**Non Atrial Arrhythmias**

**Chapter 5**

**Provisional chapter**

**Idiopathic Ventricular Arrhythmias**

**Idiopathic Ventricular Arrhythmias**

DOI: 10.5772/intechopen.77186

Idiopathic ventricular arrhythmias (VAs) occur with a mechanism that is unrelated to myocardial scar. Idiopathic VAs most commonly occur in patients without structural heart disease, but can occur in those with structural heart disease. Idiopathic VAs present as a sustained or a non-sustained ventricular tachycardia or premature ventricular contractions. Imaging examinations such as echocardiography, nuclear tests, and cardiac magnetic resonance imaging are helpful for excluding any association of an idiopathic VA occurrence with myocardial scar. For the past two decades, the sites of idiopathic VA origins, commonly endocardial but sometimes epicardial, have been increasingly recognized. Idiopathic VAs usually originate from specific anatomical structures and exhibit characteristic electrocardiograms based on their anatomical background. Idiopathic VAs are basically benign, but they require medical treatment or catheter ablation when idiopathic VAs are symptomatic, frequent, or cause tachycardia-induced cardiomyopathy. This book chapter describes the up-to-date information on the prevalence of idiopathic

VA origins relevant to the anatomy, diagnosis, and treatment of idiopathic VAs. **Keywords:** idiopathic, ventricular tachycardia, anatomy, diagnosis, treatment

Idiopathic ventricular arrhythmias (IVAs) present as ventricular tachycardias (VTs) or premature ventricular contractions (PVCs) whose mechanisms are not associated with a myocardial scar. IVAs commonly occur in patients without structural heart disease (SHD), but can occur in those with SHD [1–3]. Classically, VTs originating from the right ventricular outflow tract (RVOT) and the left posterior fascicle are well known as IVAs. However, for the past two decades, IVAs originating from other endocardial and also epicardial sites have been increasingly recognized (**Figure 1**) [3]. IVAs usually originate from the specific anatomical

> © 2016 The Author(s). Licensee InTech. This chapter is 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.

© 2018 The Author(s). Licensee IntechOpen. This chapter is 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.

Additional information is available at the end of the chapter

Additional information is available at the end of the chapter

http://dx.doi.org/10.5772/intechopen.77186

Takumi Yamada

**Abstract**

**1. Introduction**

Takumi Yamada

#### **Idiopathic Ventricular Arrhythmias Idiopathic Ventricular Arrhythmias**

#### Takumi Yamada Takumi Yamada

Additional information is available at the end of the chapter Additional information is available at the end of the chapter

http://dx.doi.org/10.5772/intechopen.77186

#### **Abstract**

Idiopathic ventricular arrhythmias (VAs) occur with a mechanism that is unrelated to myocardial scar. Idiopathic VAs most commonly occur in patients without structural heart disease, but can occur in those with structural heart disease. Idiopathic VAs present as a sustained or a non-sustained ventricular tachycardia or premature ventricular contractions. Imaging examinations such as echocardiography, nuclear tests, and cardiac magnetic resonance imaging are helpful for excluding any association of an idiopathic VA occurrence with myocardial scar. For the past two decades, the sites of idiopathic VA origins, commonly endocardial but sometimes epicardial, have been increasingly recognized. Idiopathic VAs usually originate from specific anatomical structures and exhibit characteristic electrocardiograms based on their anatomical background. Idiopathic VAs are basically benign, but they require medical treatment or catheter ablation when idiopathic VAs are symptomatic, frequent, or cause tachycardia-induced cardiomyopathy. This book chapter describes the up-to-date information on the prevalence of idiopathic VA origins relevant to the anatomy, diagnosis, and treatment of idiopathic VAs.

DOI: 10.5772/intechopen.77186

**Keywords:** idiopathic, ventricular tachycardia, anatomy, diagnosis, treatment

## **1. Introduction**

Idiopathic ventricular arrhythmias (IVAs) present as ventricular tachycardias (VTs) or premature ventricular contractions (PVCs) whose mechanisms are not associated with a myocardial scar. IVAs commonly occur in patients without structural heart disease (SHD), but can occur in those with SHD [1–3]. Classically, VTs originating from the right ventricular outflow tract (RVOT) and the left posterior fascicle are well known as IVAs. However, for the past two decades, IVAs originating from other endocardial and also epicardial sites have been increasingly recognized (**Figure 1**) [3]. IVAs usually originate from the specific anatomical

© 2016 The Author(s). Licensee InTech. This chapter is 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. © 2018 The Author(s). Licensee IntechOpen. This chapter is 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.


**Figure 1.** Idiopathic ventricular arrhythmia origins. AIVV, anterior interventricular vein; AMC, aorto-mitral continuity; APAM, anterolateral papillary muscle; GCV, great cardiac vein; LAF, left anterior fascicle; LPF, left posterior fascicle; LV, left ventricle; LVOT, LV outflow tract; MA, mitral annulus; MCV, mid-cardiac vein; PA, pulmonary artery; PAM, papillary muscle; PPAM, posteromedial papillary muscle; RV, right ventricle; RVOT, RV outflow tract; TA, tricuspid annulus.

known as the LV ostium [11, 12] (**Figure 2**). Because there is no myocardium between the aortic and the mitral valves (fibrous trigone), most idiopathic LV ventricular arrhythmias (VAs) can originate from along the LV ostium. The LV myocardium comes in direct contact with the aorta at the base of the ASCs (**Figure 2**). When IVAs arise from the most superior portion of the LV ostium (the aortic sinus of valsalva), they can be ablated within the base of the ASCs. It has been reported that some IVAs can be ablated from the junction (commissure) between the left and the right coronary cusps (L-RCC) [13]. In these VAs, catheter ablation from underneath the ASCs is often required for their elimination. Anatomically, the superior end of the LV myocardium makes a semicircular attachment to the aortic root at the bottom of the right and left coronary cusps. However, because of the semilunar nature of the attachments of the aortic valvular cusps, the superior end of the LV myocardium is located underneath the aortic valves at the L-RCC (**Figure 2**). Therefore, IVAs that can be ablated at the L-RCC should be classified into the same group as the VAs that can be ablated within the ASCs. In this setting, these IVAs may be defined as IVAs arising from the aortic root [7]. It has been reported that IVAs can rarely be ablated from within the noncoronary cusp of the aorta (NCC) [7, 14, 15]. Spatially, the aortic root occupies a central location within the heart, with the NCC anterior and superior to the paraseptal region of the left and right atria close to the superior atrioventricular junctions (**Figure 3**) [12]. In normal human hearts, the NCC is adjacent to the atrial myocardium on the epicardial aspect of the interatrial septum. When atrial tachycardias arise from that region of the atria, those atrial tachycardias can be ablated from within the NCC. It is considered that the NCC does not directly come in contact with the ventricular myocardium

**Figure 2.** Two-dimensional computed tomography (CT) images showing the relationships between the ventricular myocardium and aortic sinus cusps. The arrowheads and dotted line in the left panel indicate the ostium of the left ventricle. The arrowheads in the right panel indicate the superior edge of the ventricular myocardium connecting with the left coronary cusp and right coronary cusp (RCC), and the dotted line the ventriculo-arterial junction. Ant, anterior; Ao, aorta; IAS, interatrial septum; L, left coronary cusp; LA, left atrium; LCA, left coronary artery; LV, left ventricle; MV, mitral valve; NCC, noncoronary cusp; R, right coronary cusp; RV, right ventricle. This figure was cited from Ref. [7] with permission.

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structures and exhibit characteristic electrocardiograms based on their anatomical background. Basically, IVAs are benign and not life-threatening, but are often symptomatic and also can cause tachycardia-induced cardiomyopathy [4, 5]. Therefore, it is important for cardiologists to update their knowledge about IVAs. This chapter describes the current expertise on the prevalence of IVA origins relevant to the anatomy, diagnosis, and treatment of IVAs.

## **2. Prevalence of IVA origins relevant to the anatomy**

The sites of IVA origins have been identified by electrophysiological mapping and confirmed by successful catheter ablation. The most common site of IVA origins is the ventricular outflow tract [1, 6]. IVAs originate more often from the RVOT than from the left ventricular outflow tract (LVOT). In the RVOT, the septum is a more common site of IVA origins than the free wall. The most common site of IVA origins in the LVOT is the aortic root followed by the sites underneath the aortic sinus cusps (ASCs) (**Figure 2**) [7, 8]. Especially, the site underneath the left coronary cusp (LCC) is located in front of the mitral annulus (MA) and is termed the aorto-mitral continuity (AMC). The MA is also one of the major sites of IVA origins [9, 10]. The anteromedial aspect of the MA may overlap with the AMC. Anatomically, the aortic and mitral valves are in a direct apposition and attach to the elliptical opening at the base of the left ventricle (LV)

**Figure 2.** Two-dimensional computed tomography (CT) images showing the relationships between the ventricular myocardium and aortic sinus cusps. The arrowheads and dotted line in the left panel indicate the ostium of the left ventricle. The arrowheads in the right panel indicate the superior edge of the ventricular myocardium connecting with the left coronary cusp and right coronary cusp (RCC), and the dotted line the ventriculo-arterial junction. Ant, anterior; Ao, aorta; IAS, interatrial septum; L, left coronary cusp; LA, left atrium; LCA, left coronary artery; LV, left ventricle; MV, mitral valve; NCC, noncoronary cusp; R, right coronary cusp; RV, right ventricle. This figure was cited from Ref. [7] with permission.

structures and exhibit characteristic electrocardiograms based on their anatomical background. Basically, IVAs are benign and not life-threatening, but are often symptomatic and also can cause tachycardia-induced cardiomyopathy [4, 5]. Therefore, it is important for cardiologists to update their knowledge about IVAs. This chapter describes the current expertise on the prevalence of IVA origins relevant to the anatomy, diagnosis, and treatment of IVAs.

**Figure 1.** Idiopathic ventricular arrhythmia origins. AIVV, anterior interventricular vein; AMC, aorto-mitral continuity; APAM, anterolateral papillary muscle; GCV, great cardiac vein; LAF, left anterior fascicle; LPF, left posterior fascicle; LV, left ventricle; LVOT, LV outflow tract; MA, mitral annulus; MCV, mid-cardiac vein; PA, pulmonary artery; PAM, papillary muscle; PPAM, posteromedial papillary muscle; RV, right ventricle; RVOT, RV outflow tract; TA, tricuspid

The sites of IVA origins have been identified by electrophysiological mapping and confirmed by successful catheter ablation. The most common site of IVA origins is the ventricular outflow tract [1, 6]. IVAs originate more often from the RVOT than from the left ventricular outflow tract (LVOT). In the RVOT, the septum is a more common site of IVA origins than the free wall. The most common site of IVA origins in the LVOT is the aortic root followed by the sites underneath the aortic sinus cusps (ASCs) (**Figure 2**) [7, 8]. Especially, the site underneath the left coronary cusp (LCC) is located in front of the mitral annulus (MA) and is termed the aorto-mitral continuity (AMC). The MA is also one of the major sites of IVA origins [9, 10]. The anteromedial aspect of the MA may overlap with the AMC. Anatomically, the aortic and mitral valves are in a direct apposition and attach to the elliptical opening at the base of the left ventricle (LV)

**2. Prevalence of IVA origins relevant to the anatomy**

annulus.

80 Cardiac Arrhythmias

known as the LV ostium [11, 12] (**Figure 2**). Because there is no myocardium between the aortic and the mitral valves (fibrous trigone), most idiopathic LV ventricular arrhythmias (VAs) can originate from along the LV ostium. The LV myocardium comes in direct contact with the aorta at the base of the ASCs (**Figure 2**). When IVAs arise from the most superior portion of the LV ostium (the aortic sinus of valsalva), they can be ablated within the base of the ASCs. It has been reported that some IVAs can be ablated from the junction (commissure) between the left and the right coronary cusps (L-RCC) [13]. In these VAs, catheter ablation from underneath the ASCs is often required for their elimination. Anatomically, the superior end of the LV myocardium makes a semicircular attachment to the aortic root at the bottom of the right and left coronary cusps. However, because of the semilunar nature of the attachments of the aortic valvular cusps, the superior end of the LV myocardium is located underneath the aortic valves at the L-RCC (**Figure 2**). Therefore, IVAs that can be ablated at the L-RCC should be classified into the same group as the VAs that can be ablated within the ASCs. In this setting, these IVAs may be defined as IVAs arising from the aortic root [7]. It has been reported that IVAs can rarely be ablated from within the noncoronary cusp of the aorta (NCC) [7, 14, 15]. Spatially, the aortic root occupies a central location within the heart, with the NCC anterior and superior to the paraseptal region of the left and right atria close to the superior atrioventricular junctions (**Figure 3**) [12]. In normal human hearts, the NCC is adjacent to the atrial myocardium on the epicardial aspect of the interatrial septum. When atrial tachycardias arise from that region of the atria, those atrial tachycardias can be ablated from within the NCC. It is considered that the NCC does not directly come in contact with the ventricular myocardium

IVAs can arise from the intracavital structures including the papillary muscles (PAMs) [18–22] and moderator band (MB) [23]. PAM VAs account for approximately 7% of patients with IVAs [18–22]. LV PAM VAs are known to arise more commonly from the posteromedial PAM than from the anterolateral PAM [20]. The sites of the PAM VA origins are limited to the base of the PAMs. IVAs can rarely originate from the PMs in the RV [22]. IVAs can arise from all three RV PAMs, but half of them arise from the septal PAM [22]. It has been recently reported that the MB rarely can be a source of IVAs including PVCs, VTs, and ventricular fibrillation [23]. Anatomically, the MB is considered to be a part of the septomarginal trabeculation, crossing from the septum to the RV free wall and supporting the anterior PAM of the tricuspid valve

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Most recently, it has been reported that IVAs can arise from the muscular bands in the RV [24, 25]. The RVOT is the most common site of IVA origins. In the RV, the TA is the second most common site of IVAs, and less commonly idiopathic VAs can originate from some RV muscles [3, 17, 22, 23]. Anatomically, the muscles of the RV may be divided into three groups: (1) trabeculae, (2) papillary muscles of the tricuspid valve, and (3) infundibular muscles (**Figure 5**). The muscles of the infundibulum are thick muscular bands, consisting of the septal and parietal bands. The junction of these two bands is often indicated by a raphe or a ridge extending from the superior papillary muscle to the nadir of the posterior pulmonary leaflet. This junction has been

**Figure 4.** Twelve-lead electrocardiograms exhibiting a premature ventricular contraction originating from the moderator band (MB) (left panel) and an intracardiac echocardiographic image (middle panel) and fluoroscopic images (right panels) exhibiting the successful ablation site of the premature ventricular contraction originating from the MB. ABL, ablation catheter; APM, anterolateral papillary muscle; CS, coronary sinus; ICE, intracardiac echocardiography catheter; LAO, left anterior oblique; RAO, right anterior oblique. The other abbreviations are as in the previous figures. This figure

(**Figure 4**) [23].

was modified from Ref. [10] with permission.

**Figure 3.** Two-dimensional (right panel) and three-dimensional (left panel) CT images. The dotted line indicates the tricuspid annulus and solid circle the right ventricular His bundle (HB) region. L, left coronary cusp; N, noncoronary cusp; RA, right atrium; RCA, right coronary artery; SVC, superior vena cava. The other abbreviations are as in the previous figures. This figure was cited from Ref. [15] with permission.

(**Figure 3**). However, it has been reported that some IVAs can be ablated from within the NCC [14]. The clinical observation that a noncoronary sinus of valsalva aneurysm can rupture into the right ventricle (RV), as well as the right atrium, supports the assumption that the NCC may be attached to the ventricular myocardium where IVAs can arise from. Some IVAs can be ablated from within the pulmonary sinus cusps [16]. The ventricular muscle is attached to the pulmonary sinus cusps (PSCs) in the RVOT like the ASCs in the LVOT. The ventricular muscle extends above the PSCs, but it should be noted that ventricular myocardial extensions never occurs in the aorta [12]. The ventricular muscle may appear to extend above the right coronary cusp (RCC) because of the specific nature of the interventricular septum. However, the superior end of the *left* ventricular muscle attaches to the RCC, and the *right* ventricular muscle attaching to the *left* ventricular muscle underneath the RCC runs in the interventricular septum up to the PSCs, which is located above the ASCs. In fact, the *right* ventricular muscle in the interventricular septum is separated from the RCC and aorta by a loose connective tissue. When IVAs arise from the ventricular muscle underneath the ASCs and PSCs or above the PSCs, catheter ablation within the ASCs and PSCs is required to cure those VAs because those VA origins are likely to be epicardial.

IVAs can originate from the atrioventricular annuli including the MA [9, 10] and tricuspid annulus (TA) [17]. IVAs originating from the MA and TA account for 5 and 8% of all IVAs, respectively. MA VAs can originate from any of the regions along the MA except the septal aspect where the fibrous trigone is located with no ventricular myocardium, but the anterolateral and posteroseptal aspects of the MA are the most common and second most common sites of MA VA origins, respectively [9, 10]. TA VAs can originate from any regions along the TA, but more often originate from the septal aspect, especially in the anteroseptal or para-Hisian region than the free wall [17].

IVAs can arise from the intracavital structures including the papillary muscles (PAMs) [18–22] and moderator band (MB) [23]. PAM VAs account for approximately 7% of patients with IVAs [18–22]. LV PAM VAs are known to arise more commonly from the posteromedial PAM than from the anterolateral PAM [20]. The sites of the PAM VA origins are limited to the base of the PAMs. IVAs can rarely originate from the PMs in the RV [22]. IVAs can arise from all three RV PAMs, but half of them arise from the septal PAM [22]. It has been recently reported that the MB rarely can be a source of IVAs including PVCs, VTs, and ventricular fibrillation [23]. Anatomically, the MB is considered to be a part of the septomarginal trabeculation, crossing from the septum to the RV free wall and supporting the anterior PAM of the tricuspid valve (**Figure 4**) [23].

Most recently, it has been reported that IVAs can arise from the muscular bands in the RV [24, 25]. The RVOT is the most common site of IVA origins. In the RV, the TA is the second most common site of IVAs, and less commonly idiopathic VAs can originate from some RV muscles [3, 17, 22, 23]. Anatomically, the muscles of the RV may be divided into three groups: (1) trabeculae, (2) papillary muscles of the tricuspid valve, and (3) infundibular muscles (**Figure 5**). The muscles of the infundibulum are thick muscular bands, consisting of the septal and parietal bands. The junction of these two bands is often indicated by a raphe or a ridge extending from the superior papillary muscle to the nadir of the posterior pulmonary leaflet. This junction has been

(**Figure 3**). However, it has been reported that some IVAs can be ablated from within the NCC [14]. The clinical observation that a noncoronary sinus of valsalva aneurysm can rupture into the right ventricle (RV), as well as the right atrium, supports the assumption that the NCC may be attached to the ventricular myocardium where IVAs can arise from. Some IVAs can be ablated from within the pulmonary sinus cusps [16]. The ventricular muscle is attached to the pulmonary sinus cusps (PSCs) in the RVOT like the ASCs in the LVOT. The ventricular muscle extends above the PSCs, but it should be noted that ventricular myocardial extensions never occurs in the aorta [12]. The ventricular muscle may appear to extend above the right coronary cusp (RCC) because of the specific nature of the interventricular septum. However, the superior end of the *left* ventricular muscle attaches to the RCC, and the *right* ventricular muscle attaching to the *left* ventricular muscle underneath the RCC runs in the interventricular septum up to the PSCs, which is located above the ASCs. In fact, the *right* ventricular muscle in the interventricular septum is separated from the RCC and aorta by a loose connective tissue. When IVAs arise from the ventricular muscle underneath the ASCs and PSCs or above the PSCs, catheter ablation within the ASCs and PSCs is required to cure those VAs because those

**Figure 3.** Two-dimensional (right panel) and three-dimensional (left panel) CT images. The dotted line indicates the tricuspid annulus and solid circle the right ventricular His bundle (HB) region. L, left coronary cusp; N, noncoronary cusp; RA, right atrium; RCA, right coronary artery; SVC, superior vena cava. The other abbreviations are as in the

IVAs can originate from the atrioventricular annuli including the MA [9, 10] and tricuspid annulus (TA) [17]. IVAs originating from the MA and TA account for 5 and 8% of all IVAs, respectively. MA VAs can originate from any of the regions along the MA except the septal aspect where the fibrous trigone is located with no ventricular myocardium, but the anterolateral and posteroseptal aspects of the MA are the most common and second most common sites of MA VA origins, respectively [9, 10]. TA VAs can originate from any regions along the TA, but more often originate from the septal aspect, especially in the anteroseptal or para-

VA origins are likely to be epicardial.

previous figures. This figure was cited from Ref. [15] with permission.

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Hisian region than the free wall [17].

**Figure 4.** Twelve-lead electrocardiograms exhibiting a premature ventricular contraction originating from the moderator band (MB) (left panel) and an intracardiac echocardiographic image (middle panel) and fluoroscopic images (right panels) exhibiting the successful ablation site of the premature ventricular contraction originating from the MB. ABL, ablation catheter; APM, anterolateral papillary muscle; CS, coronary sinus; ICE, intracardiac echocardiography catheter; LAO, left anterior oblique; RAO, right anterior oblique. The other abbreviations are as in the previous figures. This figure was modified from Ref. [10] with permission.

termed the crista supraventricularis. An extension of the septal band is the MB, which usually extends inferiorly to the site of attachment of the anterior papillary muscle in the anterior wall. The parietal band extends across the tricuspid orifice onto the anterior wall, fading out above the area of the attachment of the anterior papillary muscle. IVAs rarely arise from the infundibular muscles, and parietal band IVAs are approximately three times as prevalent as septal band IVAs. IVAs can arise from the Purkinje network, most commonly from the left posterior fascicle followed by the anterior and septal fascicles [21, 26, 27]. These IVAs most often present as reentrant VTs, but sometimes as VTs or PVCs with a focal mechanism. The left anterior fascicle runs along the MA. The left septal fascicle is located between the left anterior and posterior fascicles, and there is a normal variation in its origin and distribution. The peripheral Purkinje network extends to the surface of the PAMs and MB. Therefore, these VAs have to be differen-

**Figure 7.** CT (left panels) and fluoroscopic (right panels) images exhibiting the LV summit. The LV summit was defined based on the fluoroscopy and coronary angiography as the region on the epicardial surface of the LV near the bifurcation of the left main coronary artery that is bounded by an arc (black dotted line) from the left anterior descending coronary artery (LAD) superior to the first septal perforating branch (black arrowheads) and anteriorly to the left circumflex coronary artery (LCx) laterally. The great cardiac vein (GCV) bisects the LV summit into a superior portion surrounded by the white dotted line (the *inaccessible area*) and an inferior portion surrounded by a red dotted line (the *accessible area*). The white arrowheads indicate the first diagonal branch of the LAD. AIVV, anterior interventricular cardiac vein; HB, His bundle; LMCA, left main coronary artery; PA, pulmonary artery. The other abbreviations are as in the previous

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IVAs arise commonly from the endocardial side, but can arise from the epicardial side [27] and rarely from the intramural site [28, 29]. There are two major sites of origin of idiopathic

tiated from IVAs originating from the PAMs, MB, and atrioventricular annuli.

figures. This figure was cited from Ref. [31] with permission.

**Figure 6.** Twelve-lead electrocardiograms exhibiting the ventricular arrhythmia originating from the crux of the heart (left panel) and fluoroscopic images exhibiting its successful ablation site. The abbreviations are as in the previous figures. This figure was adapted from Ref. [30] with permission.

**Figure 7.** CT (left panels) and fluoroscopic (right panels) images exhibiting the LV summit. The LV summit was defined based on the fluoroscopy and coronary angiography as the region on the epicardial surface of the LV near the bifurcation of the left main coronary artery that is bounded by an arc (black dotted line) from the left anterior descending coronary artery (LAD) superior to the first septal perforating branch (black arrowheads) and anteriorly to the left circumflex coronary artery (LCx) laterally. The great cardiac vein (GCV) bisects the LV summit into a superior portion surrounded by the white dotted line (the *inaccessible area*) and an inferior portion surrounded by a red dotted line (the *accessible area*). The white arrowheads indicate the first diagonal branch of the LAD. AIVV, anterior interventricular cardiac vein; HB, His bundle; LMCA, left main coronary artery; PA, pulmonary artery. The other abbreviations are as in the previous figures. This figure was cited from Ref. [31] with permission.

termed the crista supraventricularis. An extension of the septal band is the MB, which usually extends inferiorly to the site of attachment of the anterior papillary muscle in the anterior wall. The parietal band extends across the tricuspid orifice onto the anterior wall, fading out above the area of the attachment of the anterior papillary muscle. IVAs rarely arise from the infundibular muscles, and parietal band IVAs are approximately three times as prevalent as septal band IVAs.

IVAs can arise from the Purkinje network, most commonly from the left posterior fascicle followed by the anterior and septal fascicles [21, 26, 27]. These IVAs most often present as reentrant VTs, but sometimes as VTs or PVCs with a focal mechanism. The left anterior fascicle runs along the MA. The left septal fascicle is located between the left anterior and posterior fascicles, and there is a normal variation in its origin and distribution. The peripheral Purkinje network extends to the surface of the PAMs and MB. Therefore, these VAs have to be differentiated from IVAs originating from the PAMs, MB, and atrioventricular annuli.

IVAs arise commonly from the endocardial side, but can arise from the epicardial side [27] and rarely from the intramural site [28, 29]. There are two major sites of origin of idiopathic

**Figure 6.** Twelve-lead electrocardiograms exhibiting the ventricular arrhythmia originating from the crux of the heart (left panel) and fluoroscopic images exhibiting its successful ablation site. The abbreviations are as in the previous

**Figure 5.** Autopsy heart exhibiting the infundibular muscles. PA, pulmonary artery; PB, parietal band; SB, septal band; SPM, superior papillary muscle. The other abbreviations are as in the previous figures. This figure was adapted from

figures. This figure was adapted from Ref. [30] with permission.

Ref. [25] with permission.

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epicardial VAs such as the crux of the heart [30] and LV summit [31]. Anatomically, the crux of the heart is formed by the junction of the atrioventricular groove and the posterior interventricular groove and corresponds roughly to the junction of the middle cardiac vein and coronary sinus, near the origin of the posterior descending coronary artery (**Figure 6**) [30]. A region of the LV epicardial surface that occupies the most superior portion of the LV has been termed the LV summit by McAlpine (**Figure 7**) [11, 31]. The LV summit is bounded by the left anterior descending coronary artery and the left circumflex coronary artery. This region near where the great cardiac vein (GCV) ends and the anterior interventricular cardiac vein begins is one of the major sources of epicardial IVAs. The LV summit is bisected by the GCV into an area lateral to this structure that is accessible to epicardial catheter ablation (the *accessible area*) and a superior region that is inaccessible to catheter ablation due to the close proximity of the coronary arteries and a thick layer of epicardial fat that overlies the proximal portion of these vessels (the *inaccessible area*) [31]. The prevalence of LV summit VAs has been reported to account for 12% of idiopathic LV VAs. Among these VA origins, 70, 15, and 15% of them have been identified within the GCV, accessible area, and inaccessible area, respectively.

(**Figures 4**, **8**, and **9**) [2, 21]. An R/S wave amplitude ratio of >1 in lead V6 suggests an origin in the base (ventricular outflow tract or annuli), whereas an R/S wave amplitude ratio of <1 suggests an origin in the middle of the ventricle (papillary muscles or left fascicles) (**Figures 4**, **8**, and **9**) [2, 21]. Twelve-lead ECGs are very helpful for predicting the likely epicardial VT origins (**Figures 10** and **11**). Because in human hearts, the Purkinje network that can quickly facilitate ventricular activation throughout the ventricles is located only in the subendocardium, ventricular activation from the epicardial origin requires more time to reach the Purkinje network, resulting in a slow onset of the QRS during epicardial VTs. Based on this mechanism, several parameters predicting epicardial VT origins have been proposed: a "pseudo-delta" wave duration of >34 ms, a QRS duration of >200 ms, a delayed intrinsicoid deflection of >85 ms, an RS complex duration of >121 ms, and a maximum deflection index (MDI) (calculated by dividing the shortest time from the QRS onset to the maximum deflection in any of the precordial leads by the total QRS duration) of >0.54 (**Figure 10**) [33, 34]. When ventricular activation propagates from an epicardial origin at the LV free wall or ventricular posterior wall, the total activation vector should go from a lateral toward medial or from an inferior toward superior direction, resulting in a QS pattern in lead I or lead aVF (**Figure 11**) [32]. On the other hand, when ventricular activation propagates from an

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**Figure 8.** Representative 12-lead electrocardiograms of the QRS complexes during ventricular arrhythmias originating from the anterolateral region in the LV. APM, anterolateral papillary muscle; L, lateral portion; LAF, the left anterior fascicle; MA, mitral annulus; X-F, R, VAs with a focal or a macroreentrant mechanism. This figure was reproduced from

Ref. [21] with permission.
