44] have previously suggested a different approach (Table 4). The reference normal value interval for the IVC diameter was set at 15 – 25 mm; if the measured IVC diameter remained within these limits, and decreased with >50% after a sniff, the RA pressure was estimated at 5 – 10 mmHg; if inbreathe variation was <50%, RA pressure was estimated at 10 – 15 mmHg, and at 15 – 20 mmHg if IVC diameter was greater than 25 mm. If IVC was dilated and remained flat during the respiratory cycle, and dilated hepatic veins were also visualized, RA pressure was considered to be >20 mmHg.

**c.** Clinical Application

*3.1.4. Right ventricle systolic function*

Oblivious of the approach, estimated RA pressure is added to the tricuspid regurgitation gradient in order to calculate the systolic pulmonary artery pressure (sPAP). Usually, IVC diameter is only used to assess sPAP, and is not interpreted individually. However, one study focused on idiopathic pulmonary hypertension patients showed that an IVC diameter ≥20 mm, with respiratory variation <50%, was a prognostic factor for mortality [45]. In some cases, such as young athletes, dehydrated patients or in the presence of mechanical respiratory assistance

Right Chambers Quantification in Clinical Practice: Echocardiography Compared with Cardiac Magnetic Resonance

Assessing RV systolic function can be difficult, due to the particular morphology of the RV. Geometrical assumptions are based on pyramidal and ellipsoidal models which are not particularly accurate, as the RV has a rather irregular shape. Moreover, area and volume estimation can be impaired by the presence of trabeculations in the RV, which should be excluded from myocardial border tracings. For volume calculation, area-length and disk summation (Simpson's) methods are used, the latter being more accurate. However, volumes are underestimated by 2D echocardiography [46], when compared to 3D echocardiography [47] and cardiac MRI [34]. Cardiac computed tomography may also be used, but RV volumes tend to be overestimated using this imaging technique [48], while cardiac MRI remains the gold standard for RV assessment, although it was shown to correlate very well with real-time 3D echocardiography measurements [11]. These imaging techniques are often unavailable in most centres, rendering 2D echocardiography quite important, despite its downfalls. A complete 2D echocardiography examination should include area and volume assessment, as well as several derived parameters (Table 5), such as right ventricle fractional area change (RVFAC) and the RVEF, tricuspid annular plane systolic excursion (TAPSE), systolic velocity of the myocardium (St wave) and right ventricular myocardial performance index (RVMPI).

**dilated**

RVFAC, % 32-60 25-31 18-24 <17 RVEF, % 43–65 40-30 30-20 <20 TAPSE, mm 15-20 13-15 10-12 <10

**Table 5.** Reference limits and partition values of right ventricular systolic function as measured in the apical 4-

The RVFAC is estimated using the formula: (end-diastolic area – end-systolic area)/enddiastolic area x 100, with a lower reference value for normal RV systolic function of 35% [23] and was previously proved to diminish in primary pulmonary hypertension patients, when compared to healthy controls [49] (Figure 5). Normal RVFAC and partition values [30] are

**Moderately dilated**

**Severely dilated**

Imaging

21

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devices, IVC diameter correlates poorly with RA pressure.

**2D echocardiography Reference values Mildly**

**a.** Right ventricle fractional area change

chamber view

**Figure 4.** Measurement and view of the inferior vena cava (IVC) perpendicular to the long axis at end-expiration, just proximal to the junction of the hepatic veins that lie proximal to the ostium of the right atrium.


**Table 4.** Right atrium pressure assessment by inferior vena cava collapse and inbreathe variation

#### **c.** Clinical Application

suggested a different approach (Table 4). The reference normal value interval for the IVC diameter was set at 15 – 25 mm; if the measured IVC diameter remained within these limits, and decreased with >50% after a sniff, the RA pressure was estimated at 5 – 10 mmHg; if inbreathe variation was <50%, RA pressure was estimated at 10 – 15 mmHg, and at 15 – 20 mmHg if IVC diameter was greater than 25 mm. If IVC was dilated and remained flat during the respiratory cycle, and dilated hepatic veins were also visualized, RA pressure was

**Figure 4.** Measurement and view of the inferior vena cava (IVC) perpendicular to the long axis at end-expiration, just

**IVC diameter Change after "sniff" Estimated right atrium pressure (mmHg) Estimated right atrium pressure by Rudski [23]**

**Estimated right atrium pressure by Otto [43]**

proximal to the junction of the hepatic veins that lie proximal to the ostium of the right atrium.

≤ 21 mm Collapse "/>50% 3 mmHg (range 0 – 5 mmHg) "/> 21 mm Collapse <50% 15 mmHg (range 10 – 20 mmHg) "/>21 mm Collapse "/>50% 8 mmHg (range 5 – 10 mmHg) ≤ 21 mm Collapse <50% 8 mmHg (range 5 – 10 mmHg)

**Table 4.** Right atrium pressure assessment by inferior vena cava collapse and inbreathe variation

Normal range (15–25 mm) Collapse "/>50% 5 – 10 mmHg Normal range (15–25 mm) Collapse <50% 10 – 15 mmHg Dilated ("/>25 mm) Collapse <50% 15 – 20 mmHg Dilated ("/>25 mm) Flat "/> 20 mmHg

considered to be >20 mmHg.

20 Hot Topics in Echocardiography

Oblivious of the approach, estimated RA pressure is added to the tricuspid regurgitation gradient in order to calculate the systolic pulmonary artery pressure (sPAP). Usually, IVC diameter is only used to assess sPAP, and is not interpreted individually. However, one study focused on idiopathic pulmonary hypertension patients showed that an IVC diameter ≥20 mm, with respiratory variation <50%, was a prognostic factor for mortality [45]. In some cases, such as young athletes, dehydrated patients or in the presence of mechanical respiratory assistance devices, IVC diameter correlates poorly with RA pressure.

#### *3.1.4. Right ventricle systolic function*

Assessing RV systolic function can be difficult, due to the particular morphology of the RV. Geometrical assumptions are based on pyramidal and ellipsoidal models which are not particularly accurate, as the RV has a rather irregular shape. Moreover, area and volume estimation can be impaired by the presence of trabeculations in the RV, which should be excluded from myocardial border tracings. For volume calculation, area-length and disk summation (Simpson's) methods are used, the latter being more accurate. However, volumes are underestimated by 2D echocardiography [46], when compared to 3D echocardiography [47] and cardiac MRI [34]. Cardiac computed tomography may also be used, but RV volumes tend to be overestimated using this imaging technique [48], while cardiac MRI remains the gold standard for RV assessment, although it was shown to correlate very well with real-time 3D echocardiography measurements [11]. These imaging techniques are often unavailable in most centres, rendering 2D echocardiography quite important, despite its downfalls. A complete 2D echocardiography examination should include area and volume assessment, as well as several derived parameters (Table 5), such as right ventricle fractional area change (RVFAC) and the RVEF, tricuspid annular plane systolic excursion (TAPSE), systolic velocity of the myocardium (St wave) and right ventricular myocardial performance index (RVMPI).


**Table 5.** Reference limits and partition values of right ventricular systolic function as measured in the apical 4 chamber view

#### **a.** Right ventricle fractional area change

The RVFAC is estimated using the formula: (end-diastolic area – end-systolic area)/enddiastolic area x 100, with a lower reference value for normal RV systolic function of 35% [23] and was previously proved to diminish in primary pulmonary hypertension patients, when compared to healthy controls [49] (Figure 5). Normal RVFAC and partition values [30] are shown in Table 5. In one study, RVFAC was found to be an independent predictor of heart failure, stroke and higher mortality in patients with prior myocardial infarction [50].

**Figure 5.** Measurement of the right ventricular fractional area change (RVFAC), views for right ventricle chamber.

require special equipment and is valuable when assessing RV function after myocardial infarction, but does present with some downfalls, particularly due to the fact that it only reflects the basal segment function, ignoring other regions. Moreover, it is angle and load dependant. However, some studies have shown that it correlates well with RVFAC and Simpson's method derived RVEF [35, 54], as well as ventriculography derived RVEF [24] and that it is highly reliable as a prognostic tool in pulmonary hypertension [52, 55], heart failure [24] and dilated

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**Figure 6.** Measurement of the right ventricular ejection fraction (RVEF), views for right ventricle chamber.

Some level of correspondence has been demonstrated between TAPSE (in mm) and RVEF; a TAPSE of 5 mm corresponds to a 20% RVEF, 10 mm to a 30% RVEF, 15 mm to 40%, 20 mm to

Tissue Doppler imaging's (TDI) may be used to obtain other indices of RV performance such as the St wave, the isovolumic contraction velocity and the derived myocardial acceleration (Figure 8) during isovolumic contraction. All these parameters are quite independent of anatomical properties and do not rely on any geometrical assumptions, but may be influenced by load conditions. As they are angle dependent, Doppler beam alignment should be optimal. The isovolumic contraction velocity is measured using either pulsed or colour-coded TDI with sample volume placement on the RV free wall at the level of the tricuspid annulus. The isovolumic contraction phase starts immediately after the A' wave corresponding to ventric‐ ular filling during atrial systole and precedes the St wave which describes ventricle wall movement during the ejection phase. In one study, the isovolumic contraction velocity was shown to correlate very well with mean RA pressure and proved to have 100% sensitivity and

cardiomyopathy, oblivious of the ischemic or non-ischemic aetiology [52].

50% [56].

**d.** Tissue Doppler analysis

78% specificity for a cut-off value <6 cm/s [57-58].

**b.** Right ventricular ejection fraction

The RVEF is derived using the formula: (end-diastolic volume – end-systolic volume)/enddiastolic volume, for which the minimal normal value was established at 44% (Figure 6). Although RVEF measurement by echocardiography is impaired by geometrical assumptions, difficult endocardial border tracing and the fact that the RVOT is not included in area and volume assessment, it is still a valuable parameter, as some studies showed that RVEF is a strong and independent predictor of mortality in heart failure [51-52]. Both RVFAC and RVEF were proved to significantly correlate with other RV function parameters such as the myocar‐ dial performance index [53]. As mentioned above, the RV systolic function is dependent on the LV function and can be altered in the presence of interventricular septum movement abnormalities. The LV systolic function is mostly determined by the radial contraction, while the thin RV free wall systolic movement is predominantly determined by longitudinal shortening.

**c.** Tricuspid annular plane systolic excursion

To assess RV free wall systolic shortening, the TAPSE is measured. This parameter is assessed using the apex-4-chamber view and the M-mode; the cursor is placed at the level of the tricuspid annular plane, allowing the examiner to assess the base to apex motion of the annular plane during systole (Figure 7). The minimal reference threshold has been established at 16 mm (normal values ranging around 22 ± 4 mm) and it is inferred that higher TAPSE values correspond to a better systolic function. TAPSE is easy to measure, reproducible, does not Right Chambers Quantification in Clinical Practice: Echocardiography Compared with Cardiac Magnetic Resonance Imaging http://dx.doi.org/10.5772/55832 23

**Figure 6.** Measurement of the right ventricular ejection fraction (RVEF), views for right ventricle chamber.

require special equipment and is valuable when assessing RV function after myocardial infarction, but does present with some downfalls, particularly due to the fact that it only reflects the basal segment function, ignoring other regions. Moreover, it is angle and load dependant. However, some studies have shown that it correlates well with RVFAC and Simpson's method derived RVEF [35, 54], as well as ventriculography derived RVEF [24] and that it is highly reliable as a prognostic tool in pulmonary hypertension [52, 55], heart failure [24] and dilated cardiomyopathy, oblivious of the ischemic or non-ischemic aetiology [52].

Some level of correspondence has been demonstrated between TAPSE (in mm) and RVEF; a TAPSE of 5 mm corresponds to a 20% RVEF, 10 mm to a 30% RVEF, 15 mm to 40%, 20 mm to 50% [56].

**d.** Tissue Doppler analysis

shown in Table 5. In one study, RVFAC was found to be an independent predictor of heart

failure, stroke and higher mortality in patients with prior myocardial infarction [50].

**Figure 5.** Measurement of the right ventricular fractional area change (RVFAC), views for right ventricle chamber.

The RVEF is derived using the formula: (end-diastolic volume – end-systolic volume)/enddiastolic volume, for which the minimal normal value was established at 44% (Figure 6). Although RVEF measurement by echocardiography is impaired by geometrical assumptions, difficult endocardial border tracing and the fact that the RVOT is not included in area and volume assessment, it is still a valuable parameter, as some studies showed that RVEF is a strong and independent predictor of mortality in heart failure [51-52]. Both RVFAC and RVEF were proved to significantly correlate with other RV function parameters such as the myocar‐ dial performance index [53]. As mentioned above, the RV systolic function is dependent on the LV function and can be altered in the presence of interventricular septum movement abnormalities. The LV systolic function is mostly determined by the radial contraction, while the thin RV free wall systolic movement is predominantly determined by longitudinal

To assess RV free wall systolic shortening, the TAPSE is measured. This parameter is assessed using the apex-4-chamber view and the M-mode; the cursor is placed at the level of the tricuspid annular plane, allowing the examiner to assess the base to apex motion of the annular plane during systole (Figure 7). The minimal reference threshold has been established at 16 mm (normal values ranging around 22 ± 4 mm) and it is inferred that higher TAPSE values correspond to a better systolic function. TAPSE is easy to measure, reproducible, does not

**b.** Right ventricular ejection fraction

22 Hot Topics in Echocardiography

**c.** Tricuspid annular plane systolic excursion

shortening.

Tissue Doppler imaging's (TDI) may be used to obtain other indices of RV performance such as the St wave, the isovolumic contraction velocity and the derived myocardial acceleration (Figure 8) during isovolumic contraction. All these parameters are quite independent of anatomical properties and do not rely on any geometrical assumptions, but may be influenced by load conditions. As they are angle dependent, Doppler beam alignment should be optimal. The isovolumic contraction velocity is measured using either pulsed or colour-coded TDI with sample volume placement on the RV free wall at the level of the tricuspid annulus. The isovolumic contraction phase starts immediately after the A' wave corresponding to ventric‐ ular filling during atrial systole and precedes the St wave which describes ventricle wall movement during the ejection phase. In one study, the isovolumic contraction velocity was shown to correlate very well with mean RA pressure and proved to have 100% sensitivity and 78% specificity for a cut-off value <6 cm/s [57-58].

Vogel et al. conducted a study on pigs, proving that IVA is afterload and preload independent [61], while Hashimoto et al. conducted their research on sheep, proving that IVA correlates very well with peak positive dp/dt measured invasively by right heart catheterization [62]. In humans, studies have shown that IVA was significantly correlated with disease severity in patients with chronic obstructive pulmonary disease [63], obstructive sleep apnoea [64], RV remodelling triggered by type 2 diabetes mellitus [65], and that it may be used for early detection of RV dysfunction in patients with mitral stenosis [66] or systemic sclerosis, even before the onset of pulmonary hypertension [67]. Moreover, in one study on patients who underwent corrective surgery for transposition of the great arteries, IVA was proved to be superior to the peak systolic myocardial velocity in assessing the reduction of functional

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TDI may also be used for measuring the highest St wave. This parameter is obtained from the apical four chamber view by positioning the sample volume either at the level of the tricuspid annulus, on the lateral wall, or in the middle or apical segments segment. The latter locations are, however, avoided by most physicians as adequate signals are rarely obtained and measurements are less reproducible, with greater interobserver variability [58]. St may be measured using pulsed tissue or colour coded TDI, and is, as other TDI parameters, angle dependent, but less influenced by loading conditions or RV anatomy when compared to other systolic function parameters. Mean annular velocities have been established at 8.5 – 10 cm/s, while basal free wall velocities are slightly higher at 9.3 – 11 cm/s [23], with lower velocities in elderly subjects due to the increased stiffness of the myocardium [60, 69, 70]. The main limitation of this parameter is determined by the fact that it only reflects changes in systolic movement of the basal segment which are extrapolated as descriptive for the systolic function of the entire RV. This type of measurement may sometimes be inaccurate in the presence of segmental RV systolic dysfunction which may occur in some clinical conditions such as RV myocardial infarction, ARVD or pulmonary embolism. A St value under 10 cm/s should rise suspicion of RV dysfunction, especially in young subjects, although a minimum reference value was established at 6 cm/s by pooled data from several studies [23]. In one research, a St value of <12 cm/s showed high sensitivity (81%), specificity (82%) and negative predictive value (92%) for the diagnosis of RV myocardial infarction [71], while Meluzin et al. demon‐ strated it was significantly correlated with RVEF and that a value <11.5 cm/s predicted RV systolic dysfunction with 90% sensitivity and 85% specificity in patients with heart failure [72]. Also, St was also shown to be lower, as expected, in patients with systemic sclerosis [67].

Both the systolic and diastolic functions of the RV may be evaluated using the myocardial performance index, also known as RVMPI or Tei index. This index can be obtained either by pulsed Doppler or TDI and is defined by the ratio of isovolumic time/ejection time. The ejection time is assessed by placing the pulsed Doppler cursor at the level of the RVOT and is measured from the onset to the cessation of the systolic pulmonary artery flow. When the pulsed Doppler cursor is placed at the level of the tricuspid annulus, the time from the cessation of the A wave to the onset of the next E wave is measured and the difference between this interval and the ejection time signifies the total isovolumic time (isovolumic resting time + isovolumic con‐

reserve, in both the RV and LV [68].

**e.** Right ventricular myocardial performance index

**Figure 7.** Measurement of the tricuspid annular plane systolic excursion (TAPSE) in normal and pulmonary artery hy‐ pertension individual, in the four chamber view a straight line (M mode) is drawn through the lateral tricuspid valve annulus.

**Figure 8.** Pulsed wave tissue Doppler with the sample placed at the level of the tricuspid annulus of the RV free wall, demonstrating peak systolic velocity (St), and myocardial acceleration during isovolumic contraction (IVA).

This parameter may further be used to derive the myocardial acceleration during isovolumic contraction (IVA) which is calculated as the peak isovolumic contraction velocity divided by the time to peak velocity. Myocardial acceleration during isovolumic contraction may be measured either by pulsed-wave TDI or colour-coded TDI, but normal values seem to be different; in one study, values proved to be up to 20% higher when assessed by pulsed-wave TDI, by comparison with colour-coded TDI evaluation [23] [59]. In addition to that, normal values vary with age [60] and heart rate. For tissue Doppler assessment, pooled data from 10 studies established a lower reference value of 2.2 m/s [23]. IVA was studied on several animal models which lead to significant conclusions which may be implemented in every day practice. Vogel et al. conducted a study on pigs, proving that IVA is afterload and preload independent [61], while Hashimoto et al. conducted their research on sheep, proving that IVA correlates very well with peak positive dp/dt measured invasively by right heart catheterization [62]. In humans, studies have shown that IVA was significantly correlated with disease severity in patients with chronic obstructive pulmonary disease [63], obstructive sleep apnoea [64], RV remodelling triggered by type 2 diabetes mellitus [65], and that it may be used for early detection of RV dysfunction in patients with mitral stenosis [66] or systemic sclerosis, even before the onset of pulmonary hypertension [67]. Moreover, in one study on patients who underwent corrective surgery for transposition of the great arteries, IVA was proved to be superior to the peak systolic myocardial velocity in assessing the reduction of functional reserve, in both the RV and LV [68].

TDI may also be used for measuring the highest St wave. This parameter is obtained from the apical four chamber view by positioning the sample volume either at the level of the tricuspid annulus, on the lateral wall, or in the middle or apical segments segment. The latter locations are, however, avoided by most physicians as adequate signals are rarely obtained and measurements are less reproducible, with greater interobserver variability [58]. St may be measured using pulsed tissue or colour coded TDI, and is, as other TDI parameters, angle dependent, but less influenced by loading conditions or RV anatomy when compared to other systolic function parameters. Mean annular velocities have been established at 8.5 – 10 cm/s, while basal free wall velocities are slightly higher at 9.3 – 11 cm/s [23], with lower velocities in elderly subjects due to the increased stiffness of the myocardium [60, 69, 70]. The main limitation of this parameter is determined by the fact that it only reflects changes in systolic movement of the basal segment which are extrapolated as descriptive for the systolic function of the entire RV. This type of measurement may sometimes be inaccurate in the presence of segmental RV systolic dysfunction which may occur in some clinical conditions such as RV myocardial infarction, ARVD or pulmonary embolism. A St value under 10 cm/s should rise suspicion of RV dysfunction, especially in young subjects, although a minimum reference value was established at 6 cm/s by pooled data from several studies [23]. In one research, a St value of <12 cm/s showed high sensitivity (81%), specificity (82%) and negative predictive value (92%) for the diagnosis of RV myocardial infarction [71], while Meluzin et al. demon‐ strated it was significantly correlated with RVEF and that a value <11.5 cm/s predicted RV systolic dysfunction with 90% sensitivity and 85% specificity in patients with heart failure [72]. Also, St was also shown to be lower, as expected, in patients with systemic sclerosis [67].

#### **e.** Right ventricular myocardial performance index

**Figure 8.** Pulsed wave tissue Doppler with the sample placed at the level of the tricuspid annulus of the RV free wall,

**Figure 7.** Measurement of the tricuspid annular plane systolic excursion (TAPSE) in normal and pulmonary artery hy‐ pertension individual, in the four chamber view a straight line (M mode) is drawn through the lateral tricuspid valve

annulus.

24 Hot Topics in Echocardiography

This parameter may further be used to derive the myocardial acceleration during isovolumic contraction (IVA) which is calculated as the peak isovolumic contraction velocity divided by the time to peak velocity. Myocardial acceleration during isovolumic contraction may be measured either by pulsed-wave TDI or colour-coded TDI, but normal values seem to be different; in one study, values proved to be up to 20% higher when assessed by pulsed-wave TDI, by comparison with colour-coded TDI evaluation [23] [59]. In addition to that, normal values vary with age [60] and heart rate. For tissue Doppler assessment, pooled data from 10 studies established a lower reference value of 2.2 m/s [23]. IVA was studied on several animal models which lead to significant conclusions which may be implemented in every day practice.

demonstrating peak systolic velocity (St), and myocardial acceleration during isovolumic contraction (IVA).

Both the systolic and diastolic functions of the RV may be evaluated using the myocardial performance index, also known as RVMPI or Tei index. This index can be obtained either by pulsed Doppler or TDI and is defined by the ratio of isovolumic time/ejection time. The ejection time is assessed by placing the pulsed Doppler cursor at the level of the RVOT and is measured from the onset to the cessation of the systolic pulmonary artery flow. When the pulsed Doppler cursor is placed at the level of the tricuspid annulus, the time from the cessation of the A wave to the onset of the next E wave is measured and the difference between this interval and the ejection time signifies the total isovolumic time (isovolumic resting time + isovolumic con‐

traction time). These measurements are taken from two different acoustic windows and, implicitly, in different points in time, therefore errors can occur if the RR interval is not regular. Consequently, measurements may only be made if the rhythm is regular and are not feasible in case of atrial fibrillation. When using the TDI method, measurements are taken during a single heart beat, by placing the cursor at the level of the tricuspid annulus (Figure 9). The isovolumic contraction time (IVCT) is measured from the cessation of the At wave to the beginning of the St wave, the ejection time (ET) – from the onset to the cessation of the St wave, and the isovolumic relaxation time (IVRT) – from the end of the S' wave to the onset of the Et wave. The correlation between the tissue Doppler and pulsed Doppler methods are modest, due to differences in isovolumic times, which lead to higher cut-off points when tissue Doppler is used, as it was shown in studies focused on the LV [73, 74]. Moreover, one recent study showed that LV Tei index assessment by tissue Doppler was better correlated with the LV ejection fraction in patients with heart failure [75]. Similar results were obtained in a study on a paediatric population with congenital heart disease which showed that the TDI derived Tei index values were different from those obtained by pulsed Doppler and that they had additional utility, as they might help differentiate systolic from diastolic dysfunction by providing specific information on the isovolumetric intervals [76]. For the RVMPI, the upper reference limit has been established at 0.40 by the pulsed Doppler method and at 0.55 by the tissue Doppler method [23]. Any values above these thresholds are considered to be patho‐ logical, as stated by Brierre et al. who obtained a mean value of the Tei index of 0.90 in their research on idiopathic pulmonary artery hypertension patients; moreover, they showed that values ≥0.98 were associated with increased mortality [45].

may, however, be limited by using the tissue Doppler method which allows measurement taking during a single heart beat, but results are still unreliable in patients with atrial fibrilla‐ tion. Other disadvantages include load dependency and altered results when RA pressure is

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**Figure 9.** Measurement of right ventricular myocardial performance index (RVMPI) by pulsed wave Doppler of tricus‐ pid regurgitation and tissue Doppler with the sample placed at the level of the tricuspid annulus of the RV free wall.

RV systolic function assessment can also be performed by analyzing the tricuspid regurgitation flow, which is commonly visualized from the apical 4-chamber view. Using continuous-wave Doppler, several parameters can be derived, such as: RV-RA pressure gradient, systolic, diastolic and mean pulmonary artery pressure (sPAP; dPAP; mPAP), the rate of pressure rise in the RV (dp/dt), and the previously described right index of myocardial performance (RVMPI). To this purpose, an optimal parallel alignment of the continuous Doppler cursor to the tricuspid regurgitation (TR) flow should be obtained. The rate of pressure rise in the RV (dp/dt) was first described in 1962 and measured invasively by right heart catheterization. An echocardiographic method based on the Bernoulli equation was developed to serve the same purpose, although it was shown that continuous-wave Doppler analysis of the TR flow significantly underestimated peak RV pressures when compared to invasive measurements [87]. The rate of pressure rise is calculated by measuring the time interval in which the tricuspid flow velocity rises from 1 m/s to 2 m/s (Figure 10). Based on the Bernoulli equation, this rise in velocity corresponds to a pressure elevation of 12 mmHg. Other researchers suggest that dp/dt assessment correlates better with invasive measurements if the studied time interval is focused on a rise in velocity from 0.5 to 2 m/s, which corresponds to a 15 mmHg rise in pressure [88]. The value of dp/dt is expressed in mmHg/sec, but normal reference values have not been established so far; this parameter, although easy to obtain, has limited clinical value, also due to the fact that it is load and angle dependent. However, values <400 mmHg/s are likely to be abnormal [23]. One small study showed that the dp/dt over maximum RV pressure ratio had a significant correlation to the NYHA functional class, while dp/dt by itself had none at all [89].

**f.** Analyzing the tricuspid regurgitation flow

Nowadays, this parameter is of little interest.

elevated, due to artificial IVRT shortening which leads to lower RVMPI values [86].

Up to date, RVMPI was proved to be useful for RV function assessment in several studies. One study on patients with acute RV myocardial infarction showed that the Tei index was valuable for diagnosis, RV function quantification and, interestingly, for acute improve‐ ment assessment [77].

In another research by Blanchard et al. conducted on patients with chronic thromboembolic pulmonary hypertension, RVMPI was shown to be a valuable tool for monitoring disease severity and for assessing outcome after pulmonary thrombo-endarterectomy, and positively correlated with pulmonary vascular resistance, measured by right heart catheterization [78]. Moreover, RVMPI was shown to be a high sensitivity and specificity parameter for diagnostic purposes in patients with acute pulmonary embolism, as well as a valuable tool for assessing the response to efficient anticoagulant therapy [79-81]. In addition to that, Haddad et al. demonstrated that both the RVMPI and the RVFAC may have an incremental prognostic value in terms of mortality and morbidity after valvular heart surgery [82], while others confirmed its utility in assessing global RV function in children with congenital heart disease [83-84]. The Tei index also proved its value in RV function assessment in patients with sleep apnoea, as it was positively correlated with the anoxia-hypoxia index, while RVFAC showed inverse correlation with the same parameter [85].

The echocardiographic evaluation of RV by RVMPI has many advantages, as it is non-invasive, widely available, reproducible and independent of any geometric assumptions. If the pulsed wave Doppler method is used, errors may occur if the RR interval is variable. This downfall may, however, be limited by using the tissue Doppler method which allows measurement taking during a single heart beat, but results are still unreliable in patients with atrial fibrilla‐ tion. Other disadvantages include load dependency and altered results when RA pressure is elevated, due to artificial IVRT shortening which leads to lower RVMPI values [86].

**Figure 9.** Measurement of right ventricular myocardial performance index (RVMPI) by pulsed wave Doppler of tricus‐ pid regurgitation and tissue Doppler with the sample placed at the level of the tricuspid annulus of the RV free wall.

#### **f.** Analyzing the tricuspid regurgitation flow

traction time). These measurements are taken from two different acoustic windows and, implicitly, in different points in time, therefore errors can occur if the RR interval is not regular. Consequently, measurements may only be made if the rhythm is regular and are not feasible in case of atrial fibrillation. When using the TDI method, measurements are taken during a single heart beat, by placing the cursor at the level of the tricuspid annulus (Figure 9). The isovolumic contraction time (IVCT) is measured from the cessation of the At wave to the beginning of the St wave, the ejection time (ET) – from the onset to the cessation of the St wave, and the isovolumic relaxation time (IVRT) – from the end of the S' wave to the onset of the Et wave. The correlation between the tissue Doppler and pulsed Doppler methods are modest, due to differences in isovolumic times, which lead to higher cut-off points when tissue Doppler is used, as it was shown in studies focused on the LV [73, 74]. Moreover, one recent study showed that LV Tei index assessment by tissue Doppler was better correlated with the LV ejection fraction in patients with heart failure [75]. Similar results were obtained in a study on a paediatric population with congenital heart disease which showed that the TDI derived Tei index values were different from those obtained by pulsed Doppler and that they had additional utility, as they might help differentiate systolic from diastolic dysfunction by providing specific information on the isovolumetric intervals [76]. For the RVMPI, the upper reference limit has been established at 0.40 by the pulsed Doppler method and at 0.55 by the tissue Doppler method [23]. Any values above these thresholds are considered to be patho‐ logical, as stated by Brierre et al. who obtained a mean value of the Tei index of 0.90 in their research on idiopathic pulmonary artery hypertension patients; moreover, they showed that

Up to date, RVMPI was proved to be useful for RV function assessment in several studies. One study on patients with acute RV myocardial infarction showed that the Tei index was valuable for diagnosis, RV function quantification and, interestingly, for acute improve‐

In another research by Blanchard et al. conducted on patients with chronic thromboembolic pulmonary hypertension, RVMPI was shown to be a valuable tool for monitoring disease severity and for assessing outcome after pulmonary thrombo-endarterectomy, and positively correlated with pulmonary vascular resistance, measured by right heart catheterization [78]. Moreover, RVMPI was shown to be a high sensitivity and specificity parameter for diagnostic purposes in patients with acute pulmonary embolism, as well as a valuable tool for assessing the response to efficient anticoagulant therapy [79-81]. In addition to that, Haddad et al. demonstrated that both the RVMPI and the RVFAC may have an incremental prognostic value in terms of mortality and morbidity after valvular heart surgery [82], while others confirmed its utility in assessing global RV function in children with congenital heart disease [83-84]. The Tei index also proved its value in RV function assessment in patients with sleep apnoea, as it was positively correlated with the anoxia-hypoxia index, while RVFAC showed inverse

The echocardiographic evaluation of RV by RVMPI has many advantages, as it is non-invasive, widely available, reproducible and independent of any geometric assumptions. If the pulsed wave Doppler method is used, errors may occur if the RR interval is variable. This downfall

values ≥0.98 were associated with increased mortality [45].

ment assessment [77].

26 Hot Topics in Echocardiography

correlation with the same parameter [85].

RV systolic function assessment can also be performed by analyzing the tricuspid regurgitation flow, which is commonly visualized from the apical 4-chamber view. Using continuous-wave Doppler, several parameters can be derived, such as: RV-RA pressure gradient, systolic, diastolic and mean pulmonary artery pressure (sPAP; dPAP; mPAP), the rate of pressure rise in the RV (dp/dt), and the previously described right index of myocardial performance (RVMPI). To this purpose, an optimal parallel alignment of the continuous Doppler cursor to the tricuspid regurgitation (TR) flow should be obtained. The rate of pressure rise in the RV (dp/dt) was first described in 1962 and measured invasively by right heart catheterization. An echocardiographic method based on the Bernoulli equation was developed to serve the same purpose, although it was shown that continuous-wave Doppler analysis of the TR flow significantly underestimated peak RV pressures when compared to invasive measurements [87]. The rate of pressure rise is calculated by measuring the time interval in which the tricuspid flow velocity rises from 1 m/s to 2 m/s (Figure 10). Based on the Bernoulli equation, this rise in velocity corresponds to a pressure elevation of 12 mmHg. Other researchers suggest that dp/dt assessment correlates better with invasive measurements if the studied time interval is focused on a rise in velocity from 0.5 to 2 m/s, which corresponds to a 15 mmHg rise in pressure [88]. The value of dp/dt is expressed in mmHg/sec, but normal reference values have not been established so far; this parameter, although easy to obtain, has limited clinical value, also due to the fact that it is load and angle dependent. However, values <400 mmHg/s are likely to be abnormal [23]. One small study showed that the dp/dt over maximum RV pressure ratio had a significant correlation to the NYHA functional class, while dp/dt by itself had none at all [89]. Nowadays, this parameter is of little interest.

The severity of pulmonary hypertension may be underestimated in the presence of severe tricuspid regurgitation that leads to elevated RA pressure and, consequently, to a lesser RV-

Right Chambers Quantification in Clinical Practice: Echocardiography Compared with Cardiac Magnetic Resonance

2.9 – 3.4 m/s 37 – 50 mmHg +/-

\* dilated right chambers; increased thickness of the RV free wall; abnormal shape and function of the interventricular septum; dilated pulmonary artery; increased velocity of the pulmonary regurgitation jet; short acceleration time of RV

**Table 6.** Arbitrary criteria for the presence of pulmonary hypertension based on continuous Doppler derived systolic

Like the sPAP, the dPAP can be derived by applying the Bernoulli equation to the pulmonary regurgitationflow:dPAP=4 x (end-diastolic regurgitantvelocity)2 +RApressure.Thepulmona‐ ry regurgitation flow may also be used to calculate the mPAP pressure after the same princi‐ ple, by the formula mPAP= (4 x early PR velocity) + RA pressure, or by adding RA pressure to the velocity time integral (VTI) of the tricuspid regurgitation, the latter method being the most accurate, as it correlates better to invasive measurements by right heart catheterization [93, 94]. Previous methods relied on more vague estimations, based on the sPAP and dPAP: mPAP= 1/3 sPAP + 2/3 dPAP, or obtained by analysing the pulmonary artery continuous wave Doppler

The AT is measured from the onset of the pulmonary flow, which corresponds to the onset of the QRS complex on the ECG, to the onset of the maximum pulmonary velocity; consequently, the shorter the AT, the higher the mPAP. This formula applies when the heart rate is between 60 and 100 bpm, and the AT is below 120 msec. A study showed, however, that, in case of aggravated pulmonary hypertension, when AT shortens below this threshold, the formula mPAP= 90 – (0.62 x AT) led to more accurate results [95]. Despite the technical progress and reasonable mathematical and physical assumptions, right chamber and pulmonary pressure assessment by echocardiography is not sufficient for diagnosing pulmonary hypertension. In pulmonary artery hypertensive patients, right heart catheterisation remains the golden standard [94], as it is needed to confirm the diagnosis, to assess severity and to test for vessel reactivity if specific therapy is considered [90]. Several studies have shown that sPAP is considerably underestimated by echocardiography when compared to right heart catheteri‐ zation, oblivious of the used method [96-98]. However, despite all the limitations, the assess‐ ment of pulmonary artery pressures by echocardiography can be used as a screening method

**TR maximum velocity PAPs Other echo parameters**

**suggesting HTP\***

http://dx.doi.org/10.5772/55832

Imaging

29

RA pressure gradient and lower sPAP (Table 6).

PH unlikely ≤ 2.8 m/s ≤ 36 mmHg

PH likely >3.4 m/s >50 mmHg

ejection in the pulmonary artery; PH - pulmonary hypertension

for pulmonary hypertension [90, 94].

**g.** Regional RV Strain and Strain Rate

PH possible ≤ 2.8 m/s ≤ 36 mmHg +

pulmonary artery pressure (sPAP) and tricuspid regurgitation (TR) jet maximum velocity [90].

flow, using the formula mPAP= 79 – (0.45 x AT) (AT= acceleration time) [95].

**Figure 10.** Measurement of the rate of pressure rise in the ventricles (dp/dt) of tricuspid regurgitation in the four chamber view in pulmonary artery hypertension individual.

The RV-RA pressure gradient may also be estimated using the peak velocity of the TR flow based on the simplified Bernoulli equation: peak pressure gradient of TR= 4 x (TR maximum velocity)2 . As it is angle dependant, the best possible alignment of the continuous-wave Doppler cursor with the regurgitation jet should be obtained and several measurements, from several acoustic windows (most often, apical 4 chamber view and parasternal RV inflow view), should be taken (Figure 11). The signal with the highest velocity and density should be used; the Doppler signal may be enhanced by injecting agitated saline into the venous flow. Moreover, special attention is necessary to exclude RVOT obstruction, which often occurs in congenital heart disease. sPAP is then calculated by adding the estimated RA pressure (assessed by IVC diameter and its inbreathe variations, as described above) to the RV-RA gradient.

**Figure 11.** Doppler echocardiographic determination of systolic pulmonary artery pressure (sPAP).

A tricuspid regurgitation jet maximum velocity of ≤ 2.8 m/s renders pulmonary hypertension unlikely, a velocity of >3.4 m/s – likely, while values between 2.8 m/s and 3.4 m/s indicate that pulmonary hypertension is possible [90-91]. Normal resting values have been established at ≤36 mmHg for peak systolic pressure, assuming a RA pressure of 3-5 mmHg [23, 92].

The severity of pulmonary hypertension may be underestimated in the presence of severe tricuspid regurgitation that leads to elevated RA pressure and, consequently, to a lesser RV-RA pressure gradient and lower sPAP (Table 6).


\* dilated right chambers; increased thickness of the RV free wall; abnormal shape and function of the interventricular septum; dilated pulmonary artery; increased velocity of the pulmonary regurgitation jet; short acceleration time of RV ejection in the pulmonary artery; PH - pulmonary hypertension

**Table 6.** Arbitrary criteria for the presence of pulmonary hypertension based on continuous Doppler derived systolic pulmonary artery pressure (sPAP) and tricuspid regurgitation (TR) jet maximum velocity [90].

Like the sPAP, the dPAP can be derived by applying the Bernoulli equation to the pulmonary regurgitationflow:dPAP=4 x (end-diastolic regurgitantvelocity)2 +RApressure.Thepulmona‐ ry regurgitation flow may also be used to calculate the mPAP pressure after the same princi‐ ple, by the formula mPAP= (4 x early PR velocity) + RA pressure, or by adding RA pressure to the velocity time integral (VTI) of the tricuspid regurgitation, the latter method being the most accurate, as it correlates better to invasive measurements by right heart catheterization [93, 94]. Previous methods relied on more vague estimations, based on the sPAP and dPAP: mPAP= 1/3 sPAP + 2/3 dPAP, or obtained by analysing the pulmonary artery continuous wave Doppler flow, using the formula mPAP= 79 – (0.45 x AT) (AT= acceleration time) [95].

The AT is measured from the onset of the pulmonary flow, which corresponds to the onset of the QRS complex on the ECG, to the onset of the maximum pulmonary velocity; consequently, the shorter the AT, the higher the mPAP. This formula applies when the heart rate is between 60 and 100 bpm, and the AT is below 120 msec. A study showed, however, that, in case of aggravated pulmonary hypertension, when AT shortens below this threshold, the formula mPAP= 90 – (0.62 x AT) led to more accurate results [95]. Despite the technical progress and reasonable mathematical and physical assumptions, right chamber and pulmonary pressure assessment by echocardiography is not sufficient for diagnosing pulmonary hypertension. In pulmonary artery hypertensive patients, right heart catheterisation remains the golden standard [94], as it is needed to confirm the diagnosis, to assess severity and to test for vessel reactivity if specific therapy is considered [90]. Several studies have shown that sPAP is considerably underestimated by echocardiography when compared to right heart catheteri‐ zation, oblivious of the used method [96-98]. However, despite all the limitations, the assess‐ ment of pulmonary artery pressures by echocardiography can be used as a screening method for pulmonary hypertension [90, 94].

**g.** Regional RV Strain and Strain Rate

8

28 Hot Topics in Echocardiography

velocity)2

gradient.

chamber view in pulmonary artery hypertension individual.

**Figure 10.** Measurement of the rate of pressure rise in the ventricles (dp/dt) of tricuspid regurgitation in the four

The RV-RA pressure gradient may also be estimated using the peak velocity of the TR flow based on the simplified Bernoulli equation: peak pressure gradient of TR= 4 x (TR maximum

Doppler cursor with the regurgitation jet should be obtained and several measurements, from several acoustic windows (most often, apical 4 chamber view and parasternal RV inflow view), should be taken (Figure 11). The signal with the highest velocity and density should be used; the Doppler signal may be enhanced by injecting agitated saline into the venous flow. Moreover, special attention is necessary to exclude RVOT obstruction, which often occurs in congenital heart disease. sPAP is then calculated by adding the estimated RA pressure (assessed by IVC diameter and its inbreathe variations, as described above) to the RV-RA

**Figure 11.** Doppler echocardiographic determination of systolic pulmonary artery pressure (sPAP).

A tricuspid regurgitation jet maximum velocity of ≤ 2.8 m/s renders pulmonary hypertension unlikely, a velocity of >3.4 m/s – likely, while values between 2.8 m/s and 3.4 m/s indicate that pulmonary hypertension is possible [90-91]. Normal resting values have been established at

≤36 mmHg for peak systolic pressure, assuming a RA pressure of 3-5 mmHg [23, 92].

. As it is angle dependant, the best possible alignment of the continuous-wave

negatively with 2D-derived pulmonary arterial systolic pressure and positively with TAPSE, the peak systolic velocity, and the fractional shortening area [32]. In one study, patients with mitral valve prolapse who underwent surgical treatment had significantly lower TAPSE and peak systolic velocities of the tricuspid annulus after surgery, while 3D-derived RVEF remained the same (58.4 ± 4%) [32]. Moreover, 3D echocardiography analysis was used to describe RV systolic function in patients with various cardiovascular disorders, showing that patients with pulmonary hypertension had the largest RV volumes and RVEF, while those with idiopathic dilated cardiomyopathy had considerably lower RVEF when compared to

Right Chambers Quantification in Clinical Practice: Echocardiography Compared with Cardiac Magnetic Resonance

Imaging

31

http://dx.doi.org/10.5772/55832

In another study, normal RVEF reference values were established at 38.0% to 65.3% for women

Nowadays, cardiac MRI is considered to be the gold standard for determining RV volume and function [11]. This method should be taken into account when 3D echocardiography is not

Cardiac MRI requires a minimum 1.5 Tesla scanner, with a phased-array cardiac coil. Cine imaging acquired 2-chamber and 4-chamber views allow the positing of a retrospectively ECGgated steady-state free procession pulse sequence using following parameters: repetition time 3.5–4.2 ms, echo time 1.5–1.8 ms, flip-angle 45°, matrix 256 × 256, field of view 250–350 mm, slice thickness 5–8 mm with a gap of 0–2 mm depending on body size; 12 slices should be acquired [10]. Cardiac MRI allows an accurate delineation of the endocardial and epicardial borders in all planes and all cardiac phases; in addition to that, the systolic descent and twist of the tricuspid valve is quantified by tracking of the valve motion on the long-axis cines in order to correct for loss of systolic RV volume due to AV ring descent; thirdly, papillary muscles are delineated, with blood pool thresholding. This technique allows the calculus of RV end-systolic and end-diastolic volumes, RV ejection fraction and right ventricular mass with a great degree of precision [103-104]. Cardiac MRI allows a complete assessment of the RV inflow and outflow, regardless of ventricular size or shape. The extent of myocardial

Several reference values for RV volumes have been mentioned, with significant gender differences; consequently, larger RV volumes were documented in males when compared to females: RV end-diastolic volume 190 ± 33 mL vs. 148 ± 35 mL, RV end-systolic volume 78 ± 20 mL vs. 56 ± 18 mL [105]. Other values were obtained in another study, which compared MRI-derived volumes against 3D echocardiography volumes, proving the former were larger. The following mean normal values were established for RV end-diastolic, end-systolic, and stroke volumes: 134.2 ± 39.2 mL vs. 124.0 ± 34.4 mL; 69.7 ± 25.5 mL vs. 65.2 ± 23.5 mL; and 64.5

damage or fibrosis is evaluated using late gadolinium enhancement.

patients with valvular heart disease [32].

**3.2. Cardiac magnetic resonance imaging**

**a.** Acquisition and measurements:

and 29.9% to 58.4% for men [34].

sufficient for evaluation.

**b.** Qualitative values:

± 24.1 mL vs. 58.8 ± 18.4 mL [106].

**Figure 12.** Measurement of global right ventricular deformation by speckle-tracking with the sample placed at the level of the RV free wall in normal and pulmonary artery hypertension individual.

Strain and strain rate (SR) imaging can provide valuable data on the relative deformation of myocardial segments under stress. The resting length of the myocardium (L0) changes when submitted to a certain force (L1). Myocardial strain is best described by the L1-L0/L0 ratio, expressed in a certain percentage, which is negative when shortening occurs and positive when the myocardium lengthens. The SR can be derived using strain and the velocity of myocardial deformation, expressed in 1/s. The particular anatomy of the RV, which is mainly composed of longitudinal and oblique fibres, renders it highly susceptible to strain variations at lower stress whencomparedtotheLV[99].Rightmyocardialvelocities are,thusly,higherthanintheLVand more elevated at the apex, when compared to the base, even in normal individuals [99].

TDI-derived and speckle-tracking echocardiography-derived strain and SR can be used to assess RV dynamics and were found to be both feasible and roughly comparable. Strain and SR correlate well with radionuclide RVEF [24].

Normal strain is 19 ± 6 % in the basal RV free wall, 27 ± 6 %, in the median and 32 ± 6 % at the apex for the prediction of RVEF >50% [100]. This renders strain assessment of the RV quite strenuous, with important limitations due to the need of perfect alignment of the TDI cursor to the rather thin free wall of the RV. In addition to that, strain analysis is highly dependent on hemodynamic variations [101]. In patients with RV disease or dysfunction, peak systolic strain and SR are significantly reduced and delayed compared with individuals with normal RV function [24].

RV speckle-tracking is less challenging in terms of angle issues, provided that optimal endocardial border tracking is performed [102]. In 2D speckle-tracking analysis, a certain selected zone is studied in motion, allowing a good assessment of the longitudinal, radial and torsion movements of the RV (Figure 12); however, this method is limited by a low temporal resolution [102].

**h.** 3D echocardiography

3D echocardiography may also be used to assess right ventricle systolic and diastolic functions. It has been previously demonstrated that 3D echocardiography-derived RVEF correlated negatively with 2D-derived pulmonary arterial systolic pressure and positively with TAPSE, the peak systolic velocity, and the fractional shortening area [32]. In one study, patients with mitral valve prolapse who underwent surgical treatment had significantly lower TAPSE and peak systolic velocities of the tricuspid annulus after surgery, while 3D-derived RVEF remained the same (58.4 ± 4%) [32]. Moreover, 3D echocardiography analysis was used to describe RV systolic function in patients with various cardiovascular disorders, showing that patients with pulmonary hypertension had the largest RV volumes and RVEF, while those with idiopathic dilated cardiomyopathy had considerably lower RVEF when compared to patients with valvular heart disease [32].

In another study, normal RVEF reference values were established at 38.0% to 65.3% for women and 29.9% to 58.4% for men [34].

#### **3.2. Cardiac magnetic resonance imaging**

Nowadays, cardiac MRI is considered to be the gold standard for determining RV volume and function [11]. This method should be taken into account when 3D echocardiography is not sufficient for evaluation.

**a.** Acquisition and measurements:

Strain and strain rate (SR) imaging can provide valuable data on the relative deformation of myocardial segments under stress. The resting length of the myocardium (L0) changes when submitted to a certain force (L1). Myocardial strain is best described by the L1-L0/L0 ratio, expressed in a certain percentage, which is negative when shortening occurs and positive when the myocardium lengthens. The SR can be derived using strain and the velocity of myocardial deformation, expressed in 1/s. The particular anatomy of the RV, which is mainly composed of longitudinal and oblique fibres, renders it highly susceptible to strain variations at lower stress whencomparedtotheLV[99].Rightmyocardialvelocities are,thusly,higherthanintheLVand more elevated at the apex, when compared to the base, even in normal individuals [99].

**Figure 12.** Measurement of global right ventricular deformation by speckle-tracking with the sample placed at the

level of the RV free wall in normal and pulmonary artery hypertension individual.

TDI-derived and speckle-tracking echocardiography-derived strain and SR can be used to assess RV dynamics and were found to be both feasible and roughly comparable. Strain and

Normal strain is 19 ± 6 % in the basal RV free wall, 27 ± 6 %, in the median and 32 ± 6 % at the apex for the prediction of RVEF >50% [100]. This renders strain assessment of the RV quite strenuous, with important limitations due to the need of perfect alignment of the TDI cursor to the rather thin free wall of the RV. In addition to that, strain analysis is highly dependent on hemodynamic variations [101]. In patients with RV disease or dysfunction, peak systolic strain and SR are significantly reduced and delayed compared with individuals with normal

RV speckle-tracking is less challenging in terms of angle issues, provided that optimal endocardial border tracking is performed [102]. In 2D speckle-tracking analysis, a certain selected zone is studied in motion, allowing a good assessment of the longitudinal, radial and torsion movements of the RV (Figure 12); however, this method is limited by a low temporal

3D echocardiography may also be used to assess right ventricle systolic and diastolic functions. It has been previously demonstrated that 3D echocardiography-derived RVEF correlated

SR correlate well with radionuclide RVEF [24].

RV function [24].

30 Hot Topics in Echocardiography

resolution [102].

**h.** 3D echocardiography

Cardiac MRI requires a minimum 1.5 Tesla scanner, with a phased-array cardiac coil. Cine imaging acquired 2-chamber and 4-chamber views allow the positing of a retrospectively ECGgated steady-state free procession pulse sequence using following parameters: repetition time 3.5–4.2 ms, echo time 1.5–1.8 ms, flip-angle 45°, matrix 256 × 256, field of view 250–350 mm, slice thickness 5–8 mm with a gap of 0–2 mm depending on body size; 12 slices should be acquired [10]. Cardiac MRI allows an accurate delineation of the endocardial and epicardial borders in all planes and all cardiac phases; in addition to that, the systolic descent and twist of the tricuspid valve is quantified by tracking of the valve motion on the long-axis cines in order to correct for loss of systolic RV volume due to AV ring descent; thirdly, papillary muscles are delineated, with blood pool thresholding. This technique allows the calculus of RV end-systolic and end-diastolic volumes, RV ejection fraction and right ventricular mass with a great degree of precision [103-104]. Cardiac MRI allows a complete assessment of the RV inflow and outflow, regardless of ventricular size or shape. The extent of myocardial damage or fibrosis is evaluated using late gadolinium enhancement.

**b.** Qualitative values:

Several reference values for RV volumes have been mentioned, with significant gender differences; consequently, larger RV volumes were documented in males when compared to females: RV end-diastolic volume 190 ± 33 mL vs. 148 ± 35 mL, RV end-systolic volume 78 ± 20 mL vs. 56 ± 18 mL [105]. Other values were obtained in another study, which compared MRI-derived volumes against 3D echocardiography volumes, proving the former were larger. The following mean normal values were established for RV end-diastolic, end-systolic, and stroke volumes: 134.2 ± 39.2 mL vs. 124.0 ± 34.4 mL; 69.7 ± 25.5 mL vs. 65.2 ± 23.5 mL; and 64.5 ± 24.1 mL vs. 58.8 ± 18.4 mL [106].

**Figure 13.** Cardiac MRI steady-state free procession sequence for the assessment of right ventricular function en-dia‐ stolic and en-systolic. RV=right ventricle; LV=left ventricle.

#### **c.** Clinical Application

The efficiency of 3D echocardiography vs. cardiac MRI in RV assessment was compared in many studies. One research group conducted a study on 60 pulmonary artery hypertensive patients [4], proving that 3D echocardiography had some advantages over cardiac MRI, as it could be routinely used for serial imaging and at the bedside. Moreover, it was previously shown that both 3D echocardiography and cardiac MRI may be used to assess RV remodeling in pulmonary artery hypertension patients [11, 34, 107]. However, cardiac MRI results proved to be more reproducible in terms of assessing RV ejection fraction and RV mass [26]. Although less available, cardiovascular MRI is frequently used nowadays to describe RV systolic function; recent imaging techniques allow a good assessment of parameters such as ventricular volumes, ejection fraction, and myocardial mass, with increased accuracy when compared to echocardiography. Stroke volumes, cardiac output, and volumes routed through cardiac shunts can be derived using flow velocities and cross sectional areas. These methods are similar to those used in Doppler echocardiography, but provide a better accuracy, as MRI velocity analysis can be conducted in any orientation or plane. Tissue parameters are best visualized by contrast enhancement techniques (contrast-enhanced MRI), which typically use gadolini‐ um-based magnetic contrast agents [103]. Similar to strain echocardiography, tagged MRI is used to study the 3-dimensional motion and deformation in the heart. Tags are regions of the myocardium, whose longitudinal magnetization has been altered before imaging which render them dark in MRI. These dark areas are landmarks within the heart which allow the detection of motion. In one study on patients with idiopathic pulmonary arterial hypertension, tagged MRI was used to identify significant interventricular asynchrony caused by a pro‐ longed RV systolic contraction time, probably due to impaired electrical conductivity in the right ventricle. It was then showed that ventricular asynchrony led to impaired LV diastolic filling and, consequently, to decreased LV end-diastolic volumes [108]. Although further research would be needed to validate reproducible parameters for RV evaluation, echocar‐

9

of >0.50 [111].

**4.1. Echocardiography**

*4.1.1. Tissue Doppler analysis*

**a.** Acquisition and measurements:

diography and cardiac MRI based techniques are, for the time being, of immense value. As mentioned before, cardiovascular MRI is nowadays considered to be the gold standard for RV assessment; in one research, some 3D echocardiography-derived measurements, such as the RVEF, compared well against cardiac MRI results, with little difference (47.8 ± 8.5% vs 48.2 ± 10.8%) [106]. However, in another study, a tendency to overestimate RVEF by 3D echocar‐ diography, with a bias of approximately 13% (95% CI -52% to +27%), has been reported; moreover, in the same research, RV diastolic and RV systolic volumes were shown to be systematically and significantly underestimated by 3D echocardiography [109]. Solid correla‐ tions were established between 2D echocardiography tissue Doppler St wave velocity and MRI-derived RVEF [110]. In addition to that, it was shown that a systolic long-axis peak velocity of <11 cm/s at the lateral tricuspid annulus was associated with moderately impaired MRI-derived RVEF, while severely reduced RVEF ≤30% was best detected by RVMPI at a value

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Imaging

33

http://dx.doi.org/10.5772/55832

The assessment of RV diastolic dysfunction strongly resembles LV evaluation. Validated parameters include the tricuspid flow E and A velocities, as well as the E/A ratio, the E wave deceleration time and the IVRT, which are assessed in a similar manner to mitral flow evaluation; the previously mentioned parameters are measured using the apical 4-chamber

Several limitations undermine the accuracy of tricuspid flow parameters, particularly the preload and afterload dependency. Preload variations are significant during the respiratory cycle due to fluctuant intrathoracic pressure, which is diminished during inbreathing and rises during expiration. Low intrathoracic pressure favours venous return to the RA, leading to better atrial filling and increased pressure; as a consequence, early diastolic ventricular filling is improved, with an increase in E wave velocity, while A wave velocities remain almost the same; subsequently, the E/A ratio may change. Conversely, lower E wave velocities are obtained when preload decreases during expiration. This is why some authors suggest that at least 5 beats should be analysed in each patient in order to obtain an average value that should have clinical significance [112]. Other physiological factors that influence tricuspid flow patterns are age, gender and tachycardia [112]. Measurements may also be altered by the presence of severe tricuspid regurgitation or atrial fibrillation [23]. Moreover, the thin-walled RV is also highly sensitive to afterload variations, particularly in patients with myocardial infarction or chronic ischemia [113]. TDI is another valuable tool for assessing RV diastolic function. TDI is used to measure velocities at the level of the tricuspid annulus (Et, At, Et/At) and to derive the E/Et ratio which is gaining interest as a marker of diastolic dysfunction. In

**4. Assessment of right ventricular diastolic dysfunction**

view by placing sample volume at the tips of the tricuspid leaflets.

diography and cardiac MRI based techniques are, for the time being, of immense value. As mentioned before, cardiovascular MRI is nowadays considered to be the gold standard for RV assessment; in one research, some 3D echocardiography-derived measurements, such as the RVEF, compared well against cardiac MRI results, with little difference (47.8 ± 8.5% vs 48.2 ± 10.8%) [106]. However, in another study, a tendency to overestimate RVEF by 3D echocar‐ diography, with a bias of approximately 13% (95% CI -52% to +27%), has been reported; moreover, in the same research, RV diastolic and RV systolic volumes were shown to be systematically and significantly underestimated by 3D echocardiography [109]. Solid correla‐ tions were established between 2D echocardiography tissue Doppler St wave velocity and MRI-derived RVEF [110]. In addition to that, it was shown that a systolic long-axis peak velocity of <11 cm/s at the lateral tricuspid annulus was associated with moderately impaired MRI-derived RVEF, while severely reduced RVEF ≤30% was best detected by RVMPI at a value of >0.50 [111].

#### **4. Assessment of right ventricular diastolic dysfunction**

#### **4.1. Echocardiography**

9

**c.** Clinical Application

32 Hot Topics in Echocardiography

stolic and en-systolic. RV=right ventricle; LV=left ventricle.

The efficiency of 3D echocardiography vs. cardiac MRI in RV assessment was compared in many studies. One research group conducted a study on 60 pulmonary artery hypertensive patients [4], proving that 3D echocardiography had some advantages over cardiac MRI, as it could be routinely used for serial imaging and at the bedside. Moreover, it was previously shown that both 3D echocardiography and cardiac MRI may be used to assess RV remodeling in pulmonary artery hypertension patients [11, 34, 107]. However, cardiac MRI results proved to be more reproducible in terms of assessing RV ejection fraction and RV mass [26]. Although less available, cardiovascular MRI is frequently used nowadays to describe RV systolic function; recent imaging techniques allow a good assessment of parameters such as ventricular volumes, ejection fraction, and myocardial mass, with increased accuracy when compared to echocardiography. Stroke volumes, cardiac output, and volumes routed through cardiac shunts can be derived using flow velocities and cross sectional areas. These methods are similar to those used in Doppler echocardiography, but provide a better accuracy, as MRI velocity analysis can be conducted in any orientation or plane. Tissue parameters are best visualized by contrast enhancement techniques (contrast-enhanced MRI), which typically use gadolini‐ um-based magnetic contrast agents [103]. Similar to strain echocardiography, tagged MRI is used to study the 3-dimensional motion and deformation in the heart. Tags are regions of the myocardium, whose longitudinal magnetization has been altered before imaging which render them dark in MRI. These dark areas are landmarks within the heart which allow the detection of motion. In one study on patients with idiopathic pulmonary arterial hypertension, tagged MRI was used to identify significant interventricular asynchrony caused by a pro‐ longed RV systolic contraction time, probably due to impaired electrical conductivity in the right ventricle. It was then showed that ventricular asynchrony led to impaired LV diastolic filling and, consequently, to decreased LV end-diastolic volumes [108]. Although further research would be needed to validate reproducible parameters for RV evaluation, echocar‐

**Figure 13.** Cardiac MRI steady-state free procession sequence for the assessment of right ventricular function en-dia‐

#### *4.1.1. Tissue Doppler analysis*

**a.** Acquisition and measurements:

The assessment of RV diastolic dysfunction strongly resembles LV evaluation. Validated parameters include the tricuspid flow E and A velocities, as well as the E/A ratio, the E wave deceleration time and the IVRT, which are assessed in a similar manner to mitral flow evaluation; the previously mentioned parameters are measured using the apical 4-chamber view by placing sample volume at the tips of the tricuspid leaflets.

Several limitations undermine the accuracy of tricuspid flow parameters, particularly the preload and afterload dependency. Preload variations are significant during the respiratory cycle due to fluctuant intrathoracic pressure, which is diminished during inbreathing and rises during expiration. Low intrathoracic pressure favours venous return to the RA, leading to better atrial filling and increased pressure; as a consequence, early diastolic ventricular filling is improved, with an increase in E wave velocity, while A wave velocities remain almost the same; subsequently, the E/A ratio may change. Conversely, lower E wave velocities are obtained when preload decreases during expiration. This is why some authors suggest that at least 5 beats should be analysed in each patient in order to obtain an average value that should have clinical significance [112]. Other physiological factors that influence tricuspid flow patterns are age, gender and tachycardia [112]. Measurements may also be altered by the presence of severe tricuspid regurgitation or atrial fibrillation [23]. Moreover, the thin-walled RV is also highly sensitive to afterload variations, particularly in patients with myocardial infarction or chronic ischemia [113]. TDI is another valuable tool for assessing RV diastolic function. TDI is used to measure velocities at the level of the tricuspid annulus (Et, At, Et/At) and to derive the E/Et ratio which is gaining interest as a marker of diastolic dysfunction. In clinical practice, both pulsed and colour TDI may be used; the former technique is simpler and provides a high temporal resolution, but is hindered by low spatial resolution [114]; the latter has high spatial resolution, but lower temporal resolution and provides mean velocities [115], as opposed to pulsed TDI, by which maximum velocities are measured. Although considered superior to pulsed wave Doppler techniques, TDI measurements have their limitations. Firstly, like pulsed Doppler parameters, they are influenced by age and gender [116].

catheterization and valuable as a prognostic tool for cardiovascular events in patients with

Right Chambers Quantification in Clinical Practice: Echocardiography Compared with Cardiac Magnetic Resonance

Pseudonormal filling 0.8 – 2.1 diastolic flow predominance in the hepatic

As in the case of the left ventricle, RV diastolic function is the first to be impaired, preceding systolic dysfunction. Therefore, when RV impairment is suspected, diastolic function assess‐ ment is advised, as RV diastolic dysfunction has been confirmed as a marker of poor prognosis [23]. Most studies support the use of the following parameters: trans-tricuspid E/A ratio,

Color M-Mode flow propagation velocity (Vp) is most commonly measured by the slope method from the apical 4-chamber view, using color flow imaging with a narrow color sector; gain is adjusted to avoid noise. The M-mode cursor is placed at the center of the RV inflow blood column from the tricuspid valve to the apex. The color flow baseline is shifted to lower the Nyquist limit so that the central highest velocity jet is blue. Flow propagation velocity (Vp) is measured as the slope of the first aliasing velocity during early filling, measured from the tricuspid valve plane to 4 cm distally into the RV cavity. Alternatively, the slope of the

Vp values >50 cm/s are considered normal for the RV. The Et/Vp ratio varies proportionally with RA pressure, and may therefore be used either by itself, or in combination with IVRT to assess filling pressures. However, this rather challenging method is redundant in patients with decreasedRVejectionfractioninwhichotherparameterspreciselyidentifydiastolicdysfunction.

The slowing of tricuspid-to-apical flow propagation measured by color M-mode Doppler is valuable in identifying diastolic dysfunction. In addition, it may help in assessing filling pressures when used in conjunction with tricuspid E. Essays were made to measure noninvasively the tricuspid-to-apical pressure gradient by color M-mode Doppler, but the method

Restrictive filling > 2.1 late systolic anterograde flow in the

veins TDE < 120 msec

Imaging

35

http://dx.doi.org/10.5772/55832

pulmonary artery

**Degree of diastolic dysfunction Tricuspid E/A ratio Additional parameters**

chronic pulmonary artery hypertension [121] (Table 7).

**Table 7.** Right ventricle diastolic dysfunction assessment

*4.1.2. Color M-mode flow propagation velocity*

transition from no color to color may be measured.

**a.** Acquisition and measurements:

**c.** Clinical Application

ratio, and RA size [23].

**b.** Qualitative values:

**c.** Clinical Application

E/Et

Impaired relaxation < 0.8 E/Et >6

**Figure 14.** Pulsed wave tissue Doppler with the sample placed at the level of the tricuspid annulus of the RV free wall, demonstrating diastolic parameters (Et and At).

#### **b.** Qualitative values:

Moreover, although previous studies focused on the LV supported TDI load independency [117], Pelà et al. demonstrated in their research on healthy subjects that RV Et and At wave velocities were dependent on loading conditions; however, they also showed that Et and At velocity variations were proportional, and consequently, despite alterations in preload, the Et/ At ratio remained constant. [118]. According to Horton et al., measuring parameters from ≥ 3 different beats during apnoea may reduce errors derived from load variations and the translational motion of the myocardium [119]. Despite the limitations, several researches have confirmed that pulsed and tissue Doppler allow a clinically significant evaluation of RV diastolic function. Puwanat et al. demonstrated that a tricuspid E/Et ratio >6 was associated with a mean right atrium pressure >10 mmHg in patients with heart failure and preserved ejection fraction [120]; this finding was consistent with data from a previous research by Utsunomyia et al. who demonstrated that intraatrial pressure assessment by use of the E/Et ratio was comparable with invasive hemodynamic measurements obtained by right heart catheterization and valuable as a prognostic tool for cardiovascular events in patients with chronic pulmonary artery hypertension [121] (Table 7).


**Table 7.** Right ventricle diastolic dysfunction assessment

#### **c.** Clinical Application

clinical practice, both pulsed and colour TDI may be used; the former technique is simpler and provides a high temporal resolution, but is hindered by low spatial resolution [114]; the latter has high spatial resolution, but lower temporal resolution and provides mean velocities [115], as opposed to pulsed TDI, by which maximum velocities are measured. Although considered superior to pulsed wave Doppler techniques, TDI measurements have their limitations. Firstly,

**Figure 14.** Pulsed wave tissue Doppler with the sample placed at the level of the tricuspid annulus of the RV free wall,

Moreover, although previous studies focused on the LV supported TDI load independency [117], Pelà et al. demonstrated in their research on healthy subjects that RV Et and At wave velocities were dependent on loading conditions; however, they also showed that Et and At velocity variations were proportional, and consequently, despite alterations in preload, the Et/ At ratio remained constant. [118]. According to Horton et al., measuring parameters from ≥ 3 different beats during apnoea may reduce errors derived from load variations and the translational motion of the myocardium [119]. Despite the limitations, several researches have confirmed that pulsed and tissue Doppler allow a clinically significant evaluation of RV diastolic function. Puwanat et al. demonstrated that a tricuspid E/Et ratio >6 was associated with a mean right atrium pressure >10 mmHg in patients with heart failure and preserved ejection fraction [120]; this finding was consistent with data from a previous research by Utsunomyia et al. who demonstrated that intraatrial pressure assessment by use of the E/Et ratio was comparable with invasive hemodynamic measurements obtained by right heart

demonstrating diastolic parameters (Et and At).

**b.** Qualitative values:

34 Hot Topics in Echocardiography

like pulsed Doppler parameters, they are influenced by age and gender [116].

As in the case of the left ventricle, RV diastolic function is the first to be impaired, preceding systolic dysfunction. Therefore, when RV impairment is suspected, diastolic function assess‐ ment is advised, as RV diastolic dysfunction has been confirmed as a marker of poor prognosis [23]. Most studies support the use of the following parameters: trans-tricuspid E/A ratio, E/Et ratio, and RA size [23].

#### *4.1.2. Color M-mode flow propagation velocity*

**a.** Acquisition and measurements:

Color M-Mode flow propagation velocity (Vp) is most commonly measured by the slope method from the apical 4-chamber view, using color flow imaging with a narrow color sector; gain is adjusted to avoid noise. The M-mode cursor is placed at the center of the RV inflow blood column from the tricuspid valve to the apex. The color flow baseline is shifted to lower the Nyquist limit so that the central highest velocity jet is blue. Flow propagation velocity (Vp) is measured as the slope of the first aliasing velocity during early filling, measured from the tricuspid valve plane to 4 cm distally into the RV cavity. Alternatively, the slope of the transition from no color to color may be measured.

**b.** Qualitative values:

Vp values >50 cm/s are considered normal for the RV. The Et/Vp ratio varies proportionally with RA pressure, and may therefore be used either by itself, or in combination with IVRT to assess filling pressures. However, this rather challenging method is redundant in patients with decreasedRVejectionfractioninwhichotherparameterspreciselyidentifydiastolicdysfunction.

**c.** Clinical Application

The slowing of tricuspid-to-apical flow propagation measured by color M-mode Doppler is valuable in identifying diastolic dysfunction. In addition, it may help in assessing filling pressures when used in conjunction with tricuspid E. Essays were made to measure noninvasively the tricuspid-to-apical pressure gradient by color M-mode Doppler, but the method is not currently intended for routine clinical application, due to its difficulty. The non-invasive imaging assessment of the RV has gained raising interest and recent research has provided data which may improve standard clinical protocols. However, highly accurate reference values are yet to be established, and there are currently few available and reproducible parameters.

the time/volume curve, expressed as peak filling rate is used to quantify diastolic function. The early and active peak tricuspid filling rates (PFRE and PFRA) and their ratio may be calculated

Right Chambers Quantification in Clinical Practice: Echocardiography Compared with Cardiac Magnetic Resonance

Maceira et al [104] published the first normal ranges for MRI-derived RV diastolic function:

, PFRA=429 mL/s, or 233 mL/m2

As previously mentioned, Doppler echocardiography may be used for the non-invasive, indirect assessment of pulmonary artery pressures. To this purpose, the RV-RA pressure gradient is calculated by analyzing the tricuspid regurgitation flow and the obtained value is added to the estimated RA pressure; the latter is estimated by measuring the IVC and its collapsibility after a "sniff". The value of sPAP thusly derived is somewhat empirical. Several studies have shown that Doppler echocardiography systematically under- or overestimates pulmonary pressures, by comparison with direct, invasive measurements by right heart

Currently, right heart catheterization remains the gold standard for pulmonary artery pressure assessment, as it is necessary to confirm the diagnosis, assess hypertension severity and the reactivity to vasodilator agents [90]. Invasive measurements are particularly useful in patients with NYHA II and III heart failure who have mild pulmonary hypertension as assessed by echocardiography. In addition to that, right heart catheterization provides the advantage of vasoreactivity testing, which is compulsory before initiating vasodilator therapy and may help predict the response to treatment; nitric oxide, adenosine and epoprostenol are most com‐ monly used for this purpose [90]. Patients who have an acute response to vasoreactivity testing

In conclusion, echocardiography may be used as a screening method, as it indicates the likelihood of pulmonary artery hypertension, rather than providing an actual diagnosis. Results should always be validated by right heart catheterization, particularly if specific vasodilator treatment is intended. All in all, 2D echocardiography has some limitations, some related to the empirical assessment of sPAP, others to the imprecision in chamber measure‐ ments due to geometrical assumptions or difficult endocardial border tracing. Presently, cardiac MRI is the golden standard in RV structure and function evaluation, due to its unlimited imaging planes, higher image resolution, and the ability to calculate volumes using three-dimensional measurements; however, cardiac MRI is seldom available in many centres, and hindered by prolonged acquisition and processing times. Moreover, its use is still limited in patients with implanted metallic devices, such as pace-makers, defibrillators, metallic prostheses or insulin pumps. Right heart catheterization allows a good evaluation of sPAP, but it is an invasive procedure and is not usually performed in the absence of other evidence

, PFRE/PFRE = 0.9 were signifi‐

http://dx.doi.org/10.5772/55832

Imaging

37

[104].

**b.** Qualitative values:

PFRE=371 mL/s, or 202 mL/m2

**5. Hemodynamic assessment**

are more likely to respond to long-tem therapy [125].

cantly higher in males [104].

catheterization [96, 124].

**Figure 15.** Pulsed color M-mode Vp imaging with the sample placed at the level of the tricuspid annulus of the RV free wall in pulmonary artery hypertension individual.

#### **4.2. Cardiac magnetic resonance imaging**

**a.** Acquisition and measurements:

The assessment of RV diastolic dysfunction by cardiac MRI is similar, as a principle, to the echocardiographic evaluation. 1.5 Tesla systems can be used to characterize the transtricuspid flow. To this purpose, 4-chamber views should be acquired. ECG-gated phase-contrast pulse sequences are positioned retrospectively, in a plane perpendicular to the transtricuspid inflow, at the level of the opened tricuspid tips, just bellow the tricuspid valve annulus. Two dynamic phase-contrast series, corresponding to an entire cardiac cycle, are acquired during breathhold: 1) the transtricuspid flow velocity sequence, and 2) a myocardial longitudinal velocity sequence. Due to technical progress, cardiac MRI is increasingly being used for blood and myocardial velocities assessment. In addition to that, several studies have demonstrated the usefulness of phase-contrast MRI for measuring diastolic function parameters [122]. However, these analyses are mostly based on manual positioning of regions of interest (ROIs) within the transtricuspid flow area or the myocardium on multiple phases [122, 123]. The derivative of the time/volume curve, expressed as peak filling rate is used to quantify diastolic function. The early and active peak tricuspid filling rates (PFRE and PFRA) and their ratio may be calculated [104].

**b.** Qualitative values:

is not currently intended for routine clinical application, due to its difficulty. The non-invasive imaging assessment of the RV has gained raising interest and recent research has provided data which may improve standard clinical protocols. However, highly accurate reference values are yet to be established, and there are currently few available and reproducible

**Figure 15.** Pulsed color M-mode Vp imaging with the sample placed at the level of the tricuspid annulus of the RV

The assessment of RV diastolic dysfunction by cardiac MRI is similar, as a principle, to the echocardiographic evaluation. 1.5 Tesla systems can be used to characterize the transtricuspid flow. To this purpose, 4-chamber views should be acquired. ECG-gated phase-contrast pulse sequences are positioned retrospectively, in a plane perpendicular to the transtricuspid inflow, at the level of the opened tricuspid tips, just bellow the tricuspid valve annulus. Two dynamic phase-contrast series, corresponding to an entire cardiac cycle, are acquired during breathhold: 1) the transtricuspid flow velocity sequence, and 2) a myocardial longitudinal velocity sequence. Due to technical progress, cardiac MRI is increasingly being used for blood and myocardial velocities assessment. In addition to that, several studies have demonstrated the usefulness of phase-contrast MRI for measuring diastolic function parameters [122]. However, these analyses are mostly based on manual positioning of regions of interest (ROIs) within the transtricuspid flow area or the myocardium on multiple phases [122, 123]. The derivative of

free wall in pulmonary artery hypertension individual.

**4.2. Cardiac magnetic resonance imaging**

**a.** Acquisition and measurements:

parameters.

36 Hot Topics in Echocardiography

Maceira et al [104] published the first normal ranges for MRI-derived RV diastolic function: PFRE=371 mL/s, or 202 mL/m2 , PFRA=429 mL/s, or 233 mL/m2 , PFRE/PFRE = 0.9 were signifi‐ cantly higher in males [104].

#### **5. Hemodynamic assessment**

As previously mentioned, Doppler echocardiography may be used for the non-invasive, indirect assessment of pulmonary artery pressures. To this purpose, the RV-RA pressure gradient is calculated by analyzing the tricuspid regurgitation flow and the obtained value is added to the estimated RA pressure; the latter is estimated by measuring the IVC and its collapsibility after a "sniff". The value of sPAP thusly derived is somewhat empirical. Several studies have shown that Doppler echocardiography systematically under- or overestimates pulmonary pressures, by comparison with direct, invasive measurements by right heart catheterization [96, 124].

Currently, right heart catheterization remains the gold standard for pulmonary artery pressure assessment, as it is necessary to confirm the diagnosis, assess hypertension severity and the reactivity to vasodilator agents [90]. Invasive measurements are particularly useful in patients with NYHA II and III heart failure who have mild pulmonary hypertension as assessed by echocardiography. In addition to that, right heart catheterization provides the advantage of vasoreactivity testing, which is compulsory before initiating vasodilator therapy and may help predict the response to treatment; nitric oxide, adenosine and epoprostenol are most com‐ monly used for this purpose [90]. Patients who have an acute response to vasoreactivity testing are more likely to respond to long-tem therapy [125].

In conclusion, echocardiography may be used as a screening method, as it indicates the likelihood of pulmonary artery hypertension, rather than providing an actual diagnosis. Results should always be validated by right heart catheterization, particularly if specific vasodilator treatment is intended. All in all, 2D echocardiography has some limitations, some related to the empirical assessment of sPAP, others to the imprecision in chamber measure‐ ments due to geometrical assumptions or difficult endocardial border tracing. Presently, cardiac MRI is the golden standard in RV structure and function evaluation, due to its unlimited imaging planes, higher image resolution, and the ability to calculate volumes using three-dimensional measurements; however, cardiac MRI is seldom available in many centres, and hindered by prolonged acquisition and processing times. Moreover, its use is still limited in patients with implanted metallic devices, such as pace-makers, defibrillators, metallic prostheses or insulin pumps. Right heart catheterization allows a good evaluation of sPAP, but it is an invasive procedure and is not usually performed in the absence of other evidence of pulmonary artery hypertension. Standard 2D echocardiography is widely available, relatively cheap, does not present any risk for the patient, and may be performed even in the presence of metallic devices which would normally hinder an MRI examination. Although it only indicates the likelihood of pulmonary artery hypertension, it may be used to select candidates for right catheterization. In terms of assessing RV structure and function, further research would be needed in order to provide solid, reproducible parameters, with normal reference values.

[4] Grapsa, J, O'Regan, D.P, Pavlopoulos, H, Durighel, G, Dawson, D, & Nihoyannopou‐ los, P. Right ventricular remodelling in pulmonary arterial hypertension with threedimensional echocardiography: comparison with cardiac magnetic resonance

Right Chambers Quantification in Clinical Practice: Echocardiography Compared with Cardiac Magnetic Resonance

Imaging

39

http://dx.doi.org/10.5772/55832

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### **Acknowledgements**

This work was supported by grants 27020/24/2011 and 22714/2/2011 from the "Iuliu Hatiega‐ nu" University of Medicine and Pharmacy in Cluj-Napoca.

### **Author details**

Lucia Agoston-Coldea1 and Silvia Lupu2

\*Address all correspondence to: luciacoldea@yahoo.com

1 The "Iuliu Hatieganu" University of Medicine and Pharmacy, Cluj-Napoca, Romania

2 The University of Medicine and Pharmacy of Targu Mures, Romania

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This work was supported by grants 27020/24/2011 and 22714/2/2011 from the "Iuliu Hatiega‐

1 The "Iuliu Hatieganu" University of Medicine and Pharmacy, Cluj-Napoca, Romania

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[118] Pela, G, Regolisti, G, Coghi, P, Cabassi, A, Basile, A, Cavatorta, A, Manca, C, & Bor‐ ghetti, A. Effects of the reduction of preload on left and right myocardial velocities analysed by Doppler tissue echocardiography in healthy subjects. Eur J Echocar‐

[119] Horton, K.D, Meece, R.W, & Hill, J.C. Assessment of the right ventricle by echocar‐ diography: a primer for cardiac sonographers. J Am Soc Echocardiogr. (2009)., 22(7),

[120] Puwanat, S, Priester, T.C, Mookadam, F, Bruce, C.J, Redfield, M.M, & Chandrasekar‐ an, K. Right ventricular function in patients with heart failure and preserved ejection

[121] Utsunomiya, H, Nakatani, S, Nishihira, M, Kanzaki, H, Kyotani, S, Nakanishi, N, Ki‐ hara, Y, & Kitakaze, M. Value of Estimated Right Ventricular Filling Pressure in Pre‐

and the effects of age and heart rate. Echocardiography. (2003)., 20(1), 19-27.

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[110] Wang, J, Prakasa, K, Bomma, C, Tandri, H, Dalal, D, James, C, Tichnell, C, Corretti, M, Bluemke, D, Calkins, H, & Abraham, T.P. Comparison of novel echocardiograph‐ ic parameters of right ventricular function with ejection fraction by cardiac magnetic resonance. J Am Soc Echocardiogr. (2007)., 20(9), 1058-1064.

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[102] Cho, E.J, Jiamsripong, P, Calleja, A.M, Alharthi, M.S, McMahon, E.M, Khandheria, B.K, & Belohlavek, M. Right ventricular free wall circumferential strain reflects grad‐ ed elevation in acute right ventricular afterload. Am J Physiol Heart Circ Physi.

[103] Benza, R, Biederman, R, Murali, S, & Gupta, H. Role of cardiac magnetic resonance imaging in the management of patients with pulmonary arterial hypertension. J Am

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dicting Cardiac Events in Chronic Pulmonary Arterial Hypertension. J Am Soc Echocardiogr. (2009)., 22(12), 1368-1374.

**Chapter 3**

**Lung Ultrasound Comet Tails —**

**Technique and Clinical Significance**

Douglas T. Summerfield and Bruce D. Johnson

While often overlooked by traditional echocardiography, the lungs and evaluation of extrava‐ scular lung water (EVLW) can be assessed by direct visualization with relatively simple ultrasonographic techniques. The results can help guide clinicians towards the cause of a patient's dyspnea and in the case of pulmonary edema even semi-quantitatively asses EVLW. Additionally the exam can be repeated as often as necessary to monitor response to treatment without fear of subjecting the patient to ionizing radiation associated with conventional chest

Advancing technology has allowed for increasingly miniaturized and portable ultrasound systems to the point where exams can be performed quickly at the bedside, often by the rounding physician. The more common standard of care for quantifying pulmonary edema has been a chest radiograph which, depending on the institution, may require more time to perform and a more formal interpretation than a portable ultrasound [1]. Even when it is obtained, chest radiograph can have a low sensitivity for common causes of dyspnea such as pulmonary edema [2, 3]. This may be due in part to poor radiographic windows of the patient or the intraobserver variability and skills of those interpreting the x-ray [4, 5]. In the case of acute pulmonary edema, the practitioner using techniques of lung ultrasound, can actually visualize the edema, classify it semi-quantitatively, and prescribe interventions before other

The lung ultrasound finding of "Comet Tails" has been well studied in how it relates to alveolar-interstitial syndromes. These syndromes include conditions with diffuse involvement of the pulmonary interstitium which lead to respiratory distress through impairment of alveolar-capillary exchange. Chronic conditions include pulmonary fibrosis, whereas acute entities are acute respiratory distress syndrome (ARDS), interstitial pneumonia, and acute

> © 2013 Summerfield and Johnson; licensee InTech. This is a paper distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use,

distribution, and reproduction in any medium, provided the original work is properly cited.

traditional diagnostic techniques such as chest radiograph can even occur.

Additional information is available at the end of the chapter

http://dx.doi.org/10.5772/56198

**1. Introduction**

radiography.


### **Chapter 3**

## **Lung Ultrasound Comet Tails — Technique and Clinical Significance**

Douglas T. Summerfield and Bruce D. Johnson

Additional information is available at the end of the chapter

http://dx.doi.org/10.5772/56198

#### **1. Introduction**

dicting Cardiac Events in Chronic Pulmonary Arterial Hypertension. J Am Soc

[122] Kayser, H.W, van der Geest, R.J, van der Wall, E.E, Duchateau, C, & De Roos, A. Right ventricular function in patients after acute myocardial infarction assessed with phase contrast MR velocity mapping encoded in three directions. J Magn Reson

[123] Paelinck, B.P, De Roos, A, Bax, J.J, Bosmans, J.M, van der Geest, R.J, Dhondt, D, Pari‐ zel, P.M, Vrints, C.J, & Lamb, H.J. Feasibility of tissue magnetic resonance imaging: a pilot study in comparison with tissue Doppler imaging and invasive measurement. J

[124] Janda, S, Shahidi, N, Gin, K, & Swiston, J. Diagnostic accuracy of echocardiography for pulmonary hypertension: a systematic review and meta-analysis. Heart. (2011).,

[125] Sitbon, O, Humbert, M, Jais, X, Ioos, V, Hamid, A.M, Provencher, S, Garcia, G, Pa‐ rent, F, Herve, P, & Simonneau, G. Long-term response to calcium channel blockers in idiopathic pulmonary arterial hypertension. Circulation. (2005)., 111(23), 3105–

Echocardiogr. (2009)., 22(12), 1368-1374.

Am Coll Cardiol. (2005)., 45(7), 1109-1116.

Imaging. (2000)., 11(5), 471-475.

97(8), 612-622.

3111.

50 Hot Topics in Echocardiography

While often overlooked by traditional echocardiography, the lungs and evaluation of extrava‐ scular lung water (EVLW) can be assessed by direct visualization with relatively simple ultrasonographic techniques. The results can help guide clinicians towards the cause of a patient's dyspnea and in the case of pulmonary edema even semi-quantitatively asses EVLW. Additionally the exam can be repeated as often as necessary to monitor response to treatment without fear of subjecting the patient to ionizing radiation associated with conventional chest radiography.

Advancing technology has allowed for increasingly miniaturized and portable ultrasound systems to the point where exams can be performed quickly at the bedside, often by the rounding physician. The more common standard of care for quantifying pulmonary edema has been a chest radiograph which, depending on the institution, may require more time to perform and a more formal interpretation than a portable ultrasound [1]. Even when it is obtained, chest radiograph can have a low sensitivity for common causes of dyspnea such as pulmonary edema [2, 3]. This may be due in part to poor radiographic windows of the patient or the intraobserver variability and skills of those interpreting the x-ray [4, 5]. In the case of acute pulmonary edema, the practitioner using techniques of lung ultrasound, can actually visualize the edema, classify it semi-quantitatively, and prescribe interventions before other traditional diagnostic techniques such as chest radiograph can even occur.

The lung ultrasound finding of "Comet Tails" has been well studied in how it relates to alveolar-interstitial syndromes. These syndromes include conditions with diffuse involvement of the pulmonary interstitium which lead to respiratory distress through impairment of alveolar-capillary exchange. Chronic conditions include pulmonary fibrosis, whereas acute entities are acute respiratory distress syndrome (ARDS), interstitial pneumonia, and acute

© 2013 Summerfield and Johnson; licensee InTech. This is a paper distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

pulmonary edema [5]. With careful attention paid by the examiner at the bedside to the patient's history and monitoring the response to treatment, the ultrasonographic finding of comet tails can be extremely useful in narrowing the differential diagnosis.

#### **2. Definitions**

"A-lines and B-lines" are two separate and distinct ultrasonographic images which may be seen during examination of the lungs by ultrasound (See Figures 1 &2). Their presence is not mutually exclusive, but the formation of each arises from a different underlying structure.

objects larger than 1 mm. Instead of showing up as a distinct structure, in the right circum‐

Lung Ultrasound Comet Tails — Technique and Clinical Significance

http://dx.doi.org/10.5772/56198

53

Under normal (non-edematous or fibrotic) conditions comet tails are absent because no acoustic mismatch occurs as the beam passes through the subpleural space. However, in conditions known as alveolar-interstitial syndromes an area of high acoustic mismatch occurs at the subpleural space were interlobular septa are in contact with the pleural lining. In the case of pulmonary edema this mismatch occurs between the differing impedances of air and water, however it can also occur anytime there is an area of differing impedances at the surface of the lungs such as pleuritis, fibrosis, or even chronic obstructive pulmonary disease [9].

Even though these structures are smaller than the resolution of the ultrasound beam, the reflections cans still be generated and sent back to the ultrasound probe. Continued reflections set up the phenomenon of reverberation which acts as a continued source of reflections back to the piezoelectric crystal. Since the ultrasound interprets time as distance, and each successive echo or return to the transducer occurs over a more distant time than the original signal, the ultrasound interprets these signals as reflections from a structure more distal from the ultrasound probe [6]. In this way a "beam" or comet tail image is created on the echo screen. (See Figure 3) Histologically the interlobular septa are 7 mm apart when they reach the sub pleural space and this is roughly the distance between the origins of individual comet tails at

the pleural line [7].

**Figure 2.** Image of pleural "A-lines."

stances the areas of highly different acoustic impedance show up as a comet tail [7,8].

**Figure 1.** Image of comet tail "B-lines"

Comet-tails or "B-lines" are defined as hyperechoic reflections which originate only from and travel roughly perpendicular to the pleural line of the lung. They have a narrow base and form a ray spreading away from the transducer towards the bottom of the screen and synchronously move with lung respiration. All ultrasound images are formed when a reflection occurs at the interface of two regions with differing acoustic impedance [6]. In the case of comet tails this impedance occurs between fluid filled interlobular septa, with the acoustic impedance of water being 1.48x105 gp/cm2 and that of an air filled lung with the acoustic impedance of air being of 0.0004x105 gp/cm2 . Interlobular septa are structures within the lung containing lymphatic vessels. These septa are below the resolution of the ultrasound beam, which can only detect

**Figure 2.** Image of pleural "A-lines."

pulmonary edema [5]. With careful attention paid by the examiner at the bedside to the patient's history and monitoring the response to treatment, the ultrasonographic finding of

"A-lines and B-lines" are two separate and distinct ultrasonographic images which may be seen during examination of the lungs by ultrasound (See Figures 1 &2). Their presence is not mutually exclusive, but the formation of each arises from a different underlying structure.

Comet-tails or "B-lines" are defined as hyperechoic reflections which originate only from and travel roughly perpendicular to the pleural line of the lung. They have a narrow base and form a ray spreading away from the transducer towards the bottom of the screen and synchronously move with lung respiration. All ultrasound images are formed when a reflection occurs at the interface of two regions with differing acoustic impedance [6]. In the case of comet tails this impedance occurs between fluid filled interlobular septa, with the acoustic impedance of water

vessels. These septa are below the resolution of the ultrasound beam, which can only detect

gp/cm2 and that of an air filled lung with the acoustic impedance of air being of

. Interlobular septa are structures within the lung containing lymphatic

comet tails can be extremely useful in narrowing the differential diagnosis.

**2. Definitions**

52 Hot Topics in Echocardiography

**Figure 1.** Image of comet tail "B-lines"

gp/cm2

being 1.48x105

0.0004x105

objects larger than 1 mm. Instead of showing up as a distinct structure, in the right circum‐ stances the areas of highly different acoustic impedance show up as a comet tail [7,8].

Under normal (non-edematous or fibrotic) conditions comet tails are absent because no acoustic mismatch occurs as the beam passes through the subpleural space. However, in conditions known as alveolar-interstitial syndromes an area of high acoustic mismatch occurs at the subpleural space were interlobular septa are in contact with the pleural lining. In the case of pulmonary edema this mismatch occurs between the differing impedances of air and water, however it can also occur anytime there is an area of differing impedances at the surface of the lungs such as pleuritis, fibrosis, or even chronic obstructive pulmonary disease [9].

Even though these structures are smaller than the resolution of the ultrasound beam, the reflections cans still be generated and sent back to the ultrasound probe. Continued reflections set up the phenomenon of reverberation which acts as a continued source of reflections back to the piezoelectric crystal. Since the ultrasound interprets time as distance, and each successive echo or return to the transducer occurs over a more distant time than the original signal, the ultrasound interprets these signals as reflections from a structure more distal from the ultrasound probe [6]. In this way a "beam" or comet tail image is created on the echo screen. (See Figure 3) Histologically the interlobular septa are 7 mm apart when they reach the sub pleural space and this is roughly the distance between the origins of individual comet tails at the pleural line [7].

**Figure 3.** The hypothesized physical and anatomic basis of echocardiographic lung comet tails. Reflections of the ul‐ trasound beam between thickened interlobular septa and the pleura generate a resonance signal over a prolonged time. The increased return over time is interpreted by the ultrasound machine as a hyperechoic structure originating deeper in the tissue and is displayed as a comet-tail on the ultrasound screen. (Illustrations and images from Jambrik et al. Usefulness of ultrasound lung comets as a nonradiologic sign of extravascular lung water. Am J Cardiol 2004;93:1265-1270, with permission from Excerpta Medica, Inc.)

**3. History and origins**

\*CTS: Comet Tail Score.

decision making process.

this on chest x-ray [7].

The "comet-tail" ultrasonographic sign was first described by Ziskin and colleagues in 1982 when an intrahepatic shotgun pellet was observed to create an artifact similar to what is seen in lung comets [8]. Other conditions affecting the pleura of the lung were later noted to create a similar pattern [9]. However it was not until 1997 when Daniel Lichtenstein, a French critical care physician, described lung comet tails as an ultrasonographic sign of alveolar-interstitial syndrome. In his paper he examined 250 patients, 121 with evidence of either wide-spread (N=92) or localized (N=29) evidence of alveolar-interstitial syndrome on chest x-ray and 129 patients with a normal chest radiograph. He found the sensitivity of ultrasound in detecting this pattern was 93.4% with a specificity of 93.0% in patients who did not have evidence for

**Figure 4.** Proposed algorithm for use of lung comet tails in the evaluation of patients with acute dyspnea. In the case of pulmonary edema, serial ultrasonographic exams performed after therapeutic intervention(s) will reveal a diminish‐ ing number of comet tails. This algorithm is suggested as a possible supplement for typical clinical assessment in the

Lung Ultrasound Comet Tails — Technique and Clinical Significance

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55

When Lichtenstein compared chest computerized tomography (CT) to the ultrasound findings on 29 of his 250 patients, he found comet tails were generated diffusely across the lungs from two distinct sources. Both of these sources were lesions associated with acute pulmonary edema, thickened sub-pleural interlobular septa and ground-glass regions. Occasionally even

For the comet tail image to form, these thickened intralobular septa must be in contact with the sub pleural space as any air between them and the transducer has such a low acoustic impedance that the echo return takes too long and is simply "cancelled out" by the machine. (This is the reason lung comets are not seen in pneumothorax and can aid in the diagnosis of that condition.) [6] In a traditional chest radiograph these septa thickened by pulmonary edema are termed "Kerley B-lines" [10, 11].

A-Lines are another distinct ultrasonographic entity separate from the "B-line" comet tails. Alines are hyperechoic lines which run roughly horizontal across the ultrasound screen and are parallel to the pleural line. These lines are equidistant to each other and are the same distance from each other as the pleural line is from the skin because they are reverberations of the pleural line. Again the ultrasound machine interprets the signals it receives temporally from the reverberations as depth. Hence the reflections are seen as lines deeper on the screen. The presence of A-lines, and absence of B-lines indicates the presence of "dry" intralobular septa and is a strong predictor of a normal capillary wedge pressure [12].

**Figure 4.** Proposed algorithm for use of lung comet tails in the evaluation of patients with acute dyspnea. In the case of pulmonary edema, serial ultrasonographic exams performed after therapeutic intervention(s) will reveal a diminish‐ ing number of comet tails. This algorithm is suggested as a possible supplement for typical clinical assessment in the decision making process.

#### **3. History and origins**

**Figure 3.** The hypothesized physical and anatomic basis of echocardiographic lung comet tails. Reflections of the ul‐ trasound beam between thickened interlobular septa and the pleura generate a resonance signal over a prolonged time. The increased return over time is interpreted by the ultrasound machine as a hyperechoic structure originating deeper in the tissue and is displayed as a comet-tail on the ultrasound screen. (Illustrations and images from Jambrik et al. Usefulness of ultrasound lung comets as a nonradiologic sign of extravascular lung water. Am J Cardiol

For the comet tail image to form, these thickened intralobular septa must be in contact with the sub pleural space as any air between them and the transducer has such a low acoustic impedance that the echo return takes too long and is simply "cancelled out" by the machine. (This is the reason lung comets are not seen in pneumothorax and can aid in the diagnosis of that condition.) [6] In a traditional chest radiograph these septa thickened by pulmonary

A-Lines are another distinct ultrasonographic entity separate from the "B-line" comet tails. Alines are hyperechoic lines which run roughly horizontal across the ultrasound screen and are parallel to the pleural line. These lines are equidistant to each other and are the same distance from each other as the pleural line is from the skin because they are reverberations of the pleural line. Again the ultrasound machine interprets the signals it receives temporally from the reverberations as depth. Hence the reflections are seen as lines deeper on the screen. The presence of A-lines, and absence of B-lines indicates the presence of "dry" intralobular septa

and is a strong predictor of a normal capillary wedge pressure [12].

2004;93:1265-1270, with permission from Excerpta Medica, Inc.)

54 Hot Topics in Echocardiography

edema are termed "Kerley B-lines" [10, 11].

The "comet-tail" ultrasonographic sign was first described by Ziskin and colleagues in 1982 when an intrahepatic shotgun pellet was observed to create an artifact similar to what is seen in lung comets [8]. Other conditions affecting the pleura of the lung were later noted to create a similar pattern [9]. However it was not until 1997 when Daniel Lichtenstein, a French critical care physician, described lung comet tails as an ultrasonographic sign of alveolar-interstitial syndrome. In his paper he examined 250 patients, 121 with evidence of either wide-spread (N=92) or localized (N=29) evidence of alveolar-interstitial syndrome on chest x-ray and 129 patients with a normal chest radiograph. He found the sensitivity of ultrasound in detecting this pattern was 93.4% with a specificity of 93.0% in patients who did not have evidence for this on chest x-ray [7].

When Lichtenstein compared chest computerized tomography (CT) to the ultrasound findings on 29 of his 250 patients, he found comet tails were generated diffusely across the lungs from two distinct sources. Both of these sources were lesions associated with acute pulmonary edema, thickened sub-pleural interlobular septa and ground-glass regions. Occasionally even "normal" subjects registered the rare comet tail in the diaphragmatic regions of the lung, and this was detected in both x-ray and CT scan [7].

Mallamaci demonstrated that in dialysis patients, overall volume status was not linked to pulmonary congestion and the formation of comet tails. Rather Comet tails, and pulmonary congestion, had more to do with a patient's left ventricular function. They also demonstrated the ability of comet tails to detect patient who were asymptomatic as 57% of patients had moderate to severe pulmonary congestion but did not have symptoms suggesting such [18]. This is in keeping with Lichtenstein's original paper which discussed a patient with a fat embolism who had the sonographic sign of comet tails three days before symptoms occurred [7] and in older literature which argued that alveolar edema, which would lead to symptoms, is preceded by interstitial edema (which may or may not cause symptoms but can now be

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57

The standard technique for quantification of comet tails has been reported in a number of studies and was pioneered by Picano and colleagues [9,13, 11]. This technique has shown its utility clinically as used by the Himalayan Rescue Association to help diagnose and monitor

The exam is performed using any commercially available portable ultrasound device which has a 1-7 MHz phased array probe. We recommend the use of the 1-5 MHz cardiac probe as it is ideal for viewing between rib spaces and still allows deep enough penetration of the ultrasound beam to view distal structures. Other groups have also found adequate views with

The patient is placed in a supine or near supine position with the anterior chest wall exposed. Each intercostals space from the second to the fifth on the right and the second to the fourth on the left is scanned in four different positions. These are para-sternal, midclavicular, anterior axillary, and mid-axillary. This gives the examiner a total of 28 different windows to examine,

**Right Hemithorax Left Hemithorax**

Intercostal space

**Table 1.** Diagram of the ultrasound windows used to obtain the Comet Tail Score (CTS). This technique was proposed by Jambrik at al. and used by Jambrik, Fagenholtz, Pratali, Agricola, Picano, Mallamaci. Each window is evaluated for

Within each window, comet tails as defined above are counted. The sum of the comet tails seen can then be compiled for a comet tail score (CTS). The intra- and interobserver variability using

Para-Sternal Midclavicular Anterior axillary

Midaxillary

the degree of pulmonary edema in high-altitude pulmonary edema (HAPE). [20]

the high frequency linear probes as well as the abdominal probes as well [21].

16 on the right and 12 on the left (See graphic representation Table 1).

Para-Sternal

detected by ultrasound) [19].

**4. Technique**

Mid-Axillary Anterior axillary

Midclavicular

comet tails, and the number present is added to form a cumulative score.

Clinical applications of comet tails began after Jambrik and colleagues evaluated 121 hospi‐ talized patients with lung ultrasound (see technique below) and compared the findings to chest x-ray. They found a significant linear correlation between a comet tail score (CTS) and x-ray (r=0.78, p<.01). When patients were examined multiple times, an even higher intrapatient correlation was seen (r=0.89; p<0.01). [13]

Lichtenstein and Jambrik's observations were expanded to the medical in-patient setting by Tsereva who validated the technique in patients with diastolic heart failure [14] and by Volpicelli, who validated the use of ultrasound in diagnosis alveolar interstitial syndrome with a 85.7% sensitivity and 97.7% specificity. The lower sensitivity in the later study can be explained by the timing of the x-ray and the ultrasounds. The chest radiographs which the ultrasounds were compared to were taken at admission and guided the treatment given, whereas the lung ultrasounds were done after the initiation of therapy. Thus for some patients the lack of comet tails was merely the resolution of pulmonary edema, but in the analysis resulted in a lower sensitivity of the ultrasound technique [5]. Other researchers further validated lung ultrasound and have suggested that it is superior to chest x-ray with sensitivities similar to Nt-proBNP levels [15]. Nt-proBNP (N-terminal probrain type natriuretic peptide) has become a common biomarker for fluid overload and tracking health status in heart failure patients. However, fluid overload may not always correlate with interstitial pulmonary edema and thus may be a marker primarily of vascular fluid overload.

In an effort to help quantify the number of comet tails seen on exam, Agricola et al. evaluated post-cardiac surgery patients. They devised a relatively simple definition for a positive or negative comet tail exam. A positive comet tail test was simply multiple bilateral comet tails seen over the whole lung surface. A negative test was with the rare occasional comet tail, the absence of comet tails, or comet tails confined to the last intercostals space. They then compared the patient's comet tail test to the amount of extravascular lung water (EVLW) determined by Pulse Contour Cardiac Output (PiCCO - is an invasive technique requiring catheters and uses principals of transpulmonary thermodilution and arterial pulse contour analysis in order to estimate extravascular lung water), to the patient's wedge pressure, and to their radiologic score as determined by chest x-ray. Again good correlation was seen between the radiologic assessment of EVLW and comet tails (r=0.60, p<0.0001) and also when compared to wedge pressure (r=0.48, p<0.0001). Most useful was the comparison to EVLW. Normal EVLW is <500 mL with alveolar flooding occurring when EVLW reaches more than 75% above its normal limit [16, 17]. With this in mind, the negative test had a 90% sensitivity and 89% specificity of accurately detecting an EVLW volume <500 mL. Likewise a positive test had a 90% and 86% sensitivity and specificity of detecting EVLW >500 mL. When comparing the comet tail test to chest radiographs and PiCCO, they found they were even able to detect excess EVLW below the threshold which would cause alveolar edema (sub clinical or early stages of pulmonary edema) with 87% and 89% sensitivity and specificity [11].

Monitoring EVLW through the formation of lung comet tails was shown to be even more important than knowing a patients overall volume status. Using bioelectric impedance Mallamaci demonstrated that in dialysis patients, overall volume status was not linked to pulmonary congestion and the formation of comet tails. Rather Comet tails, and pulmonary congestion, had more to do with a patient's left ventricular function. They also demonstrated the ability of comet tails to detect patient who were asymptomatic as 57% of patients had moderate to severe pulmonary congestion but did not have symptoms suggesting such [18]. This is in keeping with Lichtenstein's original paper which discussed a patient with a fat embolism who had the sonographic sign of comet tails three days before symptoms occurred [7] and in older literature which argued that alveolar edema, which would lead to symptoms, is preceded by interstitial edema (which may or may not cause symptoms but can now be detected by ultrasound) [19].

#### **4. Technique**

"normal" subjects registered the rare comet tail in the diaphragmatic regions of the lung, and

Clinical applications of comet tails began after Jambrik and colleagues evaluated 121 hospi‐ talized patients with lung ultrasound (see technique below) and compared the findings to chest x-ray. They found a significant linear correlation between a comet tail score (CTS) and x-ray (r=0.78, p<.01). When patients were examined multiple times, an even higher intrapatient

Lichtenstein and Jambrik's observations were expanded to the medical in-patient setting by Tsereva who validated the technique in patients with diastolic heart failure [14] and by Volpicelli, who validated the use of ultrasound in diagnosis alveolar interstitial syndrome with a 85.7% sensitivity and 97.7% specificity. The lower sensitivity in the later study can be explained by the timing of the x-ray and the ultrasounds. The chest radiographs which the ultrasounds were compared to were taken at admission and guided the treatment given, whereas the lung ultrasounds were done after the initiation of therapy. Thus for some patients the lack of comet tails was merely the resolution of pulmonary edema, but in the analysis resulted in a lower sensitivity of the ultrasound technique [5]. Other researchers further validated lung ultrasound and have suggested that it is superior to chest x-ray with sensitivities similar to Nt-proBNP levels [15]. Nt-proBNP (N-terminal probrain type natriuretic peptide) has become a common biomarker for fluid overload and tracking health status in heart failure patients. However, fluid overload may not always correlate with interstitial pulmonary edema

In an effort to help quantify the number of comet tails seen on exam, Agricola et al. evaluated post-cardiac surgery patients. They devised a relatively simple definition for a positive or negative comet tail exam. A positive comet tail test was simply multiple bilateral comet tails seen over the whole lung surface. A negative test was with the rare occasional comet tail, the absence of comet tails, or comet tails confined to the last intercostals space. They then compared the patient's comet tail test to the amount of extravascular lung water (EVLW) determined by Pulse Contour Cardiac Output (PiCCO - is an invasive technique requiring catheters and uses principals of transpulmonary thermodilution and arterial pulse contour analysis in order to estimate extravascular lung water), to the patient's wedge pressure, and to their radiologic score as determined by chest x-ray. Again good correlation was seen between the radiologic assessment of EVLW and comet tails (r=0.60, p<0.0001) and also when compared to wedge pressure (r=0.48, p<0.0001). Most useful was the comparison to EVLW. Normal EVLW is <500 mL with alveolar flooding occurring when EVLW reaches more than 75% above its normal limit [16, 17]. With this in mind, the negative test had a 90% sensitivity and 89% specificity of accurately detecting an EVLW volume <500 mL. Likewise a positive test had a 90% and 86% sensitivity and specificity of detecting EVLW >500 mL. When comparing the comet tail test to chest radiographs and PiCCO, they found they were even able to detect excess EVLW below the threshold which would cause alveolar edema (sub clinical or early stages of pulmonary

Monitoring EVLW through the formation of lung comet tails was shown to be even more important than knowing a patients overall volume status. Using bioelectric impedance

this was detected in both x-ray and CT scan [7].

56 Hot Topics in Echocardiography

correlation was seen (r=0.89; p<0.01). [13]

and thus may be a marker primarily of vascular fluid overload.

edema) with 87% and 89% sensitivity and specificity [11].

The standard technique for quantification of comet tails has been reported in a number of studies and was pioneered by Picano and colleagues [9,13, 11]. This technique has shown its utility clinically as used by the Himalayan Rescue Association to help diagnose and monitor the degree of pulmonary edema in high-altitude pulmonary edema (HAPE). [20]

The exam is performed using any commercially available portable ultrasound device which has a 1-7 MHz phased array probe. We recommend the use of the 1-5 MHz cardiac probe as it is ideal for viewing between rib spaces and still allows deep enough penetration of the ultrasound beam to view distal structures. Other groups have also found adequate views with the high frequency linear probes as well as the abdominal probes as well [21].

The patient is placed in a supine or near supine position with the anterior chest wall exposed. Each intercostals space from the second to the fifth on the right and the second to the fourth on the left is scanned in four different positions. These are para-sternal, midclavicular, anterior axillary, and mid-axillary. This gives the examiner a total of 28 different windows to examine, 16 on the right and 12 on the left (See graphic representation Table 1).


**Table 1.** Diagram of the ultrasound windows used to obtain the Comet Tail Score (CTS). This technique was proposed by Jambrik at al. and used by Jambrik, Fagenholtz, Pratali, Agricola, Picano, Mallamaci. Each window is evaluated for comet tails, and the number present is added to form a cumulative score.

Within each window, comet tails as defined above are counted. The sum of the comet tails seen can then be compiled for a comet tail score (CTS). The intra- and interobserver variability using this method has been reported as 5.1% and 7.4% respectively [13]. For clinical purposes Picano and colleges report the comet tail score in a semiquantitative manner for patients in pulmonary edema (Table 2).

diseased state. With the case of patients presenting with dyspnea, the pathologic state should be considered present until "ruled out" with other diagnostic modalities. However in the research arena where "healthy" subjects may be tested, the pre-test probability that comet tails

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A diffuse bilateral comet tail pattern is not considered normal and is indicative of alveolarinterstitial syndromes (AIS). These can be brought about by a number of disease entities including chronic conditions such as pulmonary fibrosis, and acute entities such as acute respiratory distress syndrome (ARDS), interstitial pneumonia, and acute pulmonary edema [5]. Different clinical presentations can help elucidate the etiology of these different diseases which have the same comet tail pattern. The time course of the illness can differentiate chronic causes such as pulmonary fibrosis and acute causes such as pulmonary edema. Additionally slight variations in the pattern of comet tails are noted. In the case of a fibrotic lung, the comet tails are equal in both hemi thoraces, whereas in cardiac pulmonary edema they are bilateral but with a predilection for the right hemi-thorax. Also in the fibrotic lung comet tails are more

Highly dense entities such as ARDS typically give rise to comet tails only in regions where the diseased lung is in contact with the sub-pleural space. These highly dense areas give rise to multiple comet tails less than 3 mm apart, whereas comet tails arising from thickened inter‐ lobular septa are 7 mm apart [23]. Additionally an ARDS pattern also gives rise to comet tails in focal areas which coalesce together and form comet tails of differing lengths and multiple

Importantly comet tails which arise from pulmonary edema should respond to treatment and disappear as interventions are made [18]. If they do not, then an alternate diagnosis should be sought. This reenforces the need for serial exams many authors encourage repeat exams to

Since the presence of the occasional comet tail is considered normal, the lack of comet tails can be diagnostic as well. Comet tail formation requires an area of differing acoustic impedances, when this is not present no comet tails are created. Such is the case of a pneumothorax. In examining for this potential emergent condition, an additional ultrasonographic sign must be viewed, that of the "sliding lung sign." This is the hyperechoic line which is the interface between the visceral and parietal pleura. This line will slide back and forth with respiration. When there is no sliding of this line, and an absence of comet tails, a pneumothorax should be suspected [24]. The is particularly helpful when some studies show that standard chest x-ray, in addition to taking longer, misses 30% of cases [25-27]. This is contrasted to the lung ultrasound which in a large meta-analysis and systematic review looked at 8 studies repre‐ senting 1,048 patients. When using both the absence of lung comet tails and sliding lung sign ultrasound was 90.9% sensitive and 98.2% specific in making the diagnosis of pneumothorax. In the same analysis chest radiograph was only 50.2% sensitive, but with a similar specificity

In patients with minimal comet tails confined to the intercostal space above the diaphragm, or no comet tails present on lung ultrasound, but who otherwise present with dyspnea, other

localized to the last lateral intercostals spaces are normal, is high.

patchy than in pulmonary edema, and are stable with diuretic therapy [9].

irregular comet tails [7, 23, 1].

monitor response to therapy.

of 99.4% [28].


**Table 2.** Semiquantitive classification of the Comet Tail Score (CTS)as proposed by Picano and colleagues.

#### **4.1. Other techniques**

Simpler less quantitative techniques have also been described with good prediction of pulmonary edema. Volpicelli and colleagues described a technique where each hemithorax is divided into four quadrants (8 total), upper and lower anterior and upper and lower lateral divided longitudinally by the anterior axillary line and transversely by the 2nd intercostal space. An exam was considered abnormal (positive for edema) if it had all of the following features:


By using these criteria this group found a 85.7% sensitivity and 97.7% specificity when compared to chest x-ray for detecting the presence of pulmonary edema [5].

#### **5. Application and differential diagnosis**

The presence of occasional sporadic comet tails can be a normal finding. Typically these are limited to the last lateral intercostals space above the diaphragm with a hot spot often seen on the right most caudal anterior axillary window [22, 9]. Care must be taken, however, in attributing a hot spot in the lower lateral windows to a benign finding, as local lung consoli‐ dation from diseases such as ARDS, atelectasis, or pneumonia can exhibit this pattern. [22, 11]. In those cases, the clinical presentation of dyspnea with other physical signs and symptoms such as low oxygen saturations and fever should be used to help differentiate "normal" from diseased state. With the case of patients presenting with dyspnea, the pathologic state should be considered present until "ruled out" with other diagnostic modalities. However in the research arena where "healthy" subjects may be tested, the pre-test probability that comet tails localized to the last lateral intercostals spaces are normal, is high.

this method has been reported as 5.1% and 7.4% respectively [13]. For clinical purposes Picano and colleges report the comet tail score in a semiquantitative manner for patients in pulmonary

**Score Number of Comet Tails EVLW**

0 <5 No Signs

2 15-30 Moderate

3 "/>30 Severe

**Table 2.** Semiquantitive classification of the Comet Tail Score (CTS)as proposed by Picano and colleagues.

**2.** Diffusely positive with more than one scan per side containing comet tails.

compared to chest x-ray for detecting the presence of pulmonary edema [5].

Simpler less quantitative techniques have also been described with good prediction of pulmonary edema. Volpicelli and colleagues described a technique where each hemithorax is divided into four quadrants (8 total), upper and lower anterior and upper and lower lateral divided longitudinally by the anterior axillary line and transversely by the 2nd intercostal space. An exam was considered abnormal (positive for edema) if it had all of the following features:

By using these criteria this group found a 85.7% sensitivity and 97.7% specificity when

The presence of occasional sporadic comet tails can be a normal finding. Typically these are limited to the last lateral intercostals space above the diaphragm with a hot spot often seen on the right most caudal anterior axillary window [22, 9]. Care must be taken, however, in attributing a hot spot in the lower lateral windows to a benign finding, as local lung consoli‐ dation from diseases such as ARDS, atelectasis, or pneumonia can exhibit this pattern. [22, 11]. In those cases, the clinical presentation of dyspnea with other physical signs and symptoms such as low oxygen saturations and fever should be used to help differentiate "normal" from

1 5-15 Mild

edema (Table 2).

58 Hot Topics in Echocardiography

**4.1. Other techniques**

**1.** At least three comet tails per scan.

**3.** Bilateral presence of comet tails.

**5. Application and differential diagnosis**

A diffuse bilateral comet tail pattern is not considered normal and is indicative of alveolarinterstitial syndromes (AIS). These can be brought about by a number of disease entities including chronic conditions such as pulmonary fibrosis, and acute entities such as acute respiratory distress syndrome (ARDS), interstitial pneumonia, and acute pulmonary edema [5]. Different clinical presentations can help elucidate the etiology of these different diseases which have the same comet tail pattern. The time course of the illness can differentiate chronic causes such as pulmonary fibrosis and acute causes such as pulmonary edema. Additionally slight variations in the pattern of comet tails are noted. In the case of a fibrotic lung, the comet tails are equal in both hemi thoraces, whereas in cardiac pulmonary edema they are bilateral but with a predilection for the right hemi-thorax. Also in the fibrotic lung comet tails are more patchy than in pulmonary edema, and are stable with diuretic therapy [9].

Highly dense entities such as ARDS typically give rise to comet tails only in regions where the diseased lung is in contact with the sub-pleural space. These highly dense areas give rise to multiple comet tails less than 3 mm apart, whereas comet tails arising from thickened inter‐ lobular septa are 7 mm apart [23]. Additionally an ARDS pattern also gives rise to comet tails in focal areas which coalesce together and form comet tails of differing lengths and multiple irregular comet tails [7, 23, 1].

Importantly comet tails which arise from pulmonary edema should respond to treatment and disappear as interventions are made [18]. If they do not, then an alternate diagnosis should be sought. This reenforces the need for serial exams many authors encourage repeat exams to monitor response to therapy.

Since the presence of the occasional comet tail is considered normal, the lack of comet tails can be diagnostic as well. Comet tail formation requires an area of differing acoustic impedances, when this is not present no comet tails are created. Such is the case of a pneumothorax. In examining for this potential emergent condition, an additional ultrasonographic sign must be viewed, that of the "sliding lung sign." This is the hyperechoic line which is the interface between the visceral and parietal pleura. This line will slide back and forth with respiration. When there is no sliding of this line, and an absence of comet tails, a pneumothorax should be suspected [24]. The is particularly helpful when some studies show that standard chest x-ray, in addition to taking longer, misses 30% of cases [25-27]. This is contrasted to the lung ultrasound which in a large meta-analysis and systematic review looked at 8 studies repre‐ senting 1,048 patients. When using both the absence of lung comet tails and sliding lung sign ultrasound was 90.9% sensitive and 98.2% specific in making the diagnosis of pneumothorax. In the same analysis chest radiograph was only 50.2% sensitive, but with a similar specificity of 99.4% [28].

In patients with minimal comet tails confined to the intercostal space above the diaphragm, or no comet tails present on lung ultrasound, but who otherwise present with dyspnea, other commondiagnoses shouldbe considered.These includeCOPD, acutebronchitis, andpulmona‐ ry embolism [1]. The issue of COPD is a special consideration which has been studied by at least three groups. In the initial comet tail paper, Lichtenstein observed that COPD could give rise to a fibrotic pattern, bilateral comet tails [7]. However later work performed by the same author comparing ultrasound to x-ray diagnosis suggested that the presence of diffuse bilateral comet tails was absent in 92% of patient with COPD (N=26) and absent or confined only to the laster intercostal space in 98.75% of patients without respiratory disorder (N=80). The two patients in the COPD group who had a positive test (the false positives) had pneumonia in the regions viewed as positive on ultrasound. In the patients without respiratory symptoms, one patient demonstratedapositive test.Interestingly eventhoughhedidnothave any symptoms,that one patient was admittedfor acute renalfailure requiringurgentdialysis, again supporting the idea that ultrasound findings occur before symptoms [22]. Additional studies also support the lack of findings of comet tails in COPD exacerbations. In fact in one study looking at the presence of comet tails in patients with acute shortness of breath, the most common discharge diagnosis of patients who did not exhibit bilateral diffuse comet tails was COPD [1, 18, 21].

This is found on most modern portable ultrasounds. Non-solid state devices cool using fans

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61

**Figure 5.** Author (DS) demonstrating the ease of use and portability of modern ultrasound systems by performing an

Although dyspnea is a leading cause of hospital admission, determining its etiology and subsequent treatment remains one of the greatest diagnostic challenges a clinicians faces. While many have lamented the perceived loss of physical exam skills amongst practitioners, the traditional lung exam and classic findings heard on auscultation are often difficult to hear in a noisy intensive care unit or emergency department [32, 33]. Even in ideal circumstances, there is abundant literature to suggest that the physical exam may be inaccurate [14, 15]. This

assessment of EVLW at the base camp of Mt Everest, ele 5,364 M, on an elite climber.

leads the clinician to rely on adjuncts to aid in diagnosis.

**7. Conclusion**

which will over heat at extreme altitudes.

Overall this technique allows for the rapid assessment of patients in respiratory distress and can take less than three minutes [9, 15]. When used for detecting pulmonary edema, it has nearly a 95% concordance with chest radiographs [1] and, as discussed above, may be more sensitive than chest radiograph for this diagnosis [15]. A gross recognition of the comet tail pattern present, as well as the patient's history and response to treatment can guide the clinician to the correct diagnosis. In terms of application, bedside ultrasound in many emer‐ gency departments and intensive care units is readily available.

#### **6. Special situations**

Due to its ease of use, portability and relative low cost, this technology is ideally suited for remote research and clinical applications. In fact a bedside ultrasound is the only diagnostic imaging currently used on the International Space Station.

Research applications have used the ultrasonographic finding of comet tails to monitor pulmonary edema in healthy volunteers subjected to extreme environments. These include ironman athletes, breath-hold deep divers, and mountain climbers [29]. Due to the remote nature of the conditions, ultrasound is especially useful in mountaineering where up to 10% of climbers above 4,000 M develop the life-threatening condition known as High Altitude Pulmonary Edema [30]. (See Figure 5) At an altitude of 4,240 M Fagenholz, using the CTS technique described in this chapter, showed that a CTS score of 35 +/- 11 corresponded to patients suffering from HAPE which differed from those who were short of breath from other causes who had a CTS of 12 +/-6.8 [20]. Others have shown that in the presence of normal left ventricular function and normal pulmonary artery pressures, sojourners above 4790 m can develop pulmonary edema with a corresponding decrease in oxygen saturation. The comet tails describe in these studies had right lung predominance [31]. When used in the high altitude environment, care should be taken to ensure that the device employed uses solid state storage. This is found on most modern portable ultrasounds. Non-solid state devices cool using fans which will over heat at extreme altitudes.

**Figure 5.** Author (DS) demonstrating the ease of use and portability of modern ultrasound systems by performing an assessment of EVLW at the base camp of Mt Everest, ele 5,364 M, on an elite climber.

#### **7. Conclusion**

commondiagnoses shouldbe considered.These includeCOPD, acutebronchitis, andpulmona‐ ry embolism [1]. The issue of COPD is a special consideration which has been studied by at least three groups. In the initial comet tail paper, Lichtenstein observed that COPD could give rise to a fibrotic pattern, bilateral comet tails [7]. However later work performed by the same author comparing ultrasound to x-ray diagnosis suggested that the presence of diffuse bilateral comet tails was absent in 92% of patient with COPD (N=26) and absent or confined only to the laster intercostal space in 98.75% of patients without respiratory disorder (N=80). The two patients in the COPD group who had a positive test (the false positives) had pneumonia in the regions viewed as positive on ultrasound. In the patients without respiratory symptoms, one patient demonstratedapositive test.Interestingly eventhoughhedidnothave any symptoms,that one patient was admittedfor acute renalfailure requiringurgentdialysis, again supporting the idea that ultrasound findings occur before symptoms [22]. Additional studies also support the lack of findings of comet tails in COPD exacerbations. In fact in one study looking at the presence of comet tails in patients with acute shortness of breath, the most common discharge diagnosis of

patients who did not exhibit bilateral diffuse comet tails was COPD [1, 18, 21].

gency departments and intensive care units is readily available.

imaging currently used on the International Space Station.

**6. Special situations**

60 Hot Topics in Echocardiography

Overall this technique allows for the rapid assessment of patients in respiratory distress and can take less than three minutes [9, 15]. When used for detecting pulmonary edema, it has nearly a 95% concordance with chest radiographs [1] and, as discussed above, may be more sensitive than chest radiograph for this diagnosis [15]. A gross recognition of the comet tail pattern present, as well as the patient's history and response to treatment can guide the clinician to the correct diagnosis. In terms of application, bedside ultrasound in many emer‐

Due to its ease of use, portability and relative low cost, this technology is ideally suited for remote research and clinical applications. In fact a bedside ultrasound is the only diagnostic

Research applications have used the ultrasonographic finding of comet tails to monitor pulmonary edema in healthy volunteers subjected to extreme environments. These include ironman athletes, breath-hold deep divers, and mountain climbers [29]. Due to the remote nature of the conditions, ultrasound is especially useful in mountaineering where up to 10% of climbers above 4,000 M develop the life-threatening condition known as High Altitude Pulmonary Edema [30]. (See Figure 5) At an altitude of 4,240 M Fagenholz, using the CTS technique described in this chapter, showed that a CTS score of 35 +/- 11 corresponded to patients suffering from HAPE which differed from those who were short of breath from other causes who had a CTS of 12 +/-6.8 [20]. Others have shown that in the presence of normal left ventricular function and normal pulmonary artery pressures, sojourners above 4790 m can develop pulmonary edema with a corresponding decrease in oxygen saturation. The comet tails describe in these studies had right lung predominance [31]. When used in the high altitude environment, care should be taken to ensure that the device employed uses solid state storage.

Although dyspnea is a leading cause of hospital admission, determining its etiology and subsequent treatment remains one of the greatest diagnostic challenges a clinicians faces. While many have lamented the perceived loss of physical exam skills amongst practitioners, the traditional lung exam and classic findings heard on auscultation are often difficult to hear in a noisy intensive care unit or emergency department [32, 33]. Even in ideal circumstances, there is abundant literature to suggest that the physical exam may be inaccurate [14, 15]. This leads the clinician to rely on adjuncts to aid in diagnosis.

In the case of dyspnea, chest radiograph are typically employed to help narrow the differential diagnosis. However even these can be fraught with difficulties including time to obtain, and read the x-ray. Fortunately the field of ultrasound and echocardiography has greatly expanded in the past 20 years. The lung ultrasound finding of comet tails can help guide therapeutic interventions, and unlike chest radiograph, the exam can be repeated without fear of increased radiation exposure.

[6] Levitov, A. Critical Care Ultrasonography. (2009). New York, New York: McGraw-

Lung Ultrasound Comet Tails — Technique and Clinical Significance

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63

[7] Lichtenstein, Daniel et alThe Comet-tail Artifact." Am J Respir Crit Care Med.

[9] Picano, E, et al. Ultrasound lung comets: A clinically useful sign of extravascular

[11] Agricola, Eustachio, et alUltrasound Comet-tail images: A Marker of pulmonary ede‐ ma: a comparative study with wedge pressure and extravascular lung water." Chest.

[12] Lichtenstein, D. A, et al. A-lines and B-lines: lung ultrasound as a bedside tool for predicting pulmonary artery occlusion pressure in the critically ill." Chest. (2009). ,

[13] Jambrik, Z, et al. Usefulness of ultrasound lung comets as a nonradiologic sign of ex‐

[14] Tsverava, M, & Tsverava, D. Comet tail artefact in diagnosis of pulmonary conges‐ tion in patients with diastolic heart failure." Georgian Medical News. (2010). ,

[15] Vitturi, N, et al. Thoracic ultrasonography: A new method for the work-up of pa‐

[16] Stapczynski, J. S, et al. Congestive heart failure and pulmonary edema." Emergency medicine: a comprehensive study guide. New York: McGraw-Hill; (1992). , 216-219.

[17] Lange, N. R, & Schuster, D. P. The measurement of lung water." Crit Care. (1999).

[18] Mallamaci, F, et al. Detection of pulmonary congestion by chest ultrasound in dialy‐

[20] Fagenholz, P. J, et al. Chest ultrasonography for the diagnosis and monitoring of

[21] Volpicelli, G, et al. Usefulness of lung ultrasound in the bedside distinction between pulmonary edema and exacerbation of COPD." Emerg Radiol. (2008). , 15(3), 145-151.

[22] Lichtenstein, D, & Mezière, G. A lung ultrasound sign allowing bedside distinction between pulmonary edema and COPD: the comet-tail artifact." Intesive Care Med.

tients with dyspnea." Journal of Ultrasound. (2011). , 14, 147-151.

sis patients." JACC:Cardiovascular Imagin. (2010). , 3(6), 586-594.

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[8] Ziskin, M. C, et al. The comet tail artifact." J Ultrasound Med. (1982). , 1, 1-7.

lung water." J Am Soc Echocardiography. (2006). , 19(3), 356-363.

[10] Kerley, P. Radiology in heart disease. BMJ (1933).

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With the advent of small bedside machines, lung ultrasound techniques can become an extension of the physical exam. These exams can be repeated as often as necessary in response to changing clinical conditions. In this way ultrasonographers can guide real-time decision making for patient care.

#### **Acknowledgements**

Funded by grants from NIH HL71478, Mayo Clinic and The North Face Company.

#### **Author details**

Douglas T. Summerfield and Bruce D. Johnson\*

\*Address all correspondence to: Johnson.bruce@mayo.edu

Divisions of Pulmonary and Critical Care Medicine and Cardiovascular Diseases, Mayo Clinic Rochester, USA

#### **References**


In the case of dyspnea, chest radiograph are typically employed to help narrow the differential diagnosis. However even these can be fraught with difficulties including time to obtain, and read the x-ray. Fortunately the field of ultrasound and echocardiography has greatly expanded in the past 20 years. The lung ultrasound finding of comet tails can help guide therapeutic interventions, and unlike chest radiograph, the exam can be repeated without fear of increased

With the advent of small bedside machines, lung ultrasound techniques can become an extension of the physical exam. These exams can be repeated as often as necessary in response to changing clinical conditions. In this way ultrasonographers can guide real-time decision

Funded by grants from NIH HL71478, Mayo Clinic and The North Face Company.

Divisions of Pulmonary and Critical Care Medicine and Cardiovascular Diseases, Mayo

[1] Zanobetti, Maurizia, et alCan chest ultrasonography replace standard chest radiogra‐ phy for evaluation of acute dyspnea in the ED?" Chest. (2011). , 139, 1140-1147.

[2] Wang, C. S, et al. Does this dyspneic patient in the emergency department have con‐

[3] Cremona, G, et al. Pulmonary extravascular fluid accumulation in recreational climb‐

[4] Milne, E. N. et. al. "The radiologic distinction of cardiogenic and noncardiogenic ede‐

[5] Volpicelli, Giovanni, et alBedside lung ultrasound in the assessment of alveolar-in‐ terstitial syndrome." American Journal of Emergency Medicine. (2006). , 24, 689-696.

radiation exposure.

62 Hot Topics in Echocardiography

making for patient care.

**Acknowledgements**

**Author details**

Clinic Rochester, USA

**References**

Douglas T. Summerfield and Bruce D. Johnson\*

\*Address all correspondence to: Johnson.bruce@mayo.edu

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**Chapter 4**

**Ischemic Mitral Regurgitation: From Echo**

Gheorghe Cerin, Adrian Bogdan Popa,

Additional information is available at the end of the chapter

Razvan Ticulescu and Marco Diena

http://dx.doi.org/10.5772/56062

**1. Introduction**

method of diagnosis.

**Assessment to Surgical Strategy and Techniques**

Ischemic mitral regurgitation remains an underestimated and important clinical problem. It is a complex multifactorial disease that involves global and regional left ventricular remodel‐ ing as well as dysfunction and distortion of the components of the mitral valve including the chordae, annulus and leaflets. The prevalence rate of development of mild or more severe degree of mitral insufficiency after myocardial infarction has been estimated to be up to 50%

Based on the clinical presentation, the ischemic mitral regurgitation was classified as acute or chronic (Mitesh, 2009). Although the acute ischemic mitral regurgitation is relatively rare, whenever present, it has a rapid evolution, with an extremely poor survival rate. On the other hand, the chronic ischemic mitral regurgitation is much more frequent, but it's the consequence of a slower pathological process, with a better survival rate. The echocardiography identifies all patterns of ischemic mitral regurgitation; nonetheless the classification as acute, sub-acute or chronic ischemic mitral regurgitation is rather clinical, than an echocardiographic one. Beside the complete rupture of papillary muscle, other patterns of ischemic mitral regurgita‐ tion cannot be practically located in time by echo. It is possible to have the same echocardio‐ graphic feature of the lesion in acute and in chronic settings; only the clinical presentation of the patient helps in the diagnosis of acute / sub-acute or chronic ischemic mitral regurgitation. So the echo exam has to be seen as complementary to clinical data, rather than a singular

In everyday practice the management of ischemic mitral regurgitation represents a combined problem of physiopathology, quantification and diagnosis that, together, drive the individual

> © 2013 Cerin et al.; licensee InTech. This is a paper distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

and is associated with worse prognosis (Stevenson 1987, Lamas 1997, Grigioni 2001).


## **Ischemic Mitral Regurgitation: From Echo Assessment to Surgical Strategy and Techniques**

Gheorghe Cerin, Adrian Bogdan Popa, Razvan Ticulescu and Marco Diena

Additional information is available at the end of the chapter

http://dx.doi.org/10.5772/56062

#### **1. Introduction**

[23] Lichtenstein, D, et al. Comparative diagnostic performances of auscultation, chest ra‐ diography, and lung ultrasonography in acute respiratory distress syndrome." Anes‐

[24] Lichtenstein, D, & Menu, Y. A bedside ultrasound sign ruling out pneumothorax in

[25] Tocino, I. M, et al. Distribution of pneumothorax in the supine and semirecumbent

[26] Chiles, C, & Ravin, C. E. Radiographic recognition of pneumothorax in the intensive

[27] Ball, C. G, et al. Factors related to the failure of radiographic recognition of occult

[28] Alrajhi, K. Test characteristics of ultrasonography for the detection of pneumothorax:

[29] Garbella, E, et al. Pulmonary edema in healthy subjects in extreme conditions." Pulm

[30] Bärtsch, P, et al. Respiratory symptoms, radiographic and physiologic correlations at high altitude." In: Sutton JR, Coates G, Remmers JE, editors. Hypoxia: the adapta‐

[31] Pratali, L, et al. Frequent subclinical high-altitude pulmonary edema detected by chest sonography as ultrasound lung comets in recreational climbers." Crit Care

[32] Mccullough, P. A. Uncovering heart failure in patients with a history of pulmonary disease: rationale for the early use of B-type natriuretic peptide in the emergency de‐

[33] Remes, J. Validity of clinical diagnosis of heart failure in primary health care." Eur

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tions. Toronto: B.C. Decker;(1990). , 241-245.

partment." Acad Emerg Med. (2003). , 10, 198-204.

Med. (2010). , 38(9), 1818-1823.

Heart J. (1991). , 12, 315-321.

thesiology. (2004). , 100, 9-15.

64 Hot Topics in Echocardiography

Med. (2011).

Ischemic mitral regurgitation remains an underestimated and important clinical problem. It is a complex multifactorial disease that involves global and regional left ventricular remodel‐ ing as well as dysfunction and distortion of the components of the mitral valve including the chordae, annulus and leaflets. The prevalence rate of development of mild or more severe degree of mitral insufficiency after myocardial infarction has been estimated to be up to 50% and is associated with worse prognosis (Stevenson 1987, Lamas 1997, Grigioni 2001).

Based on the clinical presentation, the ischemic mitral regurgitation was classified as acute or chronic (Mitesh, 2009). Although the acute ischemic mitral regurgitation is relatively rare, whenever present, it has a rapid evolution, with an extremely poor survival rate. On the other hand, the chronic ischemic mitral regurgitation is much more frequent, but it's the consequence of a slower pathological process, with a better survival rate. The echocardiography identifies all patterns of ischemic mitral regurgitation; nonetheless the classification as acute, sub-acute or chronic ischemic mitral regurgitation is rather clinical, than an echocardiographic one. Beside the complete rupture of papillary muscle, other patterns of ischemic mitral regurgita‐ tion cannot be practically located in time by echo. It is possible to have the same echocardio‐ graphic feature of the lesion in acute and in chronic settings; only the clinical presentation of the patient helps in the diagnosis of acute / sub-acute or chronic ischemic mitral regurgitation. So the echo exam has to be seen as complementary to clinical data, rather than a singular method of diagnosis.

In everyday practice the management of ischemic mitral regurgitation represents a combined problem of physiopathology, quantification and diagnosis that, together, drive the individual

© 2013 Cerin et al.; licensee InTech. This is a paper distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

patient prognosis but, in case of patients candidate to open heart surgery this becomes a very complex issue. With intraoperative TEE echocardiography, the exact identification of the mechanism of ischemic mitral regurgitation represents a cornerstone element for surgical planning and patient management. In case of significant residual mitral regurgitation a second run of the extracorporeal circulation may be necessary requiring a well-founded experience from the echocardiographer as the TEE intraoperative findings may be sometimes misleading.

far, very limited. There are only few general recommendations and the guidelines do not include them in the systematic evaluation of the ischemic mitral regurgitation. Most of the current information focuses on regional and global ventricular remodeling, with leaflets tethering and tenting, motion restriction and annular dilatation. Frequently, the ischemic remodeling of papillary muscle is difficult to document; nevertheless with an accurate analysis, often performed in non-standard echocardiographic views, the diseased papillary muscle may

Ischemic Mitral Regurgitation: From Echo Assessment to Surgical Strategy and Technique

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67

In coronary patients with mitral insufficiency, beside the ventricular remodeling, annular dilatation and leaflets (mobility and tethering), the echocardiographer has to focus the attention on the shape, the length and the thickness of the papillary muscle, mainly in acute

**Figure 1.** Acute inferior MI with severe MR due to acute post-ischemic elongation of PP MM. Note the abnormal length and shape of the very slim PP MM. The tip reaches the level of the MV annular plane. Often (as in this case), the elongation PP MM is visible in a different plane respect of the MR at color Doppler. MI = myocardial infarction; MR =

On the other hand, in the case of **chronic ischemic mitral insufficiency**, all the remodeling processes of left ventricle causing the ischemic mitral regurgitation are slower, the evolve over time and usually the echo diagnosis is not so tricky. Generally, the patterns of chronic ischemic mitral regurgitation are quite often the same: tethering of the papillary muscle, chordae and leaflets, various degree and progressive dilation of the left ventricular cavity and mitral annulus, mitral valve tenting, with reduced / loss of coaptation and restriction of one or both leaflets (fig 2, 3). The post-infarction loss of the contractile ventricular mass is directly corre‐ lated with the remodeling process, expressed by the heart dilatation and decreasing of cardiac reserve. All the elements belonging to the mitral apparatus will be involved in this process,

Ischemic mitral regurgitation has several pathophysiological determinants. It has been defined as a ventricular disease that affects the mitral apparatus, because both myocardial infarction and ischemia generate progressive global and regional left ventricular remodeling, and consequently, a functional mitral regurgitation. Apical and posterior displacement of the papillary muscle is a typical echocardiographic finding. This process starts ordinarily with the

circumstances, when the acute remodeling process is just beginning (fig 1).

Mitral regurgitation; PP MM = papillary muscle; MV = mitral valve.

but the leaflets and the chordae are, as a matter of fact, preserved.

be identified.

The relation between the ischemic mitral regurgitation, surgery and echocardiography, as tool for surgical planning and postoperative control, will be addressed in this chapter. The suboptimal results obtained by the most commonly used surgical strategy, that is, restrictive annuloplasty combined with coronary artery bypass graft, emphasizes the need to develop alternative or concomitant surgical techniques that directly target the causal mechanisms of the disease. Recent data show that this procedure is associated with a 10% to 20% rate of persistent mitral regurgitation soon after operation and a 50% to 70% rate of recurrent mitral insufficiency at five years (Hashim 2012, Magne 2009). Hereafter, the topics will be focused mainly on the echo assessment of the patients candidate for open-heart surgery. A particular attention will be paid to the papillary muscle and to the mitral valve geometry and their role in the pathophysiology of ischemic mitral insufficiency. Understanding the mechanisms of the different types of ischemic mitral regurgitation is mandatory for echocardiographer and surgeon to tailor the right strategy for the valve repair, and it is indeed a challenging task for both.

### **2. Physiopathology: Concepts regarding post-myocardial left ventricular remodeling, acute and chronic ischemic mitral valve and the valve geometry**

It is generally assumed that the ischemic mitral regurgitation is not a valve disease, the *'engine'* of valve insufficiency being the remodeling process of the left ventricle, depending on the localization and extension of the myocardial infarction. In ischemic heart disease, the mitral leaflets (and also the chordae) are typically structurally normal, but the leaflets are tethered and their motion is relatively restricted, owing to regional and global ventricular remodeling, with apical displacement of the posteromedial papillary muscle.

Sometimes the remodeling process starts immediately after the onset of myocardial infarction causing structural ischemic mitral regurgitation, which is associated with a poor prognosis, due to the concomitant acute infarction, acute papillary muscle remodeling and **acute ischemic mitral regurgitation**. For a successful management of this acute mechanical complication the key point is the early diagnosis, which has to be done before the complete rupture of the papillary muscle occurs. This life-threatening complication has otherwise to be considered a failure due to late echocardiographic and clinic diagnosis.

Overall, there is only scanty literature concerning the echocardiographic assessment of the papillary muscle and it is no surprising then to see that its use in the everyday practice is, so far, very limited. There are only few general recommendations and the guidelines do not include them in the systematic evaluation of the ischemic mitral regurgitation. Most of the current information focuses on regional and global ventricular remodeling, with leaflets tethering and tenting, motion restriction and annular dilatation. Frequently, the ischemic remodeling of papillary muscle is difficult to document; nevertheless with an accurate analysis, often performed in non-standard echocardiographic views, the diseased papillary muscle may be identified.

patient prognosis but, in case of patients candidate to open heart surgery this becomes a very complex issue. With intraoperative TEE echocardiography, the exact identification of the mechanism of ischemic mitral regurgitation represents a cornerstone element for surgical planning and patient management. In case of significant residual mitral regurgitation a second run of the extracorporeal circulation may be necessary requiring a well-founded experience from the echocardiographer as the TEE intraoperative findings may be sometimes misleading.

The relation between the ischemic mitral regurgitation, surgery and echocardiography, as tool for surgical planning and postoperative control, will be addressed in this chapter. The suboptimal results obtained by the most commonly used surgical strategy, that is, restrictive annuloplasty combined with coronary artery bypass graft, emphasizes the need to develop alternative or concomitant surgical techniques that directly target the causal mechanisms of the disease. Recent data show that this procedure is associated with a 10% to 20% rate of persistent mitral regurgitation soon after operation and a 50% to 70% rate of recurrent mitral insufficiency at five years (Hashim 2012, Magne 2009). Hereafter, the topics will be focused mainly on the echo assessment of the patients candidate for open-heart surgery. A particular attention will be paid to the papillary muscle and to the mitral valve geometry and their role in the pathophysiology of ischemic mitral insufficiency. Understanding the mechanisms of the different types of ischemic mitral regurgitation is mandatory for echocardiographer and surgeon to tailor the right strategy for the valve repair, and it is indeed a challenging task for

**2. Physiopathology: Concepts regarding post-myocardial left ventricular**

It is generally assumed that the ischemic mitral regurgitation is not a valve disease, the *'engine'* of valve insufficiency being the remodeling process of the left ventricle, depending on the localization and extension of the myocardial infarction. In ischemic heart disease, the mitral leaflets (and also the chordae) are typically structurally normal, but the leaflets are tethered and their motion is relatively restricted, owing to regional and global ventricular remodeling,

Sometimes the remodeling process starts immediately after the onset of myocardial infarction causing structural ischemic mitral regurgitation, which is associated with a poor prognosis, due to the concomitant acute infarction, acute papillary muscle remodeling and **acute ischemic mitral regurgitation**. For a successful management of this acute mechanical complication the key point is the early diagnosis, which has to be done before the complete rupture of the papillary muscle occurs. This life-threatening complication has otherwise to be considered a

Overall, there is only scanty literature concerning the echocardiographic assessment of the papillary muscle and it is no surprising then to see that its use in the everyday practice is, so

**remodeling, acute and chronic ischemic mitral valve and the valve**

with apical displacement of the posteromedial papillary muscle.

failure due to late echocardiographic and clinic diagnosis.

both.

66 Hot Topics in Echocardiography

**geometry**

In coronary patients with mitral insufficiency, beside the ventricular remodeling, annular dilatation and leaflets (mobility and tethering), the echocardiographer has to focus the attention on the shape, the length and the thickness of the papillary muscle, mainly in acute circumstances, when the acute remodeling process is just beginning (fig 1).

**Figure 1.** Acute inferior MI with severe MR due to acute post-ischemic elongation of PP MM. Note the abnormal length and shape of the very slim PP MM. The tip reaches the level of the MV annular plane. Often (as in this case), the elongation PP MM is visible in a different plane respect of the MR at color Doppler. MI = myocardial infarction; MR = Mitral regurgitation; PP MM = papillary muscle; MV = mitral valve.

On the other hand, in the case of **chronic ischemic mitral insufficiency**, all the remodeling processes of left ventricle causing the ischemic mitral regurgitation are slower, the evolve over time and usually the echo diagnosis is not so tricky. Generally, the patterns of chronic ischemic mitral regurgitation are quite often the same: tethering of the papillary muscle, chordae and leaflets, various degree and progressive dilation of the left ventricular cavity and mitral annulus, mitral valve tenting, with reduced / loss of coaptation and restriction of one or both leaflets (fig 2, 3). The post-infarction loss of the contractile ventricular mass is directly corre‐ lated with the remodeling process, expressed by the heart dilatation and decreasing of cardiac reserve. All the elements belonging to the mitral apparatus will be involved in this process, but the leaflets and the chordae are, as a matter of fact, preserved.

Ischemic mitral regurgitation has several pathophysiological determinants. It has been defined as a ventricular disease that affects the mitral apparatus, because both myocardial infarction and ischemia generate progressive global and regional left ventricular remodeling, and consequently, a functional mitral regurgitation. Apical and posterior displacement of the papillary muscle is a typical echocardiographic finding. This process starts ordinarily with the

**Figure 2.** Inferior myocardial infarction with ischemic mitral regurgitation due to systolic restriction of posterior mitral leaflet (2D and 3D systolic frame, from two different patients). Note the systolic tension on the chordae belonging to the posterior mitral valve with limited excursion of the cusp, the asymmetrical apposition of the anterior leaflet and the reduced area of coaptation.

posterior leaflet because the posterior mitral annulus is thinner, weaker, more flexible and without a zone of resistance. On the contrary, the anterior leaflet has a more thickened and less malleable annulus. In this way the posterior leaflet became firstly restricted while the anterior is involved only later on. The echocardiography is able to assess the relationship between the LV cavity (shape, dimensions, volume), the mitral leaflets (as mobility, leaflet apposition, length and height of coaptation, annulus dimension, etc) and the valve geometry.

In the case of chronic ischemic mitral regurgitation and ischemic dilated cardiomyopathy, (generally patients with anterior and inferior infarction), the right balance between the dimen‐ sionofthemitralvalve andthe 'new'dimensionofthedouble infarctedventricular cavityis lost, so that the mitral valve becomes insufficient. Conceptually, it may be assumed that there is a phenomenon of *'mismatch'* between the *'too large'* left ventricle and *'too small'* mitral valve apparatus,whichisunabletoextendthedraperyoftheleafletsandtoadapttothenewdimension of the infarcted ventricle (fig 3). That's why, in case of critical coronary artery disease leading to left heart dilatation and ischemic mitral regurgitation, the 'standard' surgical approach of coronary artery by-pass grafting (CABG) plus undersized ring alone, may not solve complete‐ ly the mitral regurgitation and, over time, the repair may fail (Magne 2009). In these cases the annuloplasty ring alone is not enough to achieve sufficient *'fabrics'* for a stable coaptation and repair. Ideally speaking, to get a good repair more tissue is needed to enlarge the mitral valve. This concept will be addressed in the chapter of chronic ischemic mitral regurgitation.

As noted (Cerin 2006, Tesler 2009), from the geometrical point of view, the normal mitral valve presents *a triangle* delimited between the coaptation point (typically sited inside of the ventricular cavity) and two others referral points, placed on the anterior and posterior mitral annulus (standard pattern of a normal mitral valve – Fig 4). This *echocardiographic virtual tool* demonstrates to be useful in judging the mitral valve structural and functional abnormalities (Cerin 2012). When the echocardiographic presentation of ischemic mitral regurgitation is consistent with obvious deformation of this virtual triangle, this should raise the suspicion of a possible papillary muscle abnormality with elongation of sub-valvular apparatus, alongside

**Figure 3.** Ischemic dilated cardiomyopathy and the concept of "mitral - ventricular mismatch" (see the text). Patient with double myocardial infarction (anterior and inferior).Ischemic dilated cardiomyopathy and chronic ischemic mitral insufficiency. Note the spherical shape and dilatation of the left ventricular cavity, the reduced surface of coaptation of mitral leaflet (2mm), due to the annular dilatation (41mm) and the laterally migration of the papillary muscle.

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In some cases the geometry of the mitral valve may be so distorted that an elongation of the sub valvular apparatus has to be suspected or is clearly present. In these particular cases, the echocardiography examination has to be focused on the papillary muscle lesions; this might require the execution of the exam in several off axis views, beside the standard ones. Patients with distortion of mitral valve geometry (fig 5A) will not fit within the III°b of Carpentier's classification. Some of these patient may present a clear ischemic mitral valve prolapse (type II° Carpentier), but many of them will show only a distortion of the 'standard' mitral valve triangle, with the coaptation point still present inside of the left ventricular cavity. The

to reduce / loss of leaflet coaptation.

Type I° Normal leaflet motion

Type III° Restricted motion III°a Restricted opening III°b Restricted closure

Type II° Excess leaflet motion (leaflet prolapse)

**Table 1.** Carpentier's classifications of Mitral Regurgitation

The chronic ischemic mitral regurgitation is classified as a *III°b type* of mitral insufficiency essentially due to the systolic restriction of the posterior leaflet (Table 1). The practice dem‐ onstrates that in the case of ischemic mitral regurgitation this classification may be incomplete and misleading because the chronic ischemic mitral regurgitation has always a combined annular dilation of the valve, which in fact is a type I° mechanism of mitral regurgitation in Carpenter's classification (Carpentier 1983 & 2010). That's why, for a better and more precise diagnosis of the mechanisms of ischemic mitral regurgitation, **the mitral valve geometry** has to be carefully assessed.

Ischemic Mitral Regurgitation: From Echo Assessment to Surgical Strategy and Technique http://dx.doi.org/10.5772/56062 69

**Figure 3.** Ischemic dilated cardiomyopathy and the concept of "mitral - ventricular mismatch" (see the text). Patient with double myocardial infarction (anterior and inferior).Ischemic dilated cardiomyopathy and chronic ischemic mitral insufficiency. Note the spherical shape and dilatation of the left ventricular cavity, the reduced surface of coaptation of mitral leaflet (2mm), due to the annular dilatation (41mm) and the laterally migration of the papillary muscle.


#### **Table 1.** Carpentier's classifications of Mitral Regurgitation

posterior leaflet because the posterior mitral annulus is thinner, weaker, more flexible and without a zone of resistance. On the contrary, the anterior leaflet has a more thickened and less malleable annulus. In this way the posterior leaflet became firstly restricted while the anterior is involved only later on. The echocardiography is able to assess the relationship between the LV cavity (shape, dimensions, volume), the mitral leaflets (as mobility, leaflet apposition, length and height of coaptation, annulus dimension, etc) and the valve geometry.

**Figure 2.** Inferior myocardial infarction with ischemic mitral regurgitation due to systolic restriction of posterior mitral leaflet (2D and 3D systolic frame, from two different patients). Note the systolic tension on the chordae belonging to the posterior mitral valve with limited excursion of the cusp, the asymmetrical apposition of the anterior leaflet and

In the case of chronic ischemic mitral regurgitation and ischemic dilated cardiomyopathy, (generally patients with anterior and inferior infarction), the right balance between the dimen‐ sionofthemitralvalve andthe 'new'dimensionofthedouble infarctedventricular cavityis lost, so that the mitral valve becomes insufficient. Conceptually, it may be assumed that there is a phenomenon of *'mismatch'* between the *'too large'* left ventricle and *'too small'* mitral valve apparatus,whichisunabletoextendthedraperyoftheleafletsandtoadapttothenewdimension of the infarcted ventricle (fig 3). That's why, in case of critical coronary artery disease leading to left heart dilatation and ischemic mitral regurgitation, the 'standard' surgical approach of coronary artery by-pass grafting (CABG) plus undersized ring alone, may not solve complete‐ ly the mitral regurgitation and, over time, the repair may fail (Magne 2009). In these cases the annuloplasty ring alone is not enough to achieve sufficient *'fabrics'* for a stable coaptation and repair. Ideally speaking, to get a good repair more tissue is needed to enlarge the mitral valve.

This concept will be addressed in the chapter of chronic ischemic mitral regurgitation.

to be carefully assessed.

the reduced area of coaptation.

68 Hot Topics in Echocardiography

The chronic ischemic mitral regurgitation is classified as a *III°b type* of mitral insufficiency essentially due to the systolic restriction of the posterior leaflet (Table 1). The practice dem‐ onstrates that in the case of ischemic mitral regurgitation this classification may be incomplete and misleading because the chronic ischemic mitral regurgitation has always a combined annular dilation of the valve, which in fact is a type I° mechanism of mitral regurgitation in Carpenter's classification (Carpentier 1983 & 2010). That's why, for a better and more precise diagnosis of the mechanisms of ischemic mitral regurgitation, **the mitral valve geometry** has As noted (Cerin 2006, Tesler 2009), from the geometrical point of view, the normal mitral valve presents *a triangle* delimited between the coaptation point (typically sited inside of the ventricular cavity) and two others referral points, placed on the anterior and posterior mitral annulus (standard pattern of a normal mitral valve – Fig 4). This *echocardiographic virtual tool* demonstrates to be useful in judging the mitral valve structural and functional abnormalities (Cerin 2012). When the echocardiographic presentation of ischemic mitral regurgitation is consistent with obvious deformation of this virtual triangle, this should raise the suspicion of a possible papillary muscle abnormality with elongation of sub-valvular apparatus, alongside to reduce / loss of leaflet coaptation.

In some cases the geometry of the mitral valve may be so distorted that an elongation of the sub valvular apparatus has to be suspected or is clearly present. In these particular cases, the echocardiography examination has to be focused on the papillary muscle lesions; this might require the execution of the exam in several off axis views, beside the standard ones. Patients with distortion of mitral valve geometry (fig 5A) will not fit within the III°b of Carpentier's classification. Some of these patient may present a clear ischemic mitral valve prolapse (type II° Carpentier), but many of them will show only a distortion of the 'standard' mitral valve triangle, with the coaptation point still present inside of the left ventricular cavity. The

because the small ring corrects the mitral annulus deformation only, whereas the main problems of these patients are represented by the displacement of coaptation plane too 'high', nearby the mitral annulus, the distortion of the coaptation surface and plane due to the 'crash' of the tip of the mitral valve tenting and the reduced mitral leaflet coaptation (fig 5B, scheme). The mechanism of regurgitation in these patients is clearly more complex than the classical

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Often the mechanisms involved in the ischemic mitral regurgitation are multiple, complex and intricate, and the surgical planning of the valve repair must to be tailored, ignoring partially and sometimes totally the classifications; classifications often focus on the mitral leaflet only (which are practically normal) and do not include the papillary muscles, the mitral valve

Depending of the clinical context, a check list of the echocardiographic elements has to include: dimension of the left ventricular cavity (as diameter and volume), diameter of the mitral annulus (transthoracic, PSLAx systole), the sphericity index and the distance between the papillary muscle (in case of ischemic cardiomyopathy), the length of leaflets coaptation, the length of the anterior leaflet, the 'height' of the posterior leaflet, the mobility of the anterior

From this point of view, beside of the others elements involved in valve regurgitation, the use of the *triangle of coaptation* as tool of mitral valve geometry (Cerin 2010) shows to be a suitable instrument 'to judge' better the mechanisms of ischemic mitral regurgitation (Fig 4, 5A, 5B). In some cases, due to obviously papillary muscle elongation, the triangle may completely

**Figure 6.** Chronic ischemic mitral regurgitation, due to reduce leaflet coaptation (approx. 2mm), dilatation of the left ventricle (EDVol 245ml) and of the mitral annulus (Ø45mm). Note the absence of 'the coaptation triangle' due to is‐ chemic elongation of papillary muscle: the length of papillary muscle is completely unusual, having the tip situated very near to the mitral annulus. Note also the triangular shape of this muscle, with a very sharp tip, due to progressive post-ischemic remodeling with elongation: so called 'thorn papillary muscle'. Because of the abnormal post-ischemic elongation of the papillary muscle, the normal geometry of mitral valve was distorted and the triangle of coaptation

'leaflet restriction' (III°b type of Carpentier's classification).

and most of all the posterior leaflet, etc.

disappears. NB – all the images belong to the same patient.

disappear (see the Fig 6).

geometry and the grade of general or regional left ventricular remodeling.

**Figure 4. The coaptation triangle** and the mitral valve geometry. The normal pattern of mitral valve anatomy and function is characterized by the triangle of coaptation which is defined by the coaptation point (C), normally sited in‐ side of the left ventricular cavity and two other points (A, B) placed on the anterior and posterior mitral annulus.

geometrical analysis of these patients will show the disappearance of the mitral valve triangle and a progressive the transformation of it in a *'trapeze'.* (Fig 5B).

**Figure 5.** A (up) and B (down). Ischemic mitral regurgitation with **distorted mitral valve geometry**. Note the absence of the 'standard triangle of coaptation' which as a matter of fact was transformed into a 'trapeze' due to the postischemic 'crash' of the edge of the mitral valve, generated by papillary muscle elongation (drawing).

The repair strategy by the undersized rings alone may not solve the mitral regurgitation in patients with distorted mitral valve geometry (due to papillary muscle elongation). This because the small ring corrects the mitral annulus deformation only, whereas the main problems of these patients are represented by the displacement of coaptation plane too 'high', nearby the mitral annulus, the distortion of the coaptation surface and plane due to the 'crash' of the tip of the mitral valve tenting and the reduced mitral leaflet coaptation (fig 5B, scheme). The mechanism of regurgitation in these patients is clearly more complex than the classical 'leaflet restriction' (III°b type of Carpentier's classification).

Often the mechanisms involved in the ischemic mitral regurgitation are multiple, complex and intricate, and the surgical planning of the valve repair must to be tailored, ignoring partially and sometimes totally the classifications; classifications often focus on the mitral leaflet only (which are practically normal) and do not include the papillary muscles, the mitral valve geometry and the grade of general or regional left ventricular remodeling.

Depending of the clinical context, a check list of the echocardiographic elements has to include: dimension of the left ventricular cavity (as diameter and volume), diameter of the mitral annulus (transthoracic, PSLAx systole), the sphericity index and the distance between the papillary muscle (in case of ischemic cardiomyopathy), the length of leaflets coaptation, the length of the anterior leaflet, the 'height' of the posterior leaflet, the mobility of the anterior and most of all the posterior leaflet, etc.

geometrical analysis of these patients will show the disappearance of the mitral valve triangle

**Figure 4. The coaptation triangle** and the mitral valve geometry. The normal pattern of mitral valve anatomy and function is characterized by the triangle of coaptation which is defined by the coaptation point (C), normally sited in‐ side of the left ventricular cavity and two other points (A, B) placed on the anterior and posterior mitral annulus.

**Figure 5.** A (up) and B (down). Ischemic mitral regurgitation with **distorted mitral valve geometry**. Note the absence of the 'standard triangle of coaptation' which as a matter of fact was transformed into a 'trapeze' due to the post-

The repair strategy by the undersized rings alone may not solve the mitral regurgitation in patients with distorted mitral valve geometry (due to papillary muscle elongation). This

ischemic 'crash' of the edge of the mitral valve, generated by papillary muscle elongation (drawing).

and a progressive the transformation of it in a *'trapeze'.* (Fig 5B).

70 Hot Topics in Echocardiography

From this point of view, beside of the others elements involved in valve regurgitation, the use of the *triangle of coaptation* as tool of mitral valve geometry (Cerin 2010) shows to be a suitable instrument 'to judge' better the mechanisms of ischemic mitral regurgitation (Fig 4, 5A, 5B). In some cases, due to obviously papillary muscle elongation, the triangle may completely disappear (see the Fig 6).

**Figure 6.** Chronic ischemic mitral regurgitation, due to reduce leaflet coaptation (approx. 2mm), dilatation of the left ventricle (EDVol 245ml) and of the mitral annulus (Ø45mm). Note the absence of 'the coaptation triangle' due to is‐ chemic elongation of papillary muscle: the length of papillary muscle is completely unusual, having the tip situated very near to the mitral annulus. Note also the triangular shape of this muscle, with a very sharp tip, due to progressive post-ischemic remodeling with elongation: so called 'thorn papillary muscle'. Because of the abnormal post-ischemic elongation of the papillary muscle, the normal geometry of mitral valve was distorted and the triangle of coaptation disappears. NB – all the images belong to the same patient.

The echocardiographic assessment of the mechanisms of the ischemic mitral regurgitation, which is the key for the tailored surgical approach, may be sometimes complex and tricky, due to a true mosaic of intricate mechanisms, difficult to be embedded and defined by a standard classification. The echocardiographer has to be aware of the complexity of the left ventricular remodeling process and to assess the mitral valve apparatus using multiple views and to pay particular attention to the analysis of the mitral valve geometry.

Theacute ischemicmitralregurgitation(Fig8)ismoreoftendue tostructurallesionsas complete or partial rupture of the papillary muscle, and less frequent due to an elongation of the mus‐ cle. The echocardiographic diagnosis may not be easy and it is often based on the use of the TEE in the emergency facility. The key issue in the successful management of these patients is timely intervention. If the clinical conditions and the logistic allow it, the patient should be urgently taken to the operating room. Most often, the acute ischemic regurgitation is surgically treated by mitral valve replacement. Mitral valve repair is rare, but, in specific cases, it may be a valid alternative. This depends on the quality and on the entity of the structural alteration of the

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From the echocardiographic point of view, the acute structural ischemic mitral regurgitation may present three different patterns: transection of papillary muscle ("too late" diagnosis), partial rupture of the papillary muscle ("timely" diagnosis) and elongation of the papillary

**Figure 8.** Echocardiographic classification of the structural acute ischemic mitral regurgitation (scheme). The upper pictures represent a case with transection of papillary muscle, in a patient with cardiogenic shock ("too late" echo di‐ agnosis). In the bottom raw acute papillary muscle elongation (the first pictures on the left) and partial rupture of pap‐

The gloomy clinical prognosis of acute significant ischemic mitral regurgitation associated to myocardial infarction (moderate or severe degree) is illustrated by its devastating impact on short- and long-term survival: almost one out of 4 patients die at one month and more than

In most cases the acute ischemic mitral regurgitation is a syndrome with conspicuous clinical implications. Generally, the clinical presentation of these patients is compatible with a hyper acute heart failure; they are highly symptomatic and may present with overt acute pulmonary edema, cardiogenic shock or even sudden death. Only minorities of patients are mildly

Based on the echocardiography exam the acute ischemic mitral regurgitation may be divided in structural and functional. The structural ischemic mitral regurgitation is determined by

one out of 2 after one year (24% early and 54% 1-year mortality rate) (Otto, 2012).

symptomatic or asymptomatic and may present just a new systolic murmur.

subvalvular apparatus, and also on the experience of the surgical team.

muscle (the "tricky" echo diagnosis); see the scheme on the Fig 8.

illary muscle (right picture, yellow arrow); both patients were in 3rd NYHA Class.

#### **3. Acute ischemic mitral regurgitation**

**Background.** Acute ischemic mitral valve regurgitation may occur in the setting of acute myocardial infarction owing to necrosis and rupture of papillary muscle tissue or abnormal coaptation of the leaflets, due to distortion of ventricular geometry. Hemodynamically significant mitral regurgitation is possible in both anterior and inferior infarcts, but its incidence appears higher in the inferior myocardial infarction group such as 40% vs 15% - see the Fig 7 (Estes 1966, Dagum 2000, Timek 2003). Post-infarction mitral regurgitation may be associated to multiple cardiovascular risk factors such as diabetes, abnormal body mass index (>25), advanced age, female gender, coexistence of peripheral arteriopathy and prior infarction (Green, 1999).

**Figure 7.** Differences in the vascularization of the papillary muscle. Postero-medial papillary muscle usually receives the blood only form the right coronary artery (rarely from circumflex artery), respect of the antero-lateral papillary muscle which has two sources of vascularization: left anterior descending artery and circumflex artery. By courtesy of MURESIAN Horia, MD, PhD - 2009.

Theacute ischemicmitralregurgitation(Fig8)ismoreoftendue tostructurallesionsas complete or partial rupture of the papillary muscle, and less frequent due to an elongation of the mus‐ cle. The echocardiographic diagnosis may not be easy and it is often based on the use of the TEE in the emergency facility. The key issue in the successful management of these patients is timely intervention. If the clinical conditions and the logistic allow it, the patient should be urgently taken to the operating room. Most often, the acute ischemic regurgitation is surgically treated by mitral valve replacement. Mitral valve repair is rare, but, in specific cases, it may be a valid alternative. This depends on the quality and on the entity of the structural alteration of the subvalvular apparatus, and also on the experience of the surgical team.

The echocardiographic assessment of the mechanisms of the ischemic mitral regurgitation, which is the key for the tailored surgical approach, may be sometimes complex and tricky, due to a true mosaic of intricate mechanisms, difficult to be embedded and defined by a standard classification. The echocardiographer has to be aware of the complexity of the left ventricular remodeling process and to assess the mitral valve apparatus using multiple views and to pay

**Background.** Acute ischemic mitral valve regurgitation may occur in the setting of acute myocardial infarction owing to necrosis and rupture of papillary muscle tissue or abnormal coaptation of the leaflets, due to distortion of ventricular geometry. Hemodynamically significant mitral regurgitation is possible in both anterior and inferior infarcts, but its incidence appears higher in the inferior myocardial infarction group such as 40% vs 15% - see the Fig 7 (Estes 1966, Dagum 2000, Timek 2003). Post-infarction mitral regurgitation may be associated to multiple cardiovascular risk factors such as diabetes, abnormal body mass index (>25), advanced age, female gender, coexistence of peripheral arteriopathy and prior infarction

**Figure 7.** Differences in the vascularization of the papillary muscle. Postero-medial papillary muscle usually receives the blood only form the right coronary artery (rarely from circumflex artery), respect of the antero-lateral papillary muscle which has two sources of vascularization: left anterior descending artery and circumflex artery. By courtesy of

particular attention to the analysis of the mitral valve geometry.

**3. Acute ischemic mitral regurgitation**

(Green, 1999).

72 Hot Topics in Echocardiography

MURESIAN Horia, MD, PhD - 2009.

From the echocardiographic point of view, the acute structural ischemic mitral regurgitation may present three different patterns: transection of papillary muscle ("too late" diagnosis), partial rupture of the papillary muscle ("timely" diagnosis) and elongation of the papillary muscle (the "tricky" echo diagnosis); see the scheme on the Fig 8.

**Figure 8.** Echocardiographic classification of the structural acute ischemic mitral regurgitation (scheme). The upper pictures represent a case with transection of papillary muscle, in a patient with cardiogenic shock ("too late" echo di‐ agnosis). In the bottom raw acute papillary muscle elongation (the first pictures on the left) and partial rupture of pap‐ illary muscle (right picture, yellow arrow); both patients were in 3rd NYHA Class.

The gloomy clinical prognosis of acute significant ischemic mitral regurgitation associated to myocardial infarction (moderate or severe degree) is illustrated by its devastating impact on short- and long-term survival: almost one out of 4 patients die at one month and more than one out of 2 after one year (24% early and 54% 1-year mortality rate) (Otto, 2012).

In most cases the acute ischemic mitral regurgitation is a syndrome with conspicuous clinical implications. Generally, the clinical presentation of these patients is compatible with a hyper acute heart failure; they are highly symptomatic and may present with overt acute pulmonary edema, cardiogenic shock or even sudden death. Only minorities of patients are mildly symptomatic or asymptomatic and may present just a new systolic murmur.

Based on the echocardiography exam the acute ischemic mitral regurgitation may be divided in structural and functional. The structural ischemic mitral regurgitation is determined by complete papillary muscle rupture (transection), by partial detachment of one or both tips of a papillary muscle with subsequent elongation and by acute remodeling of papillary muscle with elongation (fig 8). In some cases the ischemic event may involve the point of insertion of the tendineous chord(s) which may result in a 'flail' which is an uncommon pattern for this pathology but may explain this kind of lesion.

In summary a myocardial infarction, in acute settings, may have one of the three structural damages on the papillary muscle: transection, partially rupture or elongation. The first two situations have already largely been described in many publications. This is not the case with the papillary muscle elongation, which is closer to chronic ischemic regurgitation and where the echocardiographic geometrical analysis, based on *the triangle of coaptation,* plays an essential role in diagnosis.

#### **3.1. Papillary muscle necrosis with complete rupture of papillary muscle**

Papillary muscle necrosis with complete rupture of papillary muscle is an uncommon but dramatic type of ischemic mitral insufficiency, with approx. 1.0% incidence in patients with myocardial infarction (Clements 1985). This is a life-threatening complication of myocardial infarction that requires a prompt diagnosis and surgical intervention (Fig 9). The posterome‐ dial papillary muscle is more frequently involved because of its single coronary artery blood supply (Fig 7). Chordae to both leaflets arise from each papillary muscle so that, in cases of "complete" rupture, both leaflets are affected. The echocardiography exam generally shows loss of leaflets coaptation due to the floating ruptured papillary muscle ('flail' mitral valve). In these patients the echocardiographic diagnosis is relatively simple and, generally, may be done using transthoracic exam. These patients belong to the type II° Carpentier's classification.

realityis a *'false'*mitralvalveprolapse).Anasymmetric appositionofthe *'prolapsed'*leafletis also present. Often these patients are misdiagnosed as '*mitral prolapse'*, because the echocardiogra‐ pherfocuses the attention only on the mitral valve, neglecting to assess thepapillary muscle. So, it is possible to fall into the trap, because at variance from the mitral valve, the papillary muscle is generally seen in a different echocardiographic plane, and often off axis view. If the echocar‐ diographer doesn't have the concept of possible elongation of the papillary muscle due to the

**Figure 9.** Acute severe structural ischemic mitral regurgitation due to transection of papillary muscle (2D TEE intrao‐ perative exam). Note the loss of coaptation due to complete rupture of papillary muscle and flail (arrows). Both pa‐ tients, with hemodynamic instability, were transferred to Cardiac Surgery Dpt. the same day of the transthoracic diagnosis. An emergency mitral valve replacement and CABG was successfully performed after coronary angiography.

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The take home message is to check explicitly the papillary muscle, searching it from different off axis views, starting from the clinical settings of the patient, essentially in case of abnormal geometry of the mitral valve. At any transthoracic suspicion of partial papillary muscle rupture the TEE exam must be done, chiefly in acute settings. The partial papillary muscle lesion may be otherwise missed and it may evolve to a complete rupture. At the echo, the ruptured head shows a hypermobile, redundant excursion which may mimic a degenerative lesion (e.g. Barlow disease). It is critical to remember that in most cases of papillary muscle involvement, massive mitral regurgitation is present and the surgery must be rapidly accomplished (Fig 11). In some cases mitral valve repair is possible depending on the intraoperative findings, the

Acute remodeling of the papillary muscle with elongation is the third and rare form of acute ischemic mitral regurgitation which, usually, involves the inferior-posterior papillary muscle.

structural post-necrotic lesion, the true etiology of the lesion may be missed (Fig 10).

elapsed time from the acute myocardial infarction and the surgeon experience.

**3.3. Acute remodeling of the papillary muscle with elongation**

Nonetheless the complete rupture is rare; it carries a poor prognosis for the onset of acute pulmonary oedema and low output syndrome. Without surgery, the mortality is very high, up to 75% within the first 24 hours (Tcheng, 1992, Kirklin 2012). As a consequence, the echocardiographic diagnosis must rapidly be performed and the patient must be timely taken to the operating room. In most cases the intervention is a mitral valve replacement. However the operative mortality is high, ranging from 23 to 45%, increasing in late referral. It may reach 57% in cases of reoperations (Loisance, 1990).

#### **3.2. Incomplete papillary muscle rupture**

**Sometimes the papillary muscle is only partially ruptured.** To avoid the high operative mortality in case of complete papillary muscle rupture, the diagnosis of papillary muscle rupture has to be done on this circumstance. Usually the clinical manifestation of this condition is an episode of acute heart failure occasionally with a relative stabilization and sometimes with a new systolic murmur. The echocardiographic diagnosis may be available using the transthoracic approach, but might also be relatively tricky and then the TEE should be preferred for the reasons mentioned above (unstable patient, unclear transthoracic view).

The echocardiographic presentation of this type of structural ischemic mitral regurgitation generally shows a prolapse of one leaflet; also the type II° Carpentier's classification (which in Ischemic Mitral Regurgitation: From Echo Assessment to Surgical Strategy and Technique http://dx.doi.org/10.5772/56062 75

complete papillary muscle rupture (transection), by partial detachment of one or both tips of a papillary muscle with subsequent elongation and by acute remodeling of papillary muscle with elongation (fig 8). In some cases the ischemic event may involve the point of insertion of the tendineous chord(s) which may result in a 'flail' which is an uncommon pattern for this

In summary a myocardial infarction, in acute settings, may have one of the three structural damages on the papillary muscle: transection, partially rupture or elongation. The first two situations have already largely been described in many publications. This is not the case with the papillary muscle elongation, which is closer to chronic ischemic regurgitation and where the echocardiographic geometrical analysis, based on *the triangle of coaptation,* plays an essential

Papillary muscle necrosis with complete rupture of papillary muscle is an uncommon but dramatic type of ischemic mitral insufficiency, with approx. 1.0% incidence in patients with myocardial infarction (Clements 1985). This is a life-threatening complication of myocardial infarction that requires a prompt diagnosis and surgical intervention (Fig 9). The posterome‐ dial papillary muscle is more frequently involved because of its single coronary artery blood supply (Fig 7). Chordae to both leaflets arise from each papillary muscle so that, in cases of "complete" rupture, both leaflets are affected. The echocardiography exam generally shows loss of leaflets coaptation due to the floating ruptured papillary muscle ('flail' mitral valve). In these patients the echocardiographic diagnosis is relatively simple and, generally, may be done using transthoracic exam. These patients belong to the type II° Carpentier's classification.

Nonetheless the complete rupture is rare; it carries a poor prognosis for the onset of acute pulmonary oedema and low output syndrome. Without surgery, the mortality is very high, up to 75% within the first 24 hours (Tcheng, 1992, Kirklin 2012). As a consequence, the echocardiographic diagnosis must rapidly be performed and the patient must be timely taken to the operating room. In most cases the intervention is a mitral valve replacement. However the operative mortality is high, ranging from 23 to 45%, increasing in late referral. It may reach

**Sometimes the papillary muscle is only partially ruptured.** To avoid the high operative mortality in case of complete papillary muscle rupture, the diagnosis of papillary muscle rupture has to be done on this circumstance. Usually the clinical manifestation of this condition is an episode of acute heart failure occasionally with a relative stabilization and sometimes with a new systolic murmur. The echocardiographic diagnosis may be available using the transthoracic approach, but might also be relatively tricky and then the TEE should be preferred for the reasons mentioned above (unstable patient, unclear transthoracic view).

The echocardiographic presentation of this type of structural ischemic mitral regurgitation generally shows a prolapse of one leaflet; also the type II° Carpentier's classification (which in

**3.1. Papillary muscle necrosis with complete rupture of papillary muscle**

pathology but may explain this kind of lesion.

57% in cases of reoperations (Loisance, 1990).

**3.2. Incomplete papillary muscle rupture**

role in diagnosis.

74 Hot Topics in Echocardiography

**Figure 9.** Acute severe structural ischemic mitral regurgitation due to transection of papillary muscle (2D TEE intrao‐ perative exam). Note the loss of coaptation due to complete rupture of papillary muscle and flail (arrows). Both pa‐ tients, with hemodynamic instability, were transferred to Cardiac Surgery Dpt. the same day of the transthoracic diagnosis. An emergency mitral valve replacement and CABG was successfully performed after coronary angiography.

realityis a *'false'*mitralvalveprolapse).Anasymmetric appositionofthe *'prolapsed'*leafletis also present. Often these patients are misdiagnosed as '*mitral prolapse'*, because the echocardiogra‐ pherfocuses the attention only on the mitral valve, neglecting to assess thepapillary muscle. So, it is possible to fall into the trap, because at variance from the mitral valve, the papillary muscle is generally seen in a different echocardiographic plane, and often off axis view. If the echocar‐ diographer doesn't have the concept of possible elongation of the papillary muscle due to the structural post-necrotic lesion, the true etiology of the lesion may be missed (Fig 10).

The take home message is to check explicitly the papillary muscle, searching it from different off axis views, starting from the clinical settings of the patient, essentially in case of abnormal geometry of the mitral valve. At any transthoracic suspicion of partial papillary muscle rupture the TEE exam must be done, chiefly in acute settings. The partial papillary muscle lesion may be otherwise missed and it may evolve to a complete rupture. At the echo, the ruptured head shows a hypermobile, redundant excursion which may mimic a degenerative lesion (e.g. Barlow disease). It is critical to remember that in most cases of papillary muscle involvement, massive mitral regurgitation is present and the surgery must be rapidly accomplished (Fig 11). In some cases mitral valve repair is possible depending on the intraoperative findings, the elapsed time from the acute myocardial infarction and the surgeon experience.

#### **3.3. Acute remodeling of the papillary muscle with elongation**

Acute remodeling of the papillary muscle with elongation is the third and rare form of acute ischemic mitral regurgitation which, usually, involves the inferior-posterior papillary muscle.

**Figure 10.** Ischemic mitral regurgitation due to acute elongation of papillary muscle, appearing as mitral valve pro‐ lapse. The pictures on the middle raw show prolapse of both mitral leaflet. In reality, only the focused examination on the papillary muscle shows the triangular shape of the muscle, with a sharp tip and a partial tearing beside (arrow, bottom raw, 3D TTE).

The echocardiographic presentation of these patients shows a mitral valve with excess leaflets motion and prolapse, having the coaptation point situated *'very high'* near the mitral annulus, due to an elongated papillary muscle. If the papillary muscle is difficult to visualize, the virtual tool of *triangle of coaptation* may be useful to suppose the true etiology, considering that the normal geometry of the mitral valve will be distorted, with disappearance of the standard

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**Figure 11.** Partial rupture of papillary muscle (yellow arrows); TEE 3 D and 2 D exam and intraoperative picture.

**Figure 12.** Acute post-ischemic elongation of papillary muscle (yellow arrows); scheme, intraoperative photo and 2D and 3 D Echo. Note the tip of the papillary muscle (in the intraoperative picture and Echo slides) which reaches at the level of the mitral annulus. The papillary muscle is very thin, with a slim triangular shape and a very sharp tip: 'thorn papillary muscle'. In all cases the mitral valve presents severe regurgitation. Note the absence of the triangle of coap‐

tation, due to the migration of the coaptation plane nearby the mitral valve annulus.

triangle.

At the echo, the papillary muscle has a triangular shape and appears elongated and often slim (fig 12). This elongation determines a displacement of the coaptation point towards the mitral annular plane and to the left atrium, with subsequent mitral regurgitation. In this way the appearance of mitral valve is likewise similar with the mitral valve prolapse (type II° Car‐ pentier classification), but the etiology is the myocardial necrosis and not the anomaly of the connective tissue as in Barlow / Marfan disease.

The echocardiographic documentation of the ischemic etiology in these cases might be tricky. In order to better characterize the structural anatomy of the myocardium at the level of the infarcted or ischemic papillary muscle, additive methods could prove useful such as SPECT, cardiac MRI or PET, showing the myocardial scar or necrosis. Anyway, the diagnosis is extensively based on the geometrical analysis of the mitral valve apparatus performed by echocardiography.

Ischemic Mitral Regurgitation: From Echo Assessment to Surgical Strategy and Technique http://dx.doi.org/10.5772/56062 77

The echocardiographic presentation of these patients shows a mitral valve with excess leaflets motion and prolapse, having the coaptation point situated *'very high'* near the mitral annulus, due to an elongated papillary muscle. If the papillary muscle is difficult to visualize, the virtual tool of *triangle of coaptation* may be useful to suppose the true etiology, considering that the normal geometry of the mitral valve will be distorted, with disappearance of the standard triangle.

At the echo, the papillary muscle has a triangular shape and appears elongated and often slim (fig 12). This elongation determines a displacement of the coaptation point towards the mitral annular plane and to the left atrium, with subsequent mitral regurgitation. In this way the appearance of mitral valve is likewise similar with the mitral valve prolapse (type II° Car‐ pentier classification), but the etiology is the myocardial necrosis and not the anomaly of the

**Figure 10.** Ischemic mitral regurgitation due to acute elongation of papillary muscle, appearing as mitral valve pro‐ lapse. The pictures on the middle raw show prolapse of both mitral leaflet. In reality, only the focused examination on the papillary muscle shows the triangular shape of the muscle, with a sharp tip and a partial tearing beside (arrow,

The echocardiographic documentation of the ischemic etiology in these cases might be tricky. In order to better characterize the structural anatomy of the myocardium at the level of the infarcted or ischemic papillary muscle, additive methods could prove useful such as SPECT, cardiac MRI or PET, showing the myocardial scar or necrosis. Anyway, the diagnosis is extensively based on the geometrical analysis of the mitral valve apparatus performed by

connective tissue as in Barlow / Marfan disease.

echocardiography.

bottom raw, 3D TTE).

76 Hot Topics in Echocardiography

**Figure 12.** Acute post-ischemic elongation of papillary muscle (yellow arrows); scheme, intraoperative photo and 2D and 3 D Echo. Note the tip of the papillary muscle (in the intraoperative picture and Echo slides) which reaches at the level of the mitral annulus. The papillary muscle is very thin, with a slim triangular shape and a very sharp tip: 'thorn papillary muscle'. In all cases the mitral valve presents severe regurgitation. Note the absence of the triangle of coap‐ tation, due to the migration of the coaptation plane nearby the mitral valve annulus.

The proper diagnosis and thus the management of such a serious clinical condition as the acute ischemic mitral regurgitation must rely on clear and robust echocardiographic concepts such as mitral valve geometry and functional anatomy. As already said the normal mitral valve geometry is the standard that guides both the evaluation of the various valve lesions and the surgical treatment. The central feature of the normal mitral valve geometry is represented by **the triangle of coaptation** (fig 4). The coaptation length (CL) and the coaptation height (CH) are cornerstone elements used in order to fully describe the valve geometry and to assess the result of the repair (Cerin 2012). It may be assumed that from a three dimensional geometrical perspective the triangle of coaptation corresponds roughly to an asymmetrical tent. In the course of perioperative echocardiographic study, the systematical analysis of the mitral valve apparatus is done, focusing on whether the triangle of coaptation is present or not. This geometrical concept of the mitral valve allows the repair to be performed even in some of the serious cases of acute mitral regurgitation.

infarction may develop an *acute* and dynamic process of ventricular remodeling involving the papillary muscle, which may not be perceived or checked in real time at echo and discovered

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From this point of view, the classification of ischemic mitral regurgitation in acute and chronic may be in some cases misleading; ischemic mitral regurgitation is a ventricular disease, following the same steps as the myocardial infarction. So, as the myocardial infarction recognizes an acute period, a recent (sub-acute) and then a stable (chronic) phase, it seems logical to use the same classification for ischemic mitral regurgitation. In the era of shorter hospitalization of infarcted patients the acute ischemic mitral regurgitation, being a dynamic phenomenon, may be missed at the first echo examinations and 'discovered' over time, as 'late' complication (Popa BA 2007) (fig 14); Thus, the echocardiographer has to be aware that the classification in acute or chronic may reflect mainly the moment of diagnosis and less the true period of time when the lesion occurred. This aspect is important as regard the prognosis of ischemic mitral regurgitation, because, as noted, the acute and sub-acute ischemic mitral regurgitation have a worse prognosis over a short period of time, respect of chronic ischemic

14 A 14B 14C

14D 14E 14F

**Figure 14.** Severe ischemic mitral regurgitation (14D) diagnosed by TTE 10 years after an acute 'uncomplicated' myo‐ cardial infarction. The clinical presentation of the patient was exertion dyspnea. Ten years before, at discharge from the hospital the Echo exam has been normal. Note the elongation of the papillary muscle (14 A,C,E), causing loss of leaflet coaptation (14 A,C), with marginal prolapse of A2 scallop (14B,C). Apparently the patient presents an A2 local‐ ized prolapse (14BC), which, in reality is caused by an elongated papillary muscle. The tip of the papillary muscle is shown (14E, yellow arrows), arriving till the mitral annular plane (which is categorically abnormal). The transthoracic postoperative echo after mitral repair (mitral ring + suture and shortening of the papillary muscle), shows trivial resid‐

later, as *'chronic'* mitral regurgitation.

mitral regurgitation.

ual mitral regurgitation (14F).

Nevertheless, it should be underlined that this condition, even if rare, is a very severe cardio‐ logical emergency, often characterized by low cardiac output and high early mortality; with medical therapy about 90% of patients with acute ischemic mitral regurgitation will died in the first two months. This is the reason why surgical correction must not be delayed. The predictors of better survival are: early operation, short duration of shock and mild degree of left/right ventricular impairment. For the management of these patients the use of intra-aortic balloon pumping and / or ventricular assist device (fig 13), out of inotropic pharmacologic support, is mandatory. Surgery might be delayed up to 2-3 weeks only when patient is stable; in this setting, as noted, the surgery is performed with lower risk.

**Figure 13.** Acute heart failure due to ischemic mitral regurgitation. TEE intraoperative picture showing the assessment of the right position of the ventricular assist device (Impella) into the left ventricular outflow tract.

### **4. Chronic ischemic mitral regurgitation**

#### **4.1. Physiopathological consideration**

Largely, the chronic ischemic mitral regurgitation is considered a long-lasting developing process of LV remodeling after myocardial infarction, causing mitral regurgitation by dys‐ function and distortion of the components of the mitral valve including the chordae, the annulus and the leaflets. Nevertheless, this is not always true: some patient with acute infarction may develop an *acute* and dynamic process of ventricular remodeling involving the papillary muscle, which may not be perceived or checked in real time at echo and discovered later, as *'chronic'* mitral regurgitation.

The proper diagnosis and thus the management of such a serious clinical condition as the acute ischemic mitral regurgitation must rely on clear and robust echocardiographic concepts such as mitral valve geometry and functional anatomy. As already said the normal mitral valve geometry is the standard that guides both the evaluation of the various valve lesions and the surgical treatment. The central feature of the normal mitral valve geometry is represented by **the triangle of coaptation** (fig 4). The coaptation length (CL) and the coaptation height (CH) are cornerstone elements used in order to fully describe the valve geometry and to assess the result of the repair (Cerin 2012). It may be assumed that from a three dimensional geometrical perspective the triangle of coaptation corresponds roughly to an asymmetrical tent. In the course of perioperative echocardiographic study, the systematical analysis of the mitral valve apparatus is done, focusing on whether the triangle of coaptation is present or not. This geometrical concept of the mitral valve allows the repair to be performed even in some of the

Nevertheless, it should be underlined that this condition, even if rare, is a very severe cardio‐ logical emergency, often characterized by low cardiac output and high early mortality; with medical therapy about 90% of patients with acute ischemic mitral regurgitation will died in the first two months. This is the reason why surgical correction must not be delayed. The predictors of better survival are: early operation, short duration of shock and mild degree of left/right ventricular impairment. For the management of these patients the use of intra-aortic balloon pumping and / or ventricular assist device (fig 13), out of inotropic pharmacologic support, is mandatory. Surgery might be delayed up to 2-3 weeks only when patient is stable;

**Figure 13.** Acute heart failure due to ischemic mitral regurgitation. TEE intraoperative picture showing the assessment

Largely, the chronic ischemic mitral regurgitation is considered a long-lasting developing process of LV remodeling after myocardial infarction, causing mitral regurgitation by dys‐ function and distortion of the components of the mitral valve including the chordae, the annulus and the leaflets. Nevertheless, this is not always true: some patient with acute

of the right position of the ventricular assist device (Impella) into the left ventricular outflow tract.

**4. Chronic ischemic mitral regurgitation**

**4.1. Physiopathological consideration**

serious cases of acute mitral regurgitation.

78 Hot Topics in Echocardiography

in this setting, as noted, the surgery is performed with lower risk.

From this point of view, the classification of ischemic mitral regurgitation in acute and chronic may be in some cases misleading; ischemic mitral regurgitation is a ventricular disease, following the same steps as the myocardial infarction. So, as the myocardial infarction recognizes an acute period, a recent (sub-acute) and then a stable (chronic) phase, it seems logical to use the same classification for ischemic mitral regurgitation. In the era of shorter hospitalization of infarcted patients the acute ischemic mitral regurgitation, being a dynamic phenomenon, may be missed at the first echo examinations and 'discovered' over time, as 'late' complication (Popa BA 2007) (fig 14); Thus, the echocardiographer has to be aware that the classification in acute or chronic may reflect mainly the moment of diagnosis and less the true period of time when the lesion occurred. This aspect is important as regard the prognosis of ischemic mitral regurgitation, because, as noted, the acute and sub-acute ischemic mitral regurgitation have a worse prognosis over a short period of time, respect of chronic ischemic mitral regurgitation.

**Figure 14.** Severe ischemic mitral regurgitation (14D) diagnosed by TTE 10 years after an acute 'uncomplicated' myo‐ cardial infarction. The clinical presentation of the patient was exertion dyspnea. Ten years before, at discharge from the hospital the Echo exam has been normal. Note the elongation of the papillary muscle (14 A,C,E), causing loss of leaflet coaptation (14 A,C), with marginal prolapse of A2 scallop (14B,C). Apparently the patient presents an A2 local‐ ized prolapse (14BC), which, in reality is caused by an elongated papillary muscle. The tip of the papillary muscle is shown (14E, yellow arrows), arriving till the mitral annular plane (which is categorically abnormal). The transthoracic postoperative echo after mitral repair (mitral ring + suture and shortening of the papillary muscle), shows trivial resid‐ ual mitral regurgitation (14F).

The chronic ischemic mitral regurgitation, comparing with the acute one, is a much more gradual and more complex process, because of the slow progression over time of the left heart remodeling (fig 14). This clinical condition recognizes two main mechanisms: a structural alteration of the subvalvular apparatus (papillary muscle and the corresponding LV wall), alongside of the phenomenon of left ventricular cavity remodeling.

#### **4.2. Left ventricle post infarction remodeling process**

From the physiopathological point of view the left ventricular post myocardial infarction remodeling is considered to be a phenomenon which can be divided in two parts: a regional and a global process of remodeling.

**Regional remodeling** is more often found after the inferior infarction (but not only), and may evolve over time in two different ways:

**1.** mainly a process of inferior wall remodeling with displacement of the papillary muscles. This type is associated with overt systolic restriction of posterior mitral leaflet.

with 'limited' LV remodeling (inferior infarction) and *asymmetric mitral valve remodeling*, due to

**Figure 15.** Limited LV remodeling: TTE (left) and TEE 2-chamber view (right) showing systolic restriction of the posteri‐ or mitral leaflet and minimal leaflet coaptation. Necrosis of the inferior wall is evident, with mild left ventricular dilata‐ tion (EDVol 170ml), mild systolic dysfunction (EF 43%) and chronic ischemic mitral regurgitation due to clear systolic

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These two main echocardiographic patterns of LV remodeling, when associated with chronic ischemic mitral regurgitation, are easy to identify by transthoracic echocardiographic exam and the transesophageal examination is not necessary. Sometimes, these configurations may be less definite, as in patients with regional or global remodeling, combined with coincident papillary muscle elongation. In these cases there is an additional phenomenon of migration of the LV infarcted wall, associated with post ischemic elongation of the papillary muscle.

A geometrical analysis of the mitral apparatus, by use of the echocardiographic tool of *triangle of coaptation* may identify these patients with regional or global remodeling, combined with elongation of the papillary muscle. As already has been mentioned, the patients with papillary muscle elongation present a distortion of the triangle of coaptation with progressive alteration of the standard trilateral shape (fig 5), till the complete disappearance of it (fig.6). The mech‐ anism of mitral insufficiency in these patients is more complex and the surgical strategy has

The elongation of the papillary muscle may often be unnoticed if the operator mostly focuses the attention on the mitral leaflet, on the valve coaptation and on the degree of mitral regur‐ gitation. Moreover, the papillary muscles are difficult and rarely seen in the same plane with the mitral valve leaflets, being sited distant from the coaptation valve plane; only a specific and vigilant off axis assessment of them may reveal the muscularly post-ischemic remodeling. When the papillary muscles elongation is obvious, the surgical strategy has to be adapted and sometimes a shortening of them or use of the artificial chordae may be necessary to restore a

Therefore, as message for the everyday practice, in acute or in chronic ischemic mitral regurgita‐

Consequently, in the analysis of ischemic mitral regurgitation the starting points are restricted motion of the posterior mitral leaflet (type III° Carpentier's classification), combined with mitral annular dilatation, secondary to migration of the wall and left ventricular enlargement

tion, the marker of the papillary muscle elongation is the distorted coaptation triangle.

*solitary* migration of the postero-medial papillary muscle (scallops P3/P2).

to be tailored accordingly.

restriction of posterior leaflet.

good plane of valve coaptation and valve geometry.

**2.** inferior wall remodeling and displacement of the papillary muscles, *combined with postischemic elongation of papillary muscles*. In this kind of inferior post infarction remodeling the systolic restriction of the posterior mitral leaflet may be less evident or even absent in some cases. Respect of the first type, the geometry of mitral valve in this sort of ventricular remodeling will be different.

**Global left ventricular remodeling** is generally seen after two heart attacks (multiple myo‐ cardial infarctions and in cases with ischemic dilated cardiomyopathy) and it is characterized by restriction of both mitral leaflets, tethering of the mitral valve apparatus with mitral valve tenting, due to progressive migration of the papillary muscles simultaneously with overall left cavity dilatation.

In the patients with left ventricular remodeling and chronic ischemic mitral regurgitation, these physiopathological concepts are expressed by **two main echocardiographic patterns of left heart remodeling:**


Bothtypes of chronic ischemicmitralregurgitationpresent amitral annulardilatation, obvious‐ ly more evident in patients with double myocardial infarction. A form of *symmetric remodeling of the mitral valve apparatus* is present in patients with ischemic dilated cardiomyopathies ('extensive' LV remodeling) due to bilateral migration of *both* the papillary muscle (scallops P1/ P2/P3).Conversely, a limitaryprocessofmitralvalve apparatus remodelingispresentinpatients Ischemic Mitral Regurgitation: From Echo Assessment to Surgical Strategy and Technique http://dx.doi.org/10.5772/56062 81

The chronic ischemic mitral regurgitation, comparing with the acute one, is a much more gradual and more complex process, because of the slow progression over time of the left heart remodeling (fig 14). This clinical condition recognizes two main mechanisms: a structural alteration of the subvalvular apparatus (papillary muscle and the corresponding LV wall),

From the physiopathological point of view the left ventricular post myocardial infarction remodeling is considered to be a phenomenon which can be divided in two parts: a regional

**Regional remodeling** is more often found after the inferior infarction (but not only), and may

**1.** mainly a process of inferior wall remodeling with displacement of the papillary muscles. This type is associated with overt systolic restriction of posterior mitral leaflet.

**2.** inferior wall remodeling and displacement of the papillary muscles, *combined with postischemic elongation of papillary muscles*. In this kind of inferior post infarction remodeling the systolic restriction of the posterior mitral leaflet may be less evident or even absent in some cases. Respect of the first type, the geometry of mitral valve in this sort of ventricular

**Global left ventricular remodeling** is generally seen after two heart attacks (multiple myo‐ cardial infarctions and in cases with ischemic dilated cardiomyopathy) and it is characterized by restriction of both mitral leaflets, tethering of the mitral valve apparatus with mitral valve tenting, due to progressive migration of the papillary muscles simultaneously with overall left

In the patients with left ventricular remodeling and chronic ischemic mitral regurgitation, these physiopathological concepts are expressed by **two main echocardiographic patterns of**

**a.** the echocardiographic pattern of **limited LV remodeling:** inferior or lateral infarction scar, mild left ventricular dilatation, mild systolic dysfunction and chronic ischemic mitral regurgitation due to unambiguous systolic restriction of posterior leaflet (fig 15), and **b.** the echocardiographic pattern of **extensive LV remodeling:** major left ventricular cavity dilatation with dysfunction and distortion (by anterior and inferior myocardial infarc‐ tion), typically with poor systolic function, but also with a diastolic one and the tethering

Bothtypes of chronic ischemicmitralregurgitationpresent amitral annulardilatation, obvious‐ ly more evident in patients with double myocardial infarction. A form of *symmetric remodeling of the mitral valve apparatus* is present in patients with ischemic dilated cardiomyopathies ('extensive' LV remodeling) due to bilateral migration of *both* the papillary muscle (scallops P1/ P2/P3).Conversely, a limitaryprocessofmitralvalve apparatus remodelingispresentinpatients

alongside of the phenomenon of left ventricular cavity remodeling.

**4.2. Left ventricle post infarction remodeling process**

and a global process of remodeling.

80 Hot Topics in Echocardiography

evolve over time in two different ways:

remodeling will be different.

of both mitral leaflets (fig 3).

cavity dilatation.

**left heart remodeling:**

**Figure 15.** Limited LV remodeling: TTE (left) and TEE 2-chamber view (right) showing systolic restriction of the posteri‐ or mitral leaflet and minimal leaflet coaptation. Necrosis of the inferior wall is evident, with mild left ventricular dilata‐ tion (EDVol 170ml), mild systolic dysfunction (EF 43%) and chronic ischemic mitral regurgitation due to clear systolic restriction of posterior leaflet.

with 'limited' LV remodeling (inferior infarction) and *asymmetric mitral valve remodeling*, due to *solitary* migration of the postero-medial papillary muscle (scallops P3/P2).

These two main echocardiographic patterns of LV remodeling, when associated with chronic ischemic mitral regurgitation, are easy to identify by transthoracic echocardiographic exam and the transesophageal examination is not necessary. Sometimes, these configurations may be less definite, as in patients with regional or global remodeling, combined with coincident papillary muscle elongation. In these cases there is an additional phenomenon of migration of the LV infarcted wall, associated with post ischemic elongation of the papillary muscle.

A geometrical analysis of the mitral apparatus, by use of the echocardiographic tool of *triangle of coaptation* may identify these patients with regional or global remodeling, combined with elongation of the papillary muscle. As already has been mentioned, the patients with papillary muscle elongation present a distortion of the triangle of coaptation with progressive alteration of the standard trilateral shape (fig 5), till the complete disappearance of it (fig.6). The mech‐ anism of mitral insufficiency in these patients is more complex and the surgical strategy has to be tailored accordingly.

The elongation of the papillary muscle may often be unnoticed if the operator mostly focuses the attention on the mitral leaflet, on the valve coaptation and on the degree of mitral regur‐ gitation. Moreover, the papillary muscles are difficult and rarely seen in the same plane with the mitral valve leaflets, being sited distant from the coaptation valve plane; only a specific and vigilant off axis assessment of them may reveal the muscularly post-ischemic remodeling.

When the papillary muscles elongation is obvious, the surgical strategy has to be adapted and sometimes a shortening of them or use of the artificial chordae may be necessary to restore a good plane of valve coaptation and valve geometry.

Therefore, as message for the everyday practice, in acute or in chronic ischemic mitral regurgita‐ tion, the marker of the papillary muscle elongation is the distorted coaptation triangle.

Consequently, in the analysis of ischemic mitral regurgitation the starting points are restricted motion of the posterior mitral leaflet (type III° Carpentier's classification), combined with mitral annular dilatation, secondary to migration of the wall and left ventricular enlargement (fig 15). The consequent mitral regurgitation leads to left ventricular volume overload, closing the vicious circle of ischemic mitral regurgitation and of left ventricular remodeling. The echocardiographic examination will show the tethering of one or both mitral leaflets, which is the 'standard' pattern of chronic ischemic mitral regurgitation. However, around 10% of patients with chronic ischemic mitral regurgitation may show a different pattern of regurgi‐ tation with 'false mitral prolapse', by elongation of the papillary muscle due to local ischemia, necrosis and/or fibrosis (false because the etiology is not degenerative, but ischemic one).

**Indication to surgery:** With an ever increasing population of patients with coronary artery disease complicated by chronic ischemic mitral regurgitation, the question whether to perform a mitral valve repair in addition to CABG is one of the most common and controversial clinical dilemmas faced by cardiac surgeons and cardiologists today. There is a general agreement regarding the indication for surgery in patients with severe ischemic mitral regurgitation. The problem arises for moderate ischemic mitral regurgitation. At present, there is no definitive randomized, prospective trial that clarifies which approach should be taken. The 2011 ACCF/ AHA guidelines on CABG state that patients undergoing CABG who have severe ischemic mitral valve regurgitation not likely to resolve with revascularization, should have concomi‐ tant mitral valve repair or replacement at the time of CABG (Class I, Level of evidence B) (Gillinov 2001, Trichon BH 2003, Fattouch K 2009 & 2010, Zoghbi W 2003). Operative mortality is considered to be around 10% (Rankin 1988, Cohn 1995, Grossi 2001). Some studies advocate mitral valve repair to all patients that undergo CABG even when the degree of mitral regur‐ gitation is mild. This strategy seems to be reasonable if the chronic ischemic mitral regurgita‐ tion is considered to be expression of the LV deformation / remodeling process, which is not still reversible in the chronic phase of the myocardial infarction. A careful echocardiographic analysis focused mainly on the quality of leaflet coaptation and on the extension of LV

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deformation (limited or extensive remodeling), may guide the surgeon.

**5. Assessment of ischemic mitral regurgitation severity**

ones due to Coandă effect (hugging of the adjacent wall of the left atrium).

than in other contexts (see below the PISA method).

advisable whenever their determination is possible.

Due to the hemodynamic conditions in ischemic heart disease and the particular shape of the regurgitant orifice, assessment of the severity of mitral regurgitation may be challenging. Mitral regurgitation in an ischemic setting has a profound impact on patient's prognosis and therefore its quantification plays a key role in the revascularization plan because moderate and severe mitral regurgitation have indication to surgery. Given this special impact on prognosis, the thresholds of defining a severe mitral regurgitation in ischemic patients are much lower

**The qualitative method,** based on regurgitant jet area, is not reliable. This is true especially when an exact assessment of mitral regurgitation is need, because this approach is prone to many biases, being so dependent upon loading conditions and on equipment settings (for example color gain). The gradient between left ventricle and left atrium will highly influence the size of the jet. In an acute mitral regurgitation, in which left atrium pressure is elevated and the left ventricle-left atrium gradient is low, the regurgitant jet may be small, even though the real regurgitant volume is important. Conversely, in a high blood pressure setting (i.e. a high left ventricle-left atrium gradient) the regurgitant jet will be bigger. Last but not the least, eccentric jets (like the ones found in posterior leaflet restriction), seem smaller than the central

**The semi-quantitative** (vena contracta) and **quantitative methods** (PISA) are therefore

In these patients, from the echocardiographic point of view, there are three elements that may suggest the suspicion of ischemic etiology of the prolapsed valve:


**Figure 16.** A,B,C,D. Four different cases with chronic post ischemic elongation of the papillary muscle: 2D transthora‐ cic exam (16B) and live 3D (A,C,D). Note the progressive thinning of the papillary muscle, with the sharp aspect of the tip of it: so called 'thorny papillary muscle'.

Chronic ischemic mitral regurgitation may also be synonymous with ruptured tendineous chordae. Due to ischemia or necrosis the insertion place of the mitral chords on the tip of the papillarymusclemaybecome friable, andoftena limited*'ischemic flail'*,maybe apparent(fig17).

**Figure 17.** Loss of leaflet coaptation (B,C), with flail (B) and eccentric jet. The free ruptured chordae is visible in systole (C) and also in diastole (D). The pictures belong to the same patient.

**Indication to surgery:** With an ever increasing population of patients with coronary artery disease complicated by chronic ischemic mitral regurgitation, the question whether to perform a mitral valve repair in addition to CABG is one of the most common and controversial clinical dilemmas faced by cardiac surgeons and cardiologists today. There is a general agreement regarding the indication for surgery in patients with severe ischemic mitral regurgitation. The problem arises for moderate ischemic mitral regurgitation. At present, there is no definitive randomized, prospective trial that clarifies which approach should be taken. The 2011 ACCF/ AHA guidelines on CABG state that patients undergoing CABG who have severe ischemic mitral valve regurgitation not likely to resolve with revascularization, should have concomi‐ tant mitral valve repair or replacement at the time of CABG (Class I, Level of evidence B) (Gillinov 2001, Trichon BH 2003, Fattouch K 2009 & 2010, Zoghbi W 2003). Operative mortality is considered to be around 10% (Rankin 1988, Cohn 1995, Grossi 2001). Some studies advocate mitral valve repair to all patients that undergo CABG even when the degree of mitral regur‐ gitation is mild. This strategy seems to be reasonable if the chronic ischemic mitral regurgita‐ tion is considered to be expression of the LV deformation / remodeling process, which is not still reversible in the chronic phase of the myocardial infarction. A careful echocardiographic analysis focused mainly on the quality of leaflet coaptation and on the extension of LV deformation (limited or extensive remodeling), may guide the surgeon.

#### **5. Assessment of ischemic mitral regurgitation severity**

(fig 15). The consequent mitral regurgitation leads to left ventricular volume overload, closing the vicious circle of ischemic mitral regurgitation and of left ventricular remodeling. The echocardiographic examination will show the tethering of one or both mitral leaflets, which is the 'standard' pattern of chronic ischemic mitral regurgitation. However, around 10% of patients with chronic ischemic mitral regurgitation may show a different pattern of regurgi‐ tation with 'false mitral prolapse', by elongation of the papillary muscle due to local ischemia, necrosis and/or fibrosis (false because the etiology is not degenerative, but ischemic one).

In these patients, from the echocardiographic point of view, there are three elements that may

**2.** papillary muscle - specific appearance of the papillary muscle: elongated, hyperechogenic,

**3.** valve geometry - the abnormal mitral valve geometry, with distortion of the triangle of

**Figure 16.** A,B,C,D. Four different cases with chronic post ischemic elongation of the papillary muscle: 2D transthora‐ cic exam (16B) and live 3D (A,C,D). Note the progressive thinning of the papillary muscle, with the sharp aspect of the

Chronic ischemic mitral regurgitation may also be synonymous with ruptured tendineous chordae. Due to ischemia or necrosis the insertion place of the mitral chords on the tip of the papillarymusclemaybecome friable, andoftena limited*'ischemic flail'*,maybe apparent(fig17).

17A 17B 17C 17D

**Figure 17.** Loss of leaflet coaptation (B,C), with flail (B) and eccentric jet. The free ruptured chordae is visible in systole

**1.** leaflets - prolapse limited to one of the mitral leaflets, often of the anterior one,

thinning and triangularly shaped; *"thorny"* papillary muscle (fig 16);

16 A 16 B 16 C 16 D

coaptation, until its complete extinction (see also the Fig 5, 6)

tip of it: so called 'thorny papillary muscle'.

82 Hot Topics in Echocardiography

(C) and also in diastole (D). The pictures belong to the same patient.

suggest the suspicion of ischemic etiology of the prolapsed valve:

Due to the hemodynamic conditions in ischemic heart disease and the particular shape of the regurgitant orifice, assessment of the severity of mitral regurgitation may be challenging. Mitral regurgitation in an ischemic setting has a profound impact on patient's prognosis and therefore its quantification plays a key role in the revascularization plan because moderate and severe mitral regurgitation have indication to surgery. Given this special impact on prognosis, the thresholds of defining a severe mitral regurgitation in ischemic patients are much lower than in other contexts (see below the PISA method).

**The qualitative method,** based on regurgitant jet area, is not reliable. This is true especially when an exact assessment of mitral regurgitation is need, because this approach is prone to many biases, being so dependent upon loading conditions and on equipment settings (for example color gain). The gradient between left ventricle and left atrium will highly influence the size of the jet. In an acute mitral regurgitation, in which left atrium pressure is elevated and the left ventricle-left atrium gradient is low, the regurgitant jet may be small, even though the real regurgitant volume is important. Conversely, in a high blood pressure setting (i.e. a high left ventricle-left atrium gradient) the regurgitant jet will be bigger. Last but not the least, eccentric jets (like the ones found in posterior leaflet restriction), seem smaller than the central ones due to Coandă effect (hugging of the adjacent wall of the left atrium).

**The semi-quantitative** (vena contracta) and **quantitative methods** (PISA) are therefore advisable whenever their determination is possible.

*Vena contracta* is the narrowest region of the regurgitant jet, which is found not at the level of the leaflets, but just below the regurgitant orifice (because the blood is still converging for a few millimeters before re-expanding in left atrium) (fig 18). Its width is a marker of the regurgitant orifice area. It should be measured in a window perpendicular to the coaptation line, like parasternal long axis or four chambers views. A value of < 3mm is compatible with a mild regurgitation, while a value of >7mm is indicative of severe regurgitation. Values inbetween are not diagnostic of a moderate mitral regurgitation, because of an important overlap. In ischemic mitral regurgitation, the shape of the regurgitant orifice is not round, but rather elliptic. For this reason, assessment of vena contracta width should be done in two orthogonal planes (e.g. parasternal and apical four chambers) and an average of these two should be reported. A value > 8 mm is diagnostic of severe regurgitation. The 3D echo can be a solution for assessment of vena contracta in an ischemic setting.

**Figure 19.** Assessment of mitral regurgitation severity according to PISA method (MR ERO, MR Flow). The baseline of color Doppler is moved toward the regurgitant jet direction and the hemisphere radius is measured (left). On the mi‐

In eccentric jets (posterior leaflet restriction) the largest PISA is to be found in the parasternal

The elliptic shape of regurgitant orifice found in ischemic mitral regurgitation leads the PISA method to underestimate the real regurgitant volume (PISA is bigger than a hemisphere). Considering the profound deleterious effect of mitral regurgitation in an ischemic context, cut off levels of severity are lower than in organic mitral regurgitation, i.e. an EROA more than

Due to the dynamic characteristic of ischemic mitral regurgitation, PISA is not the same throughout the whole systole, being usually smaller in mesosystole when the regurgitation

If hemispheric floor is not flat (i.e. 180º), an angle correction can be made. In this situation

In multiple jets, both vena contracta width and PISA method are not additives and cannot

**Surgical approaches. Overview.** The surgical treatment of acute or chronic ischemic mitral regurgitation is strongly influenced by the echocardiographic assessment, which remains the only tool for surgical planning and postoperative control. The complex mechanisms of ischemic mitral regurgitation are analyzed by echo and the surgical planning is done after transthoracic and usually elaborate after intraoperative transesophageal examination. Based on echocardiographic analysis, various approaches have been proposed for the management of ischemic mitral regurgitation. So far, both medical treatments and classical surgical techniques are not always sufficient. Within the next paragraphs a rapid overview of some of the various surgical techniques implied in the treatment of ischemic mitral regurgitation will

**1. Undersized mitral valve annuloplasty.** The strategy of over-reduction of mitral annulus, combined with the coronary by-pass surgery is the most diffused surgical approach, especially in patients with dilated heart and chronic ischemic mitral regurgitation. As

in organic mitral regurgitation) and a regurgitant volume greater than

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long axis view, while in central jets the apical four chambers view should be used.

tral regurgitation envelope (continuous Doppler) maximum velocity and TVI are determined

30ml (vs. >60ml) defines a severe ischemic mitral regurgitation.

*EROA adjusted=EROA x α/180,* where *α* is the angle of convergence.

20mm2

be used.

be done.

(vs. >40mm2

tends to decrease.

**Figure 18.** Vena contracta depth measurement at the narrowest point of the regurgitant jet. The three components of the jet are visible: convergence zone, vena contracta and the flow into the left atrium.

*Quantitative approaches* and especially PISA (proximal isovelocity surface area) are the most indicated. PISA is based on the fact that near the regurgitant orifice, the blood (which should pass throw a restricted area) is disposed in hemispheric layers, having the same velocity at a certain distance from the orifice. Lowering the Nyquist limit at 15-40 cm/s (the velocity at which aliasing is appearing), all the "layers" with a higher velocity will have the aliasing phenom‐ enon. Measuring the first aliasing hemisphere we'll have a marker of regurgitation degree.

PISA method permits assessment of:

**• the flow rate** (FR) as *FR= 2 x π x R <sup>2</sup> x Val*

where *R* is the PISA radius and *Val* is the aliasing velocity

**•** effective regurgitant orifice area (ROA) as *EROA=FR/V max*

where *FR* is the flow rate and *V max* is the maximum velocity measured on mitral regurgitation envelope in continuous Doppler

**• regurgitant volume** (RV) as *RV=ROA x TVI*, where *EROA* is effective regurgitant orifice area and *TVI* is the time-velocity integral measured on mitral regurgitation envelope in contin‐ uous Doppler (fig 19).

Ischemic Mitral Regurgitation: From Echo Assessment to Surgical Strategy and Technique http://dx.doi.org/10.5772/56062 85

*Vena contracta* is the narrowest region of the regurgitant jet, which is found not at the level of the leaflets, but just below the regurgitant orifice (because the blood is still converging for a few millimeters before re-expanding in left atrium) (fig 18). Its width is a marker of the regurgitant orifice area. It should be measured in a window perpendicular to the coaptation line, like parasternal long axis or four chambers views. A value of < 3mm is compatible with a mild regurgitation, while a value of >7mm is indicative of severe regurgitation. Values inbetween are not diagnostic of a moderate mitral regurgitation, because of an important overlap. In ischemic mitral regurgitation, the shape of the regurgitant orifice is not round, but rather elliptic. For this reason, assessment of vena contracta width should be done in two orthogonal planes (e.g. parasternal and apical four chambers) and an average of these two should be reported. A value > 8 mm is diagnostic of severe regurgitation. The 3D echo can be

**Figure 18.** Vena contracta depth measurement at the narrowest point of the regurgitant jet. The three components

*Quantitative approaches* and especially PISA (proximal isovelocity surface area) are the most indicated. PISA is based on the fact that near the regurgitant orifice, the blood (which should pass throw a restricted area) is disposed in hemispheric layers, having the same velocity at a certain distance from the orifice. Lowering the Nyquist limit at 15-40 cm/s (the velocity at which aliasing is appearing), all the "layers" with a higher velocity will have the aliasing phenom‐ enon. Measuring the first aliasing hemisphere we'll have a marker of regurgitation degree.

where *FR* is the flow rate and *V max* is the maximum velocity measured on mitral regurgitation

**• regurgitant volume** (RV) as *RV=ROA x TVI*, where *EROA* is effective regurgitant orifice area and *TVI* is the time-velocity integral measured on mitral regurgitation envelope in contin‐

a solution for assessment of vena contracta in an ischemic setting.

of the jet are visible: convergence zone, vena contracta and the flow into the left atrium.

PISA method permits assessment of:

84 Hot Topics in Echocardiography

envelope in continuous Doppler

uous Doppler (fig 19).

**• the flow rate** (FR) as *FR= 2 x π x R <sup>2</sup> x Val*

where *R* is the PISA radius and *Val* is the aliasing velocity

**•** effective regurgitant orifice area (ROA) as *EROA=FR/V max*

**Figure 19.** Assessment of mitral regurgitation severity according to PISA method (MR ERO, MR Flow). The baseline of color Doppler is moved toward the regurgitant jet direction and the hemisphere radius is measured (left). On the mi‐ tral regurgitation envelope (continuous Doppler) maximum velocity and TVI are determined

In eccentric jets (posterior leaflet restriction) the largest PISA is to be found in the parasternal long axis view, while in central jets the apical four chambers view should be used.

The elliptic shape of regurgitant orifice found in ischemic mitral regurgitation leads the PISA method to underestimate the real regurgitant volume (PISA is bigger than a hemisphere). Considering the profound deleterious effect of mitral regurgitation in an ischemic context, cut off levels of severity are lower than in organic mitral regurgitation, i.e. an EROA more than 20mm2 (vs. >40mm2 in organic mitral regurgitation) and a regurgitant volume greater than 30ml (vs. >60ml) defines a severe ischemic mitral regurgitation.

Due to the dynamic characteristic of ischemic mitral regurgitation, PISA is not the same throughout the whole systole, being usually smaller in mesosystole when the regurgitation tends to decrease.

If hemispheric floor is not flat (i.e. 180º), an angle correction can be made. In this situation

*EROA adjusted=EROA x α/180,* where *α* is the angle of convergence.

In multiple jets, both vena contracta width and PISA method are not additives and cannot be used.

**Surgical approaches. Overview.** The surgical treatment of acute or chronic ischemic mitral regurgitation is strongly influenced by the echocardiographic assessment, which remains the only tool for surgical planning and postoperative control. The complex mechanisms of ischemic mitral regurgitation are analyzed by echo and the surgical planning is done after transthoracic and usually elaborate after intraoperative transesophageal examination. Based on echocardiographic analysis, various approaches have been proposed for the management of ischemic mitral regurgitation. So far, both medical treatments and classical surgical techniques are not always sufficient. Within the next paragraphs a rapid overview of some of the various surgical techniques implied in the treatment of ischemic mitral regurgitation will be done.

**1. Undersized mitral valve annuloplasty.** The strategy of over-reduction of mitral annulus, combined with the coronary by-pass surgery is the most diffused surgical approach, especially in patients with dilated heart and chronic ischemic mitral regurgitation. As noted, this technique addressed just the annular dilation. The echocardiographic exami‐ nation plays an essential role because it confirms the dilation of the mitral annulus, and the subsequent reduced and/or loss of leaflet coaptation in case of advanced left ventric‐ ular and annular dilatation ('extended' LV remodeling pattern). As a rule, Echo indicates the presence of tethering of the mitral leaflets, and also the systolic and, in cases with advanced heart remodeling and ischemic dilative cardiomyopathy, the diastolic restric‐ tion of the posterior mitral leaflets.

Carpentier classification). It is a physiologically coherent and relatively simple approach, intended to increase the surface and the mobility of the posterior mitral leaflet, in order

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**Figure 20.** Posterior mitral leaflet after extension with pericardial patch (arrows) in a patient with ischemic dilated car‐

This technique allows the extension of the surface of the posterior leaflet, especially in the area of the scallops P3 and P2, which is normally more restricted by the post-ischemic tethering. Furthermore, this procedure provides an additional anatomical leaflet reserve: in case of continuing left ventricular remodeling after surgery, which may be present in about 50% of the patients, according to some authors. Leaflet extension by autologous pericardial patch has been widely and successfully used in the reconstruction of other mitral valve pathologies such as rheumatic disease and endocarditis, with acceptable long-term results (Zegdi, 2007). This procedure can be performed within 15-20 extra minutes of aortic cross-clamping, and allows implanting larger sizes mitral prosthetic rings, with minor diastolic gradient through the mitral valve. Further studies with larger number of patients and adequate long-term follow-up are needed to assess the efficiency of this simple and promising approach to the treatment of

Once more the echo plays an essential role by identifying the patient candidates to LEX. Typically the Echo aspect demonstrates small posterior mitral leaflets, systolic and, sometimes, diastolic leaflets restriction, with significant mitral regurgitation due to reduced coaptation and asymmetrical apposition of the anterior leaflet. Consequently, at the postoperative examination Echo evaluates not only the mitral valve function as expressed by the degree of residual regurgitation, but, more important, the anatomical (leaflet length) and functional

**1.** Chronic ischemic mitral regurgitation determined by restriction of the posterior leaflet and apical displacement of the papillary muscle in patients with inferior myocardial infarction (or inferior and lateral myocardial infarction), mild left ventricular dilatation

and mild systolic dysfunction: so called 'limited' LV remodeling pattern.

diomyopathy: extended LV remodeling (intraoperative view - left and TTE preoperative picture; right).

ischemic mitral regurgitation, in case of ischemic dilated cardiomyopathy.

For every day practice three main situations will be considered:

reserve (the coaptation length).

to allow a better leaflet coaptation.

Concomitant coronary revascularization and downsizing of the mitral annulus by prosthetic rings, showed promising results with 80% good competence of the mitral valve at 2-years follow-up, but only 50% at five years (McGee, 2004, Klein 2011). Better results were published by Dion (2004) according to a proper algorithm. Patients treated with this technique showed almost always the echocardiographic picture of the so-called "monoleaflet" mitral valve, where the anterior leaflet covers the entire mitral orifice and the posterior leaflet remains restricted in its diastolic position. At the time of surgery the preoperative TEE Echo assists the surgical mitral repair by estimating the length of the medial scallop of the anterior mitral leaflet (scallop A2). This is usually performed from the distal-esophageal 135° view (three chamber view) and is essential in choosing the size of the annuloplasty ring. The choice of the size of the prosthetic ring is still empirical, but usually a ring two to three sizes smaller than measured is used.

The other determinant of the ischemic mitral regurgitation in the advanced stage of left ventricular remodeling is the restricted motion of the posterior mitral leaflet and loss of the anatomical and functional leaflet reserve both in systole and also in diastole. The existence of the anatomical and functional reserve of posterior mitral leaflet is a key element for having a competent mitral valve and, unfortunately, this aspect is not resolved by the over-reduction technique alone. To overcome the leaflet restriction some authors cut a limited number of basal chordae tendinae with the intent of reducing leaflet tethering and improving the coaptation. This simple procedure reduced tenting without creating valve prolapse, and the consequence is a decrease in mitral regurgitation (Messas 2001).


Carpentier classification). It is a physiologically coherent and relatively simple approach, intended to increase the surface and the mobility of the posterior mitral leaflet, in order to allow a better leaflet coaptation.

noted, this technique addressed just the annular dilation. The echocardiographic exami‐ nation plays an essential role because it confirms the dilation of the mitral annulus, and the subsequent reduced and/or loss of leaflet coaptation in case of advanced left ventric‐ ular and annular dilatation ('extended' LV remodeling pattern). As a rule, Echo indicates the presence of tethering of the mitral leaflets, and also the systolic and, in cases with advanced heart remodeling and ischemic dilative cardiomyopathy, the diastolic restric‐

Concomitant coronary revascularization and downsizing of the mitral annulus by prosthetic rings, showed promising results with 80% good competence of the mitral valve at 2-years follow-up, but only 50% at five years (McGee, 2004, Klein 2011). Better results were published by Dion (2004) according to a proper algorithm. Patients treated with this technique showed almost always the echocardiographic picture of the so-called "monoleaflet" mitral valve, where the anterior leaflet covers the entire mitral orifice and the posterior leaflet remains restricted in its diastolic position. At the time of surgery the preoperative TEE Echo assists the surgical mitral repair by estimating the length of the medial scallop of the anterior mitral leaflet (scallop A2). This is usually performed from the distal-esophageal 135° view (three chamber view) and is essential in choosing the size of the annuloplasty ring. The choice of the size of the prosthetic ring is still empirical, but usually a ring two to three sizes smaller than measured

The other determinant of the ischemic mitral regurgitation in the advanced stage of left ventricular remodeling is the restricted motion of the posterior mitral leaflet and loss of the anatomical and functional leaflet reserve both in systole and also in diastole. The existence of the anatomical and functional reserve of posterior mitral leaflet is a key element for having a competent mitral valve and, unfortunately, this aspect is not resolved by the over-reduction technique alone. To overcome the leaflet restriction some authors cut a limited number of basal chordae tendinae with the intent of reducing leaflet tethering and improving the coaptation. This simple procedure reduced tenting without creating valve prolapse, and the consequence

**2.** Because of these unsatisfactory results with the undersizing technique alone, the **reposi‐ tioning of the posterior papillary muscle** has been proposed, mainly in patients with ischemic dilated cardiomyopathy, as adjunctive approach to the annuloplasty; the outcome is currently under evaluation (Hvass 2010). The role of intraoperative TEE is to define the deformation of the subvalvular apparatus from the geometrical point of view. On one hand, it must preoperatively assess the distance between the base of the papillary muscles (usually from the transgastric short axis view), and on the other hand it has to

**3. Elongation of the posterior mitral leaflet with pericardial patch** (LEX), represents a relatively novel surgical approach to relief ischemic systolic restriction, despite some controversy regarding this technique (fig 20). Some encouraging results of LEX were reported but the number of treated patients is, so far, very limited (Dobre 2000, Langer 2006, de Varennes 2009). Surgical leaflet extension by autologous pericardial patch addresses directly the problem of ischemic leaflet restriction and tethering (type III°b

evaluate the geometry of the left ventricle using the sphericity index.

tion of the posterior mitral leaflets.

86 Hot Topics in Echocardiography

is a decrease in mitral regurgitation (Messas 2001).

is used.

**Figure 20.** Posterior mitral leaflet after extension with pericardial patch (arrows) in a patient with ischemic dilated car‐ diomyopathy: extended LV remodeling (intraoperative view - left and TTE preoperative picture; right).

This technique allows the extension of the surface of the posterior leaflet, especially in the area of the scallops P3 and P2, which is normally more restricted by the post-ischemic tethering. Furthermore, this procedure provides an additional anatomical leaflet reserve: in case of continuing left ventricular remodeling after surgery, which may be present in about 50% of the patients, according to some authors. Leaflet extension by autologous pericardial patch has been widely and successfully used in the reconstruction of other mitral valve pathologies such as rheumatic disease and endocarditis, with acceptable long-term results (Zegdi, 2007). This procedure can be performed within 15-20 extra minutes of aortic cross-clamping, and allows implanting larger sizes mitral prosthetic rings, with minor diastolic gradient through the mitral valve. Further studies with larger number of patients and adequate long-term follow-up are needed to assess the efficiency of this simple and promising approach to the treatment of ischemic mitral regurgitation, in case of ischemic dilated cardiomyopathy.

Once more the echo plays an essential role by identifying the patient candidates to LEX. Typically the Echo aspect demonstrates small posterior mitral leaflets, systolic and, sometimes, diastolic leaflets restriction, with significant mitral regurgitation due to reduced coaptation and asymmetrical apposition of the anterior leaflet. Consequently, at the postoperative examination Echo evaluates not only the mitral valve function as expressed by the degree of residual regurgitation, but, more important, the anatomical (leaflet length) and functional reserve (the coaptation length).

For every day practice three main situations will be considered:

**1.** Chronic ischemic mitral regurgitation determined by restriction of the posterior leaflet and apical displacement of the papillary muscle in patients with inferior myocardial infarction (or inferior and lateral myocardial infarction), mild left ventricular dilatation and mild systolic dysfunction: so called 'limited' LV remodeling pattern.

**2.** Chronic ischemic mitral regurgitation by systolic (and sometimes diastolic) restriction of mitral leaflets motion (tethering of mitral leaflets) in patients with history of double or multiple infarction, overt left ventricular dilatation and depression of systolic function (ischemic cardiomyopathy): 'extended' LV remodeling pattern.

**Geometrical echocardiographic analysis.** As already mentioned, the echocardiographic presentation of systolic restriction of the posterior mitral leaflet is typical: in presence of an inferior and/or lateral myocardial infarction, the posterior leaflet appears fixed in systole (and sometimes also in diastole), instead of the normal thickness of it and of the absence of fibrosis and/or calcification. The anterior leaflet is overlapping the posterior restricted leaflet (asym‐ metrical apposition), due to the deficit of a supporting surface in systole. The transthoracic exam is sufficient to identify the mechanism of mitral regurgitation and, equally important, to evaluate the degree of mitral regurgitation (Monin JL, 2005). The algorithm of evaluation of mitral valve geometry should be focused on the assessment of the triangle of coaptation and coaptation length (normally >6mm). In this specific condition there is an insufficient leaflet coaptation due to systolic restriction of the posterior leaflet, asymmetric apposition of the

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**Figure 22.** Restriction of posterior leaflet with typical asymmetric apposition of the anterior one (2DE and 3DE TT pic‐ tures) in a patient with inferior MI. The tip of the anterior mitral leaflet is heading towards the left atrium due to

The evaluation of the anatomical and functional reserve of the posterior mitral leaflet plays an essential role for those patients who will undergo reconstructive surgery. For example, when the posterior leaflet is too small (<1mm of length) and particularly restricted (*fixed* leaflet), it is a clear sign of reduced anatomical reserve. This key point will indicate the need of a more aggressive surgical approach where reductive annuloplasty should be associated to leaflet

**Echo-surgical messages:** As general rule, in coronary patients undergoing revascularization, the assessment of the severity of valve regurgitation (and so of decision to treat the regurgi‐ tation), should be done by transthoracic exam, as general anesthesia may significantly decrease the severity of regurgitation*.* When necessary, in the operating room, a preload and/or afterload test provides an additional estimation of the severity of mitral regurgitation (Aklog 2001, Gisbert A, 2006). Intraoperative transesophageal echocardiography is routinely per‐ formed in order to confirm the mechanism of mitral regurgitation and mainly to control the

anterior leaflet and annular dilatation.

chronic loss of the systolic resistance plane.

extension as discussed before.

outcome of repair.

**3.** Chronic ischemic mitral regurgitation by papillary muscle elongation (with various degree of false prolapse of the mitral leaflets) (Hashim 2012); usually patients with inferior myocardial infarction, chronic ischemic mitral regurgitation and *distortion of the coaptation triangle.*

#### **5.1. Chronic ischemic mitral regurgitation due to restriction**

Chronic ischemic mitral regurgitation due to restriction of the posterior mitral leaflet and asymmetrical apposition of the anterior one, by apical displacement of the posterior papillary muscle and left ventricular wall. Fig 21.

**Background.** This is the most common type of ischemic mitral regurgitation (about 2/3 of all cases of chronic ischemic mitral regurgitation), belongs to the Carpantier's type III°b classifi‐ cation and has been extensively described. The valve leakage is here the result of alteration of subvalvular apparatus secondary to left ventricle remodeling following myocardial infarction. Frequently, they present with a myocardial scar caused by a previous myocardial infarction and the remodeling process of the left heart is less expressed, with mild systolic dysfunction. Respect of patients with ischemic dilated cardiomyopathy, this category of patients has less dilatation of the left ventricular cavity, and, as a rule, history of inferior (or lateral) myocardial infarction: echocardiographic pattern of limited LV remodeling. An infarction at the basal side of the left ventricle, involving the postero-medial papillary muscle will lead to a posterior and apical displacement of the papillary muscle, which will pull the posterior leaflet toward the posterior wall, impeding it to arrive to the normal coaptation plane during systole (figure 22). The postero-medial papillary muscle is more prone to ischemic remodeling than the antero-lateral one, having only a vascular source (from circumflex or right coronary), while the latter has a double vascularization (from both left anterior descending and circumflex) – see also the fig 7.

**Geometrical echocardiographic analysis.** As already mentioned, the echocardiographic presentation of systolic restriction of the posterior mitral leaflet is typical: in presence of an inferior and/or lateral myocardial infarction, the posterior leaflet appears fixed in systole (and sometimes also in diastole), instead of the normal thickness of it and of the absence of fibrosis and/or calcification. The anterior leaflet is overlapping the posterior restricted leaflet (asym‐ metrical apposition), due to the deficit of a supporting surface in systole. The transthoracic exam is sufficient to identify the mechanism of mitral regurgitation and, equally important, to evaluate the degree of mitral regurgitation (Monin JL, 2005). The algorithm of evaluation of mitral valve geometry should be focused on the assessment of the triangle of coaptation and coaptation length (normally >6mm). In this specific condition there is an insufficient leaflet coaptation due to systolic restriction of the posterior leaflet, asymmetric apposition of the anterior leaflet and annular dilatation.

**2.** Chronic ischemic mitral regurgitation by systolic (and sometimes diastolic) restriction of mitral leaflets motion (tethering of mitral leaflets) in patients with history of double or multiple infarction, overt left ventricular dilatation and depression of systolic function

**3.** Chronic ischemic mitral regurgitation by papillary muscle elongation (with various degree of false prolapse of the mitral leaflets) (Hashim 2012); usually patients with inferior myocardial infarction, chronic ischemic mitral regurgitation and *distortion of the coaptation*

Chronic ischemic mitral regurgitation due to restriction of the posterior mitral leaflet and asymmetrical apposition of the anterior one, by apical displacement of the posterior papillary

**Figure 21.** Systolic restriction of posterior papillary muscle; 3D and 2D transthoracic echocardiography and drawing.

**Background.** This is the most common type of ischemic mitral regurgitation (about 2/3 of all cases of chronic ischemic mitral regurgitation), belongs to the Carpantier's type III°b classifi‐ cation and has been extensively described. The valve leakage is here the result of alteration of subvalvular apparatus secondary to left ventricle remodeling following myocardial infarction. Frequently, they present with a myocardial scar caused by a previous myocardial infarction and the remodeling process of the left heart is less expressed, with mild systolic dysfunction. Respect of patients with ischemic dilated cardiomyopathy, this category of patients has less dilatation of the left ventricular cavity, and, as a rule, history of inferior (or lateral) myocardial infarction: echocardiographic pattern of limited LV remodeling. An infarction at the basal side of the left ventricle, involving the postero-medial papillary muscle will lead to a posterior and apical displacement of the papillary muscle, which will pull the posterior leaflet toward the posterior wall, impeding it to arrive to the normal coaptation plane during systole (figure 22). The postero-medial papillary muscle is more prone to ischemic remodeling than the antero-lateral one, having only a vascular source (from circumflex or right coronary), while the latter has a double vascularization (from both left anterior descending and circumflex) –

(ischemic cardiomyopathy): 'extended' LV remodeling pattern.

**5.1. Chronic ischemic mitral regurgitation due to restriction**

muscle and left ventricular wall. Fig 21.

*triangle.*

88 Hot Topics in Echocardiography

see also the fig 7.

**Figure 22.** Restriction of posterior leaflet with typical asymmetric apposition of the anterior one (2DE and 3DE TT pic‐ tures) in a patient with inferior MI. The tip of the anterior mitral leaflet is heading towards the left atrium due to chronic loss of the systolic resistance plane.

The evaluation of the anatomical and functional reserve of the posterior mitral leaflet plays an essential role for those patients who will undergo reconstructive surgery. For example, when the posterior leaflet is too small (<1mm of length) and particularly restricted (*fixed* leaflet), it is a clear sign of reduced anatomical reserve. This key point will indicate the need of a more aggressive surgical approach where reductive annuloplasty should be associated to leaflet extension as discussed before.

**Echo-surgical messages:** As general rule, in coronary patients undergoing revascularization, the assessment of the severity of valve regurgitation (and so of decision to treat the regurgi‐ tation), should be done by transthoracic exam, as general anesthesia may significantly decrease the severity of regurgitation*.* When necessary, in the operating room, a preload and/or afterload test provides an additional estimation of the severity of mitral regurgitation (Aklog 2001, Gisbert A, 2006). Intraoperative transesophageal echocardiography is routinely per‐ formed in order to confirm the mechanism of mitral regurgitation and mainly to control the outcome of repair.

**Surgical planning and management.** Most of the times, the surgical technique consists in mitral annuloplasty using an undersized complete prosthetic ring or in alternative only a posterior prosthetic ring which should reduce the annular dilation especially in the region of the medial scallops (P3). Depending on the functional and anatomical reserve of the posterior leaflet, cusp extension using a pericardial patch may be taken into consideration. The newly inserted pericardial patch should be as large as possible because, by sewing usually it remains smaller and also because it has a natural tendency to shrink overtime.

**6. Unfavorable characteristics for mitral valve repair (table 2, fig 24)**

unfavorable characteristics for valve repair.

**Table 2.** Unfavorable characteristics for mitral valve repair.

• Coaptation distance ≥ 1 cm • Tenting area > 2,5 – 3 cm2

• Posterolateral angle > 45°

EDD - end diastolic diameter, ESD - end systolic diameter, ESV - end systolic volume.

• Interpapillary muscle distance > 20 mm • EDD > 65 mm, ESD > 51 mm (ESV > 140 mL)

• Complex jets

When the global remodeling of the left ventricle is too advanced, with loss of the normal shape and important dilatation of the LV cavity, overt tethering of the mitral leaflet and important annular dilatation, the mitral valve repair may be difficult to accomplish (Troubil 2010). A remodeled, dilated ventricle, with an interpapillary muscle distance more than 20mm, is a marker of poor scenario for mitral valve repair. A left ventricular cavity remodeled and dilated with a value above 65mm for LV end diastolic diameter (EDD) and above 51mm for end systolic diameter (ESD), corresponding to an end systolic volume above 140ml, are also considered

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**Figure 24.** Assessment of the tenting area (5,74cm2, left) and of the coaptation distance (13mm, right) in a coronary patient with chronic ischemic mitral insufficiency; both criteria suggest low probability for mitral valve repair.

Due to the deteriorated contractile status of the LV, the diminish force of closing contributes to the generation of mitral insufficiency, but this phenomenon alone is not enough. There are indeed forms of dilated cardiomyopathy with very large ventricle and severely reduced ejection fraction without an important mitral regurgitation, or even without any mitral regurgitation. Important in this situation is the impairment of the geometry at the papillary

muscles level. Asymmetrical and symmetrical pattern can coexist in the same patient.

#### **5.2. Ischemic dilatative cardiomyopathy (fig 23)**

**Background.** This situation is the final stage of an unfavorable evolution of ischemic heart disease. Usually, in anamnesis, there are more than one myocardial infarction and a long story of percutaneous interventions and/or surgical treatments.

**Mechanism.** This category of patients presents the phenomenon of "mitral – ventricular mismatch". Due to progressive dilatation of the left cavity, the rightly balance between the mitral valve apparatus and the dimension of the multiinfarcted left ventricle will be lost, and in this condition, the mitral valve will become insufficient. Any tentative to repair the mitral valve has to take into consideration this aspect. More remodeled and dilated the left cavity will be, more difficult will be to accomplish the valve repair and the plasty will be less stable over time. Some elements as diameter of the LV cavity, the volumes, dilatation of the mitral annulus and migration of the papillary muscle, may be documented by a series of echocar‐ diographic parameters. So, the remodeling of the left heart will be expressed by a series of factor as: tenting area, coaptation distance, left ventricular diameter and volume, the interpa‐ pillary distance. Some studies showed negative correlation between these parameters and the feasibility of mitral repair.

**Figure 23.** Ischemic dilated cardiomyopathy with chronic mitral regurgitation due to important dilatation of the LV cavity, annular dilatation and loss of leaflet coaptation (arrow). TEE transgastric short and long axis views. Notice also the systolic restriction of the posterior leaflet (right picture).

### **6. Unfavorable characteristics for mitral valve repair (table 2, fig 24)**

When the global remodeling of the left ventricle is too advanced, with loss of the normal shape and important dilatation of the LV cavity, overt tethering of the mitral leaflet and important annular dilatation, the mitral valve repair may be difficult to accomplish (Troubil 2010). A remodeled, dilated ventricle, with an interpapillary muscle distance more than 20mm, is a marker of poor scenario for mitral valve repair. A left ventricular cavity remodeled and dilated with a value above 65mm for LV end diastolic diameter (EDD) and above 51mm for end systolic diameter (ESD), corresponding to an end systolic volume above 140ml, are also considered unfavorable characteristics for valve repair.


ESV - end systolic volume.

**Surgical planning and management.** Most of the times, the surgical technique consists in mitral annuloplasty using an undersized complete prosthetic ring or in alternative only a posterior prosthetic ring which should reduce the annular dilation especially in the region of the medial scallops (P3). Depending on the functional and anatomical reserve of the posterior leaflet, cusp extension using a pericardial patch may be taken into consideration. The newly inserted pericardial patch should be as large as possible because, by sewing usually it remains

**Background.** This situation is the final stage of an unfavorable evolution of ischemic heart disease. Usually, in anamnesis, there are more than one myocardial infarction and a long story

**Mechanism.** This category of patients presents the phenomenon of "mitral – ventricular mismatch". Due to progressive dilatation of the left cavity, the rightly balance between the mitral valve apparatus and the dimension of the multiinfarcted left ventricle will be lost, and in this condition, the mitral valve will become insufficient. Any tentative to repair the mitral valve has to take into consideration this aspect. More remodeled and dilated the left cavity will be, more difficult will be to accomplish the valve repair and the plasty will be less stable over time. Some elements as diameter of the LV cavity, the volumes, dilatation of the mitral annulus and migration of the papillary muscle, may be documented by a series of echocar‐ diographic parameters. So, the remodeling of the left heart will be expressed by a series of factor as: tenting area, coaptation distance, left ventricular diameter and volume, the interpa‐ pillary distance. Some studies showed negative correlation between these parameters and the

**Figure 23.** Ischemic dilated cardiomyopathy with chronic mitral regurgitation due to important dilatation of the LV cavity, annular dilatation and loss of leaflet coaptation (arrow). TEE transgastric short and long axis views. Notice also

smaller and also because it has a natural tendency to shrink overtime.

**5.2. Ischemic dilatative cardiomyopathy (fig 23)**

feasibility of mitral repair.

90 Hot Topics in Echocardiography

the systolic restriction of the posterior leaflet (right picture).

of percutaneous interventions and/or surgical treatments.

**Table 2.** Unfavorable characteristics for mitral valve repair.

**Figure 24.** Assessment of the tenting area (5,74cm2, left) and of the coaptation distance (13mm, right) in a coronary patient with chronic ischemic mitral insufficiency; both criteria suggest low probability for mitral valve repair.

Due to the deteriorated contractile status of the LV, the diminish force of closing contributes to the generation of mitral insufficiency, but this phenomenon alone is not enough. There are indeed forms of dilated cardiomyopathy with very large ventricle and severely reduced ejection fraction without an important mitral regurgitation, or even without any mitral regurgitation. Important in this situation is the impairment of the geometry at the papillary muscles level. Asymmetrical and symmetrical pattern can coexist in the same patient.

**Geometrical echocardiographic analysis.** These patients have a high degree of tenting in both leaflets (papillary far from each other), a very dilated annulus and a large defect of coaptation in the central part of the valve conditioning a severe mitral regurgitation, with a large vena contracta. They also present a larger area than normal of the coaptation triangle, express by a larger tenting area and a higher coaptation distance (fig 24).

**Surgery.** Given the seriousness of this clinical condition, the surgical management of this syndrome requires the most aggressive approach. Restrictive and undersized annuloplasty usually with a complete rigid is often combined with other surgical techniques as leaflet extension and/or papillary muscle repositioning. There are some techniques used in these situations, like re-approaching the papillary muscles with a Gore-Tex band (Hvass 2010) thus decreasing the degree of tenting or the use of an external mesh for preventing further dilatation. Even if the immediate outcome could be satisfactory medium and long term results are to be evaluated.

The clue of the diagnosis is the visualization of the papillary muscles, which can be done transthoracic in parasternal or apical long axis views, modified for the exposure of the papillary, or transoesophageal at 60º (bicommissural view) or transgastric view at 90º. The prolapse at the level of one scallop can coexist with the restriction of another scallop, hence

**Figure 25.** Several patients with chronic ischemic regurgitation and papillary muscle elongation. The papillary muscle appears elongated, thinly and sharply, like a thorn, with a hyperechogenic tip, which is very close to the mitral valve

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**Surgical planning and management:** In these cases a rebuilding of the triangle of coaptation is performed by means of PTFE Gore-Tex neochords which will correct the normal mitral geometry. Depending on the intraoperative finding and surgical exposition and access, plication of the elongated papillary muscle may be performed. Annuloplasty is always

**Dyssynchrony as a cause of chronic ischemic mitral regurgitation.** Due to the high prevalence of left bundle branch block in the ischemic heart disease, the assyncronism of contraction is a frequent cause of mitral regurgitation. Significant mitral regurgitation is twice more often in patients with a QRS duration longer than 130 msec. The delayed activation of the antero-lateral papillary muscle leads to a misalignment of the leaflets during systole. The resynchronization therapy has good results in this type of mitral regurgitation. The pacing wires are better attached intraoperatively, the surgeon having the possibility to choose the place without the

On one hand, though, the currently available techniques still need validation and, on the other,

Ischemic mitral regurgitation has important prognosis implications in patients with coronary heart disease. It should not be underestimated and this underlines the need for a complete evaluation in which the 2DE and the Doppler echocardiography plays a major role, but should

be interpreted specifically, in particular as regards quantification of the regurgitation.

the importance to visualize the entire valve prior to surgery.

restriction imposed by the anatomy of the cardiac veins.

the optimal therapy /combination of therapies needs clarification.

performed in order to stabilize the repair.

annulus plane (so called "thorny papillary muscle").

**8. Conclusions**

### **7. Chronic ischemic mitral regurgitation due to elongation of papillary muscle (fig 24)**

**Background.** This type of ischemic mitral regurgitation is considered to be rare (about 2% of all cases of ischemic mitral regurgitation), belonging to the Carpantier's type II classifica‐ tion. Nevertheless, it is possible that this type of regurgitation is indeed more frequent and in every day practice but also underestimated. The valve leakage is, here, the result of alteration of subvalvular apparatus secondary to ischemic elongation of the papillary muscle following myocardial necrosis, chronic ischemia and mechanical stress. The papillary muscle elongation is never solitary, being an associated process in the general context of postinfarction remodeling.

**Mechanism.** The partially infarcted and/or ischemic posterior papillary muscle suffers a chronic remodeling with elongation that expresses itself at the level of the mitral leaflets by alteration of the coaptation triangle and valve geometry.

**Geometrical echocardiographic analysis:** in this specific condition there is an insufficient leaflet coaptation due to various degree of ischemic prolapse of the posterior and/or anterior mitral leaflet. Often the echocardiographic aspect is an unusual anterior leaflet prolapse or that of a prolapse of more corresponding scallops (e.g. A2/P2 and A3/P3). The papillary muscle appears elongated, triangular shaped, with the tip very close to the mitral annulus. As a consequence, the normal configuration of mitral valve, defined by the coaptation triangle, will suffer various degree of alteration, till the complete disappearance (see also fig 5, 6). An annular dilation is often associated, depending on the extension of myocardial infarction. All these elements will lead to a complex holosystolic regurgitant jet. This entity may be caused by a limited infarction at the papillary muscle level, which lead to fibrosis and elongation of the muscle. The papillary muscle will develop a thin and sharp appearance, like a thorn, and will be more hyperechogenic.

Ischemic Mitral Regurgitation: From Echo Assessment to Surgical Strategy and Technique http://dx.doi.org/10.5772/56062 93

**Figure 25.** Several patients with chronic ischemic regurgitation and papillary muscle elongation. The papillary muscle appears elongated, thinly and sharply, like a thorn, with a hyperechogenic tip, which is very close to the mitral valve annulus plane (so called "thorny papillary muscle").

The clue of the diagnosis is the visualization of the papillary muscles, which can be done transthoracic in parasternal or apical long axis views, modified for the exposure of the papillary, or transoesophageal at 60º (bicommissural view) or transgastric view at 90º. The prolapse at the level of one scallop can coexist with the restriction of another scallop, hence the importance to visualize the entire valve prior to surgery.

**Surgical planning and management:** In these cases a rebuilding of the triangle of coaptation is performed by means of PTFE Gore-Tex neochords which will correct the normal mitral geometry. Depending on the intraoperative finding and surgical exposition and access, plication of the elongated papillary muscle may be performed. Annuloplasty is always performed in order to stabilize the repair.

**Dyssynchrony as a cause of chronic ischemic mitral regurgitation.** Due to the high prevalence of left bundle branch block in the ischemic heart disease, the assyncronism of contraction is a frequent cause of mitral regurgitation. Significant mitral regurgitation is twice more often in patients with a QRS duration longer than 130 msec. The delayed activation of the antero-lateral papillary muscle leads to a misalignment of the leaflets during systole. The resynchronization therapy has good results in this type of mitral regurgitation. The pacing wires are better attached intraoperatively, the surgeon having the possibility to choose the place without the restriction imposed by the anatomy of the cardiac veins.

On one hand, though, the currently available techniques still need validation and, on the other, the optimal therapy /combination of therapies needs clarification.

#### **8. Conclusions**

**Geometrical echocardiographic analysis.** These patients have a high degree of tenting in both leaflets (papillary far from each other), a very dilated annulus and a large defect of coaptation in the central part of the valve conditioning a severe mitral regurgitation, with a large vena contracta. They also present a larger area than normal of the coaptation triangle, express by a

**Surgery.** Given the seriousness of this clinical condition, the surgical management of this syndrome requires the most aggressive approach. Restrictive and undersized annuloplasty usually with a complete rigid is often combined with other surgical techniques as leaflet extension and/or papillary muscle repositioning. There are some techniques used in these situations, like re-approaching the papillary muscles with a Gore-Tex band (Hvass 2010) thus decreasing the degree of tenting or the use of an external mesh for preventing further dilatation. Even if the immediate outcome could be satisfactory medium and long term results are to be

**7. Chronic ischemic mitral regurgitation due to elongation of papillary**

**Background.** This type of ischemic mitral regurgitation is considered to be rare (about 2% of all cases of ischemic mitral regurgitation), belonging to the Carpantier's type II classifica‐ tion. Nevertheless, it is possible that this type of regurgitation is indeed more frequent and in every day practice but also underestimated. The valve leakage is, here, the result of alteration of subvalvular apparatus secondary to ischemic elongation of the papillary muscle following myocardial necrosis, chronic ischemia and mechanical stress. The papillary muscle elongation is never solitary, being an associated process in the general context of post-

**Mechanism.** The partially infarcted and/or ischemic posterior papillary muscle suffers a chronic remodeling with elongation that expresses itself at the level of the mitral leaflets by

**Geometrical echocardiographic analysis:** in this specific condition there is an insufficient leaflet coaptation due to various degree of ischemic prolapse of the posterior and/or anterior mitral leaflet. Often the echocardiographic aspect is an unusual anterior leaflet prolapse or that of a prolapse of more corresponding scallops (e.g. A2/P2 and A3/P3). The papillary muscle appears elongated, triangular shaped, with the tip very close to the mitral annulus. As a consequence, the normal configuration of mitral valve, defined by the coaptation triangle, will suffer various degree of alteration, till the complete disappearance (see also fig 5, 6). An annular dilation is often associated, depending on the extension of myocardial infarction. All these elements will lead to a complex holosystolic regurgitant jet. This entity may be caused by a limited infarction at the papillary muscle level, which lead to fibrosis and elongation of the muscle. The papillary muscle will develop a thin and sharp appearance, like a thorn, and will

larger tenting area and a higher coaptation distance (fig 24).

alteration of the coaptation triangle and valve geometry.

evaluated.

**muscle (fig 24)**

92 Hot Topics in Echocardiography

infarction remodeling.

be more hyperechogenic.

Ischemic mitral regurgitation has important prognosis implications in patients with coronary heart disease. It should not be underestimated and this underlines the need for a complete evaluation in which the 2DE and the Doppler echocardiography plays a major role, but should be interpreted specifically, in particular as regards quantification of the regurgitation.

A complete assessment of left ventricular geometry and function and of the mitral valve configuration prior to surgery may help improve patient risk stratification and better indi‐ vidualize the surgical strategy based on the patient's specific characteristics.

tation is considered to range between 10 to 20% of the cases, and, at five years of follow up,

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95

Thus, in advanced stage of left ventricular post infarction remodeling with over dilatation and important mitral valve tethering, the ring annuloplasty has to be completed with leaflet extension. This approach seems coherent with the mechanism of mitral regurgitation, with the echocardiographic data and with the concept of "mitral valve – LV chamber mismatch".

The major challenge for cardiologists and surgeons is how to integrate data from different imaging techniques that assess mitral valve geometry and left ventricular size, geometry, function and potential functional recovery. This in order to tailor and optimize the surgical

Even today, we have no reliable predictors of recurrent and persistent mitral regurgitation. However, the surgical treatment of ischemic mitral insufficiency continues to evolve and new methods addressing ventricular structures are being introduced: left ventricular restoration, papillary muscle's relocation, sling, imbrication or reapproximation, chordal cutting or translocation. Despite remarkable progress in reparative surgery, further investigation is still

, Razvan Ticulescu2

1 The Cardioteam Foundation, Cardiac Surgery Dpt, San Gaudenzio Clinic, Novara, Italy

[1] "Kirklin/Barratt-Boyes Cardiac Surgery": Nicholas T. Kouchoukos, Eugene H. Black‐ stone, Frank L. Hanley, James K. Kirklin. 4Th edition, Publisher: Saunders; 4th Re‐

[2] Popa B A, Diena M, Cerin G, Lanzillo G., Tesler UF.Severe Post-Ischemic Elongation of the Anterior Papillary Muscle. An Unusual Cause of Mitral Insufficiency in a 75-

[3] Carpentier's Reconstructive Valve Surgery, Alain Carpentier, David Adams, Farzan‐

and Marco Diena1

approach to patients with chronic ischemic mitral regurgitation.

, Adrian Bogdan Popa1

\*Address all correspondence to: gheorghe.cerin@gmail.com

2 Cardiac Surgery Dpt, The 'Monza' Hospital, Bucharest, Romania

Year-Old Man; Tex Heart Inst J. (2007); 34(2): 222-224.

necessary to find the best approach to treat ischemic mitral regurgitation.

half of the patient may develop recurrence.

**Author details**

Gheorghe Cerin1

**References**

vised edition

Filsoufi, Saunders, 2010.

The acute ischemic mitral regurgitation is a rare mechanical complication after myocardial infarction, due to elongation, partial or complete rupture of papillary muscle but has a poor prognosis and it needs urgent diagnosis and surgery. A careful echocardiographic exam, performed in ICU, is mandatory in acute patients with myocardial infarction, focusing the attention on the presence of mitral regurgitation. In case of any suspicion of structural acute ischemic mitral regurgitation the transesophageal exam must be done, to avoid the transfor‐ mation of partial rupture of papillary muscle in a complete one. The complete rupture of papillary muscle is often fatal and has to be considered a too late clinical and echocardiographic diagnosis; these patients need an emergent operation and very intensive perioperative pharmacologic and mechanical support.

From a conceptual point of view, chronic ischemic mitral regurgitation witnesses the loss of contractile myocardial tissue parallel with the presence of the post-infarction remodeling process. As known, ischemic mitral insufficiency develops on normally mitral leaflets. As the myocardial mass loss is larger, the remodeling processes and regurgitation become greater.

Recognizing the mechanism of valve incompetence is an essential point for the surgical planning and for a good result of the mitral repair. In the patient's candidates to surgery, the role of the echocardiographic exam is to identify the mechanisms of valve regurgitation and to quantify it. As noted, in most cases of chronic ischemic mitral regurgitation the mechanism is the restriction of one or both leaflets, caused by the tethering exercised by the displaced papillary muscle.

The transthoracic exam is commonly enough to clarify the mechanism of the chronic ischemic mitral regurgitation. Only patients with papillary muscle elongation may raise difficulties in diagnosis. Loss of the normal shape of the 'triangle of coaptation' is one of the key character‐ istics of chronic ischemic mitral regurgitation. In case of post-ischemic elongation of the papillary muscle, the clue of the diagnosis is obtained by looking not only to the mitral valve, but by focusing the exam on the papillary muscles, particularly when the patient presents a deformation of the 'coaptation triangle'. In patients with type II° Carpentier's classifications (elongated papillary muscle and leaflets prolapse), alongside of ring annuloplasty use of PTFE Gore-Tex chordae is often required.

In patients with chronic ischemic mitral insufficiency the echocardiography may identify two different patterns of post infarction remodeling: a *limited* process of post infarction remodeling and an *extensive* one. The mitral repair is usually more challenging in patients with extensive pattern of post infarction remodeling, where, due to left heart cavity enlargement a phenom‐ enon of "mitral valve – LV chamber mismatch" is present.

Although the mechanisms of ischemic mitral regurgitation are often complex, currently, undersized annuloplasty is considered the standard approach to reducing mitral insufficiency. Unfortunately this technique does not resolve the real mechanism of disease, the remodeled and sphericalized left ventricle. By this technique the persistence of ischemic mitral regurgi‐ tation is considered to range between 10 to 20% of the cases, and, at five years of follow up, half of the patient may develop recurrence.

Thus, in advanced stage of left ventricular post infarction remodeling with over dilatation and important mitral valve tethering, the ring annuloplasty has to be completed with leaflet extension. This approach seems coherent with the mechanism of mitral regurgitation, with the echocardiographic data and with the concept of "mitral valve – LV chamber mismatch".

The major challenge for cardiologists and surgeons is how to integrate data from different imaging techniques that assess mitral valve geometry and left ventricular size, geometry, function and potential functional recovery. This in order to tailor and optimize the surgical approach to patients with chronic ischemic mitral regurgitation.

Even today, we have no reliable predictors of recurrent and persistent mitral regurgitation. However, the surgical treatment of ischemic mitral insufficiency continues to evolve and new methods addressing ventricular structures are being introduced: left ventricular restoration, papillary muscle's relocation, sling, imbrication or reapproximation, chordal cutting or translocation. Despite remarkable progress in reparative surgery, further investigation is still necessary to find the best approach to treat ischemic mitral regurgitation.

#### **Author details**

A complete assessment of left ventricular geometry and function and of the mitral valve configuration prior to surgery may help improve patient risk stratification and better indi‐

The acute ischemic mitral regurgitation is a rare mechanical complication after myocardial infarction, due to elongation, partial or complete rupture of papillary muscle but has a poor prognosis and it needs urgent diagnosis and surgery. A careful echocardiographic exam, performed in ICU, is mandatory in acute patients with myocardial infarction, focusing the attention on the presence of mitral regurgitation. In case of any suspicion of structural acute ischemic mitral regurgitation the transesophageal exam must be done, to avoid the transfor‐ mation of partial rupture of papillary muscle in a complete one. The complete rupture of papillary muscle is often fatal and has to be considered a too late clinical and echocardiographic diagnosis; these patients need an emergent operation and very intensive perioperative

From a conceptual point of view, chronic ischemic mitral regurgitation witnesses the loss of contractile myocardial tissue parallel with the presence of the post-infarction remodeling process. As known, ischemic mitral insufficiency develops on normally mitral leaflets. As the myocardial mass loss is larger, the remodeling processes and regurgitation become greater. Recognizing the mechanism of valve incompetence is an essential point for the surgical planning and for a good result of the mitral repair. In the patient's candidates to surgery, the role of the echocardiographic exam is to identify the mechanisms of valve regurgitation and to quantify it. As noted, in most cases of chronic ischemic mitral regurgitation the mechanism is the restriction of one or both leaflets, caused by the tethering exercised by the displaced

The transthoracic exam is commonly enough to clarify the mechanism of the chronic ischemic mitral regurgitation. Only patients with papillary muscle elongation may raise difficulties in diagnosis. Loss of the normal shape of the 'triangle of coaptation' is one of the key character‐ istics of chronic ischemic mitral regurgitation. In case of post-ischemic elongation of the papillary muscle, the clue of the diagnosis is obtained by looking not only to the mitral valve, but by focusing the exam on the papillary muscles, particularly when the patient presents a deformation of the 'coaptation triangle'. In patients with type II° Carpentier's classifications (elongated papillary muscle and leaflets prolapse), alongside of ring annuloplasty use of PTFE

In patients with chronic ischemic mitral insufficiency the echocardiography may identify two different patterns of post infarction remodeling: a *limited* process of post infarction remodeling and an *extensive* one. The mitral repair is usually more challenging in patients with extensive pattern of post infarction remodeling, where, due to left heart cavity enlargement a phenom‐

Although the mechanisms of ischemic mitral regurgitation are often complex, currently, undersized annuloplasty is considered the standard approach to reducing mitral insufficiency. Unfortunately this technique does not resolve the real mechanism of disease, the remodeled and sphericalized left ventricle. By this technique the persistence of ischemic mitral regurgi‐

vidualize the surgical strategy based on the patient's specific characteristics.

pharmacologic and mechanical support.

papillary muscle.

94 Hot Topics in Echocardiography

Gore-Tex chordae is often required.

enon of "mitral valve – LV chamber mismatch" is present.

Gheorghe Cerin1 , Adrian Bogdan Popa1 , Razvan Ticulescu2 and Marco Diena1


#### **References**


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**Chapter 5**

**Real-Time 3D Echocardiography in Percutaneous**

Since Dr Kanji Inoue introduced the Inoue balloon catheter in 1984, percutaneous balloon valvuloplasty (PBMV) has become the treatment of choice forpatients with symptomatic mitral valve stenosis and favorable valve morphology. PBMV is the preferred treatment for mitral stenosis as it is less invasive and provides longer-lasting results than closed commissurotomy. 1 PMBV is not suited for patients with mitral stenosis due to severe annular calcification or markedly degenerated valves. PBMV can be performed either an in antegrade fashion through a transseptal puncture or retrograde from the aorta to the mitral valve. Serial balloon dila‐ tions of the mitral valve using the self-centering Inoue balloon catheter (or alternatively, a standard valvuloplasty balloon catheter) are performed to physically split the mitral valve leaflet commissures and subsequently improve leaflet motion and hemodynamics. In success‐ ful cases,percutaneous balloonmitral valvuloplasty typicallydoubles themitral valve area and decreases the mitral valve gradient by half. Splitting of the commissures is the principle mechanism that leads to improvement of hemodynamics and patient symptomatology.

The anatomy of the mitral valve is complex, and echocardiographic imaging plays a critical role in both the diagnosis and guidance of management of patients with mitral stenosis. Although Doppler hemodynamics and 2D transthoracic echocardiography are a mainstay in the echocardiographic assessment of mitral stenosis (Figure 1), real-time three-dimensional echocardiography (RT3DE) is an emerging imaging tool for not only the diagnosis of mitral stenosis (Figure 2), but also for the guidance of percutaneous balloon mitral valvuloplasty

> © 2013 Navarro et al.; licensee InTech. This is a paper distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

**Balloon Mitral Valvuloplasty**

Additional information is available at the end of the chapter

Mark A. Navarro, Michael Kim and

procedures in the catheterization laboratory.

Ernesto E. Salcedo

**1. Introduction**

http://dx.doi.org/10.5772/56433
