*3.10.2.3 Echocardiography*

Echocardiography serves as the principal modality for and quantitating AS. 2D imaging provides information on chamber size, degree of hypertrophy, LV systolic function, valve mobility, and calcification. Doppler measurement of transvalvular blood flow velocity can be used to ermine peak and mean pressure gradients using the.

The symptomatic triad of AS is angina, exertional syncope, and symptoms of congestive heart failure, such as shortness of breath. The mechanisms for angina and congestive heart failure are explained in the previous section. The mechanism for syncope is likely related to the blunting of exercise-induced augmentation in stroke volume as a result of outflow obstruction coupled with exercise-induced peripheral vasodilation. These changes cause a drop in systemic blood pressure leading to cerebral hypoperfusion and syncope.

The classic physical finding is a systolic ejection murmur heard loudest at the second right intercostal space, which commonly radiates to the carotid arteries. And maybe associated with severe cases of AS palpable thrill may be present. Palpation of the pulse may reveal a weak and delayed pulse known as *pulsus parvus et tardus*.

### **3.11 Diagnosis and grading**

The most common method for the diagnosis and grading of AS is two-dimensional transthoracic echocardiography Doppler velocity measurement (**Table 1**). In most patients, this modality can reliably establish aortic jet velocity, aortic valve peak and mean gradients, and aortic valve area [39].

### **3.12 Natural history**

Without valve replacement symptomatic AS has a bleak outcome. Numerous studies consistently reported survivals of 3 years for angina and syncope and 1.5–2 years for dyspnea and heart failure. These findings have determined the recommendations for timely surgical intervention in patients with symptomatic AS. Thirty percent of truly asymptomatic severe AS patients will become symptomatic in 2 years with mortality risks of less than 1–5% each year to 5% each year. Progression rate correlates with AS severity, which seems to progress faster with higher mean gradient. Moderate AS progress, with aortic valve area, decreases on average by 0.1 cm<sup>2</sup> per cent annually the pressure gradient across the valve rises on average by 7 mm Hg per year, and the jet velocity increases by 0.3 m/s per year [40, 41].

**25**

*Aortic Valve Disease: State of the Art*

Aortic valve area (cm2

**Table 1.**

planning therapy [42].

**3.13 Aortic regurgitation**

*3.13.1 Epidemiology and aetiology*

such as Marfan syndrome) [43].

*3.13.2 Pathophysiology*

rapidly [44, 45].

*3.13.3 Clinical features*

*DOI: http://dx.doi.org/10.5772/intechopen.93311*

*The severity of aortic stenosis according to echocardiographic criteria.*

The definitions of the conditions "low-gradient AS" and "high-gradient AS" are the most relevant new changes in the recommendations for the management of aortic valve stenosis (AS). Precise thresholds of biomarkers and pulmonary hypertension are considered, and the emphasis is focused on computed tomography, particularly for assessing the degree of calcification of the aortic valve and for

**Parameter Mild Moderate Severe**

Mean pressure gradient (mm Hg) <20 20–39 ≥40 Aortic jet velocity (m/s) 2.0–2.9 3.0–3.9 ≥4.0

) 1.6–2.5 1.1–1.5 ≤1.0

The reasons of aortic regurgitation (AR) are many and can be credited to a disruption of any components of the functional unit of the aortic root valve composite (e.g., cusps, sinuses of Valsalva, sinotubular junction, annulus). In general, the causes can be divided into those that involve the valve cusps (e.g., calcific degeneration, congenitally bicuspid valve, infective endocarditis, rheumatic disease, myxomatous degeneration) and those that encompass the aortic root (e.g., aortic dissection, aortitis of various etiologies such as syphilis, connective tissue disorders

The pathophysiology of AR is determined by the speed of onset and duration of the disease process. In acute AR, typically caused by aortic dissection, infective endocarditis, trauma, or valve prosthesis failure, there is an abrupt escalation in left ventricular end-diastolic volume because of the regurgitation. Since the left ventricle has restricted compliance and does not have enough time to gradually adapt to the extra volume, the left ventricular end-diastolic pressure (LVEDP) rises

In chronic AR, there is a gradual and stealthy evolution of left ventricular (LV) dilation and eccentric hypertrophy because of an increase in left ventricular end-diastolic volume, LVEDP, and wall stress. Dilation of the LV maintains normal systolic function and forward flow but requiring extra work to achieve normality. Sooner or later, the hypertrophic response is exhausted, and LVEF deteriorates as afterload

Patients with acute AR present with unexpected or precipitously cardiovascular

increases, resulting in heart failure and its related clinical presentation [44].

collapse, which is a life-threatening emergency. They often demonstrate ischemic symptoms because of the diminished coronary blood flow and heightened myocardial oxygen demand. In comparison, patients with chronic AR are often asymptomatic for an extended time because of the compensator remodelling of their LV mentioned earlier. Once the compensatory response is depleted, the patients

*Aortic Valve Disease: State of the Art DOI: http://dx.doi.org/10.5772/intechopen.93311*


### **Table 1.**

*Advances in Complex Valvular Disease*

*3.10.2.1 Electrocardiogram*

*3.10.2.2 Radiography*

*3.10.2.3 Echocardiography*

**3.11 Diagnosis and grading**

**3.12 Natural history**

decreases on average by 0.1 cm<sup>2</sup>

0.3 m/s per year [40, 41].

leading to cerebral hypoperfusion and syncope.

peak and mean gradients, and aortic valve area [39].

*3.10.2 Ejection systolic crescendo murmur at the second aortic area*

when calcification extends from the valve into the induction system.

apparent. Note, these findings are neither highly sensitive nor specific.

Standard features on the electrocardiogram include ventricular hypertrophy (LVH) with a strain and a biphasic p wave in V1 corresponding to atrial (LA) hypertrophy. Atrioventricular and intra ventricular conduction abnormalities maybe

The chest X-ray rounding of the left heart border and apex, post stenotic dilation of the aorta calcification of the aortic valve, and pulmonary congestion may be

Echocardiography serves as the principal modality for and quantitating AS. 2D imaging provides information on chamber size, degree of hypertrophy, LV systolic function, valve mobility, and calcification. Doppler measurement of transvalvular blood flow velocity can be used to ermine peak and mean pressure gradients using the. The symptomatic triad of AS is angina, exertional syncope, and symptoms of congestive heart failure, such as shortness of breath. The mechanisms for angina and congestive heart failure are explained in the previous section. The mechanism for syncope is likely related to the blunting of exercise-induced augmentation in stroke volume as a result of outflow obstruction coupled with exercise-induced peripheral vasodilation. These changes cause a drop in systemic blood pressure

The classic physical finding is a systolic ejection murmur heard loudest at the second right intercostal space, which commonly radiates to the carotid arteries. And maybe associated with severe cases of AS palpable thrill may be present. Palpation of the pulse may reveal a weak and delayed pulse known as *pulsus parvus et tardus*.

The most common method for the diagnosis and grading of AS is two-dimensional transthoracic echocardiography Doppler velocity measurement (**Table 1**). In most patients, this modality can reliably establish aortic jet velocity, aortic valve

Without valve replacement symptomatic AS has a bleak outcome. Numerous studies consistently reported survivals of 3 years for angina and syncope and 1.5–2 years for dyspnea and heart failure. These findings have determined the recommendations for timely surgical intervention in patients with symptomatic AS. Thirty percent of truly asymptomatic severe AS patients will become symptomatic in 2 years with mortality risks of less than 1–5% each year to 5% each year. Progression rate correlates with AS severity, which seems to progress faster with higher mean gradient. Moderate AS progress, with aortic valve area,

the valve rises on average by 7 mm Hg per year, and the jet velocity increases by

per cent annually the pressure gradient across

**24**

*The severity of aortic stenosis according to echocardiographic criteria.*

The definitions of the conditions "low-gradient AS" and "high-gradient AS" are the most relevant new changes in the recommendations for the management of aortic valve stenosis (AS). Precise thresholds of biomarkers and pulmonary hypertension are considered, and the emphasis is focused on computed tomography, particularly for assessing the degree of calcification of the aortic valve and for planning therapy [42].
