1160
Clinical Review Section Editor: Bruce D. Lindsay, M.D.
Catheter Ablation of Idiopathic Epicardial Ventricular Arrhythmias Originating from the Vicinity of the Coronary Sinus System YI-HE CHEN, M.D., and JIA-FENG LIN, M.D. From the Department of Cardiology, Second Affiliated Hospital of Wenzhou Medical College, Wenzhou Zhejiang, China
Catheter Ablation of Idiopathic Epicardial Ventricular Arrhythmias. Idiopathic epicardial ventricular arrhythmias (IEVAs) originating from the vicinity of the coronary sinus system are not uncommon, accounting for about 9% of idiopathic ventricular arrhythmia cases. IEVAs share clinical presentation and electrophysiological characteristics with ventricular arrhythmias arising from the right ventricular outflow tract possibly as manifestations of cAMP-mediated triggered activity and delayed after-depolarizations. Detailed analysis of standard 12-lead electrocardiogram morphology by using unique variables and algorithms allows clinicians to predict probable location of epicardial foci and informs optimal catheter ablation strategy. Epicardial mapping and ablation through the coronary sinus and its branches is effective and safe, and increasingly favored. However, it is important because of the common perivascular origin of IEVAs to perform coronary angiography prior to or after ablation and to select the appropriate ablation energy form to avoid serious complications. (J Cardiovasc Electrophysiol, Vol. 26, pp. 1160-1167, October 2015) catheter ablation, coronary sinus system, outflow tract, premature ventricular complexes, ventricular tachycardia Introduction Idiopathic ventricular arrhythmias, presenting as monomorphic nonsustained ventricular tachycardia (VT) or frequent premature ventricular contractions (PVCs), are the most common ventricular arrhythmias (VAs) in patients without overt underlying heart disease.1 First described as repetitive monomorphic VT arising from the right ventricular outflow tract (RVOT), idiopathic VAs were later found to also originate from the left ventricular outflow tract (LVOT),2,3 pulmonary artery,4,5 papillary muscle,6 aortic cusp and epicardium.7,8 Although true prevalence of idiopathic epicardial ventricular arrhythmias (IEVAs) is not known precisely, it was estimated at 9% in earlier studies,8 and in the 2.5% to 15% range in more recent single-center studies with selected cohorts and influenced by underlying heart disease.9,10 Clinical presentation of IEVAs is similar to that of VAs originating from the RVOT, with patients usually suffering from palpitation, chest pain, and shortness of This work was partially supported by Wenzhou Municipal Science and Technology Commision (Grant No. Y2008086). Disclosures: None. Address for correspondence: Prof. Jia-Feng Lin, M.D., Department of Cardiology, Second Affiliated Hospital of Wenzhou Medical College, Wenzhou 325000, 109 Xueyuan Road, Wenzhou Zhejiang, China. Fax: 86-577-88832693; E-mail: [email protected].
Manuscript received 25 May 2015; Revised manuscript received 18 June 2015; Accepted for publication 8 July 2015. doi: 10.1111/jce.12756
breath and less commonly syncope.11 Symptoms tend to be more pronounced during exercise and emotional stress. In electrocardiogram evaluation, most IEVA patients present with incessant or consecutive PVCs, and occasionally nonsustained VT, which might precipitate tachycardia mediated cardiomyopathy that is reversible after catheter ablation. Although the prognosis of idiopathic VAs is relatively good with most patients having a benign course, there are rare cases of VAs arising from RVOT that evolve into polymorphic VT or occasionally into ventricular fibrillation.12 It is therefore important to exclude potential malignant VAs among patients with idiopathic VAs who are admitted to the hospital with unexplained syncope. It is well known that most idiopathic VAs can be eliminated by radiofrequency catheter ablation (RFCA) at the endocardium, which is not successful in those of LVOT epicardial origin13-15 sharing a perivascular origin, usually located at the transitional area from the great cardiac vein to the anterior interventricular vein or sporadically the middle cardiac vein.8,9,16,17 As reported by most authors and in our experience, most IEVAs can be completely ablated through the coronary venous system (CVS), and the remaining through a percutaneous or transthoracic approach.18,19 In this article, we review previous studies on IEVAs and focus on their mechanism, distinctive ECG morphology of different origin sites, and catheter ablation through the CVS. Mechanism of IEVAs Idiopathic VAs are usually caused by triggered activity or automaticity of normal cardiomyocytes,20 while VAs in patients with underlying heart disease are scar mediated and present as macroreentrant arrhythmias around the scar and
Chen and Lin Catheter Ablation of Idiopathic Epicardial Ventricular Arrhythmias
1161
Figure 1. Schematic view of the coronary sinus system, the distal great cardiac vein (GCV) divided into 2 regions (DGCV1 and DGCV2). AIV: anterior interventricular vein; CS: coronary sinus; DGCV1: epicardium of anterolateral wall of mitral annulus; DGCV2: AIV opening proximal end; EDGCV: extended tributary of the distal great cardiac vein; LVOT: left ventricular outflow tract; MA: mitral annulus; MCV: middle cardiac vein; RVOT: right ventricular outflow tract; SCV: small cardiac vein; TA: tricuspid annulus. (Modified from Li Yue-Chun: International journal of cardiology; from Li Ji-Wu: International journal of cardiology.) For a high quality, full color version of this figure, please see Journal of Cardiovascular Electrophysiology’s website: www.wileyonlinelibrary.com/journal/jce
surviving myocytes.21,22 Lerman et al.23 found that the most prevalent form of idiopathic RVOT VAs, which present as frequent PVCs, ventricular couplets, or nonsustained VT usually at rest, is cAMP-mediated triggered activity and delayed after-depolarizations (DADs); these also are described as adenosine-sensitive VAs. IEVAs, a subtype of LVOT VAs,24 have the same electrophysiological and pharmacologic properties as RVOT VAs, such as inability to be concealed or manifest entrainment, and inducibility by programmed stimulation, burst pacing or isoproterenol infusion. Therefore, these VAs appear to share the same underlying mechanism and should be regarded as a single entity originating from different sites. The underlying mechanism of triggered activity has been demonstrated to be cAMP-stimulated intracellular calcium overload, with subsequent Na+ /Ca2+ exchanger function enhancement and inward current increase leading to DADs, and eventually to VT or PVCs.25-27 Thus, lowering stimulated intracellular cAMP levels with adenosine or vagus nerve stimulation terminates triggered activity and eliminates ventricular arrhythmia. Anatomical Considerations of CVS A systematic understanding of IEVAs originating from the CVS requires a thorough understanding of CVS anatomy. Use of coronary venography by retrograde injection of contrast medium into the coronary sinus usually allows clear visualization of the architecture of this system throughout various radiographic projections (anteroposterior, left and right anterior oblique, and lateral).28,29 The coronary venous tree presents greater variation than the coronary artery one; however, it commonly comprises the coronary sinus, and great, middle and small cardiac veins.30 The coronary sinus, which is located around the atrioventricular groove in close association with the left circumflex artery, runs along the posterior and lateral part of the mitral valve and ends in the right atrium. After crossing the posterior interventricular sulcus, it directly continues as the great cardiac vein (GCV) that runs around the anterior and lateral portions of the mitral valve, and turns anteriorly along the outer surface of the anterobasal left ventricular outflow, beneath the left atrium and the aortic valve cusp. The distal GCV continues as the anterior interventricular vein (AIV),
which runs parallel to the left anterior descending coronary artery. The middle cardiac vein, also known as the inferior interventricular vein, starts at the apex of the heart adjacent to the posterior descending artery, lies in the inferior interventricular sulcus and eventually empties into the coronary sinus. The aforementioned veins, constituting the left CVS, are by far the most important venous network of the heart, practically draining approximately three-quarters of coronary blood flow. The remaining venous return, which usually empties into the coronary sinus through the cardiac small vein, occasionally may infuse blood flow directly into the right atrium. The cardiac small vein runs along the atrioventricular groove in the epicardial surface of the right ventricle. In some patients, coronary venous angiography also shows a distinct branch located distal to the transitional area between the GCV and the AIV, which is known as the extended tributary of the distal great cardiac vein (EDGCV). A small left atrial vein named Marshall (or Marshall ligament) is the remnant of the embryonic left superior cardinal vein and runs diagonally on the posterior left atrial surface.31 Marshall vein (or ligament) drains into the coronary sinus at the point where the great cardiac vein turns into the coronary sinus; according to the study by El-Maasarany et al.,29 15% of patients have a well-developed Vieussens valve at this site that might preclude ablation catheter advancement because of a decrease in GCV diameter. Moreover, there is also a small folded tissue known as Thebesian valve at the ostium of the coronary sinus, which might occasionally be an obstacle to catheterization.32,33 The architecture of the coronary sinus system is shown in Figure 1. The anatomic structure of the CVS provides unique access to the left ventricular epicardium with minimal injury and is currently used for drug delivery, placement of left ventricular leads in cardiac resynchronization therapy, stem cell treatment for heart failure or ischemic heart disease, and increasingly for catheter ablation of various arrhythmias.30,34,35 Electrocardiographic Characteristics of IEVAs Although epicardial VTs had been reported, no ECG criteria to predict an epicardial origin of VTs had been described until Berruezo et al.36 analyzed the ECG
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Vol. 26, No. 10, October 2015
characteristics of 14 consecutive patients with VTs that were unsuccessfully ablated via an endocardial approach. Three variables, namely pseudo delta wave (PdW), intrinsicoid deflection time (IDT), and RS complex duration time, emerged as high sensitivity and specificity significant predictors of an epicardial origin. Subsequently, Daniels et al.8 introduced a new variable, the maximum deflection index (MDI), to identify epicardial VTs with remote origin relative to the aortic sinus of Valsalva; MDI ࣙ0.55 indicated such an origin with a sensitivity of 100% and specificity of 98.5%. However, Yamada et al.37 posited that a delayed MDI was less reliable for discriminating endocardial from epicardial VTs arising from the great cardiac vein or anterior interventricular cardiac vein because of preferential conduction or intramural origin. Other variables and algorithms38,39 to predict epicardial foci are summarized in (Table 1). Recently, our study10 suggested that IDT >70 ms and MDI >0.54 strongly predict idiopathic VTs arising from the CVS. However, inconsistent with previous studies, no significant differences in PdW time were found among VTs originating in the epicardial region adjacent to the transitional area from the GCV to the AIV, right ventricular endocardial outflow tract, aortic sinus of Valsalva or left ventricular endocardium. Heterogeneity in baseline clinical characteristics among patients in other studies with underlying heart disease might be responsible for the differing results.40 Idiopathic VTs arising from a different epicardial region manifest different ECG morphology (Table 2). A large number of epicardial VTs can be ablated within CVS, which as mentioned above mainly can be divided into GCV, middle cardiac vein, and AIV, with rarely a small EDGCV located distal to the origin of AIV.10 The inconsistent presence of the latter vein among patients might underlie the lack of reports of idiopathic VTs originating from the region adjacent to EDGCV and of distinctive ECG characteristics before publication of our study. Generally, most IEVAs that originate from the CVS present with left or right bundle-branch block morphology with slurring R wave; R wave transition zone in precordial leads earlier than V3 ; with or without S(s) wave in leads V5 or V6 ;9,41 and on the frontal plane leads, most with an inferior axis with rS, R, qr complex in lead I and QS complex in lead aVR/aVL. With some exceptions, IEVAs ablated from within the proximal coronary sinus or middle cardiac vein are characterized by left superior axis; deeply negative deltoid wave caused by the lower spatial location in frontal plane; and activation wave deviated from the inferior leads.42 Moreover, previous studies described the ECG features of VTs ablated from within the left coronary veins, however, without detailed distinction of QRS morphology of VTs originating at different sites within the CVS. Our studies documented differential ECG characteristics of VAs arising originating from the distal GCV, AIV and EDGCV.10 VTs originating from distal GCV have S wave in leads V5 –V6 without S wave in lead V1 , and precordial transition zone always earlier than V1 . The PdW time of VTs originating at the distal CGV is significantly longer than that of VTs from AIV and EDGCV because the distal GCV is located at the lateral left ventricular wall and much more time is required by VTs originating at this site to activate the entire heart. The area of the distal GCV can be further subdivided into 2 regions with distinctive ECG characteristics (Fig. 2). AIV is located more anteriorly than the distal GCV, and
VTs originating at AIV show rS wave in lead V1 and no s wave in leads V5 –V6 ; greater r wave amplitude in lead V1 than V2 is unique to VTs of AIV origin. Both of the sites present rS and qr in lead I. The anatomic location of EDGCV is distal to AIV and close to the septum, and more rightward and posterior than distal CGV, which results in higher R wave in lead I and shorter PdW time, an Rs pattern in lead V1 , and R wave in leads V5 –V6 . However, target sites of IEVAs determined by detailed electrophysiological examination are not always in accord with those inferred from surface ECG because clockwise or counterclockwise rotation, displacement of ECG electrodes, or movement of diaphragm may alter the intrathoracic position of the heart, thereby influencing QRS morphology. In summary, VTs of CVS origin present distinctive ECG patterns. Analysis of ECG morphology and use of algorithms or variables allow one to predict possible sites of origin of IEVTs before mapping and to establish an optimal strategy for catheter ablation. Catheter Ablation Although antiarrhythmic agents partly attenuate VAs, they are not devoid of side effects. Recently, RFCA has become an increasingly favored option because of its high efficacy in the treatment of idiopathic VAs with a low incidence of complications. Epicardial ablation by percutaneous approach is required for more than 30% of epicardial VAs in postinfarction patients and in those with nonischemic cardiomyopathy; however, several potential risks including pericardial bleeding, injury to the esophagus, vessels, and/or phrenic nerve or pericarditis limit the utilization of epicardial access.18 Epicardial fat in some patients also is a potential barrier to pacing and catheter ablation. Because most idiopathic epicardial VAs are of perivascular origin and usually adjacent to a coronary vein, CVS provides a safer, more convenient, and minimally invasive access to the ventricular epicardial regions, especially to the transition area between the GCV and the AIV. Previous investigators had achieved pace mapping and earliest ventricular activation of VTs from within the CVS; however, ablation was not attempted because of safety concerns and technical challenges.47,48 In 1997, Stellbrink et al.16 published a case report of idiopathic ventricular tachycardia originating from the left ventricular free wall; and after failing to completely ablate it through the left ventricular endocardium, they finally eliminated it by transcoronary venous catheter ablation within coronary sinus and its branch, therefore providing a new approach for ablating epicardial VT. Similarly, Obel et al.46 described a group of patients with idiopathic epicardial outflow tract VT that was successfully eliminated in all cases by ablation within the distal great coronary vein, demonstrating that epicardial VAs can be successfully and safely ablated within the different sites of CVS. More recently, in a study of 27 consecutive patients, Baman et al.9 found that idiopathic epicardial VAs were acutely eliminated within the CVS in 20 of 27 (74%) patients. These studies and our more recent ones show a high success rate, with epicardial VAs being eliminated in almost all patients through a coronary venous approach.10,37,49 However, Steven et al.50 reported only 6 of 14 (43%) patients in whom initially successful ablation was achieved from the GCV; longterm success rate decreased because of PVC recurrence. The
Chen and Lin Catheter Ablation of Idiopathic Epicardial Ventricular Arrhythmias
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TABLE 1 Sensitivity, Specificity, Positive Predictive Value, and Negative Predictive Value of Different ECG Variables and Algorithms in Predicting the Epicardial Origin of Idiopathic VAs in Different Studies Underlying Disease
ECG Variables
Berruezo et al. [36]
Ischemic/dilated
Ito et al. [38] Daniels et al. [8] Yamada et al. [37]
Idiopathic Idiopathic Idiopathic
PdW ࣙ34 milliseconds IDT ࣙ85 milliseconds RS ࣙ121 milliseconds aVR/aVL >1.4 Or S ࣙ1.2 mV* MDI ࣙ0.55 RS >121 milliseconds MDI >0.55 Inferior q waves PdW ࣙ75 milliseconds MDI ࣙ0.59 q wave in lead I IDT >70 milliseconds MDI >0.54 IDT ࣙ70 milliseconds MDI ࣙ0.54
Vall`es et al. [43]
NICM
Li et al. [10]
Idiopathic
Li et al. [64]
Idiopathic
Sensitivity 83 87 76 86 100 67 67 88#
Specificity
PPV
95 90 85 97 98.5 69 82 88#
83.33 83.33 90.0 83.3
NA NA NA 75 NA 33 46 NA
95.83 97.22 94.3 96.2
97.18 97.22 81.8 86.2
NPV NA NA NA 99 NA 90 91 NA
76.92 83.33 97.1 95.3
NICM = nonischemic cardiomyopathies; PPV = positive predictive value; NPV = negative predictive value; pseudo delta wave; IDT = intrinsicoid deflection time; RS = RS complex duration; MDI = maximum deflection index; aVR/aVL = the Q wave amplitude in aVL to aVR; S = the S wave amplitude in V1; NA = not available; *a step in the ECG algorithm; # sensitivity and specificity of the algorithm including the 4 steps. TABLE 2 ECG Characteristics of Idiopathic Epicardial Ventricular Arrhythmias Arising from the Coronary Sinus System QRS Complex Morphology Origin GCV DGCV1 DGCV2 AIV EDGCV Crux pCS MCV
QRS Axis
Transition Zone
Ⅰ
Ⅱ/Ⅲ/aVF
aVR
aVL
V1
V2 –V3
V4
V5 –V6
References
Inferior Inferior Inferior Inferior
Clinical Review Section Editor: Bruce D. Lindsay, M.D.
Catheter Ablation of Idiopathic Epicardial Ventricular Arrhythmias Originating from the Vicinity of the Coronary Sinus System YI-HE CHEN, M.D., and JIA-FENG LIN, M.D. From the Department of Cardiology, Second Affiliated Hospital of Wenzhou Medical College, Wenzhou Zhejiang, China
Catheter Ablation of Idiopathic Epicardial Ventricular Arrhythmias. Idiopathic epicardial ventricular arrhythmias (IEVAs) originating from the vicinity of the coronary sinus system are not uncommon, accounting for about 9% of idiopathic ventricular arrhythmia cases. IEVAs share clinical presentation and electrophysiological characteristics with ventricular arrhythmias arising from the right ventricular outflow tract possibly as manifestations of cAMP-mediated triggered activity and delayed after-depolarizations. Detailed analysis of standard 12-lead electrocardiogram morphology by using unique variables and algorithms allows clinicians to predict probable location of epicardial foci and informs optimal catheter ablation strategy. Epicardial mapping and ablation through the coronary sinus and its branches is effective and safe, and increasingly favored. However, it is important because of the common perivascular origin of IEVAs to perform coronary angiography prior to or after ablation and to select the appropriate ablation energy form to avoid serious complications. (J Cardiovasc Electrophysiol, Vol. 26, pp. 1160-1167, October 2015) catheter ablation, coronary sinus system, outflow tract, premature ventricular complexes, ventricular tachycardia Introduction Idiopathic ventricular arrhythmias, presenting as monomorphic nonsustained ventricular tachycardia (VT) or frequent premature ventricular contractions (PVCs), are the most common ventricular arrhythmias (VAs) in patients without overt underlying heart disease.1 First described as repetitive monomorphic VT arising from the right ventricular outflow tract (RVOT), idiopathic VAs were later found to also originate from the left ventricular outflow tract (LVOT),2,3 pulmonary artery,4,5 papillary muscle,6 aortic cusp and epicardium.7,8 Although true prevalence of idiopathic epicardial ventricular arrhythmias (IEVAs) is not known precisely, it was estimated at 9% in earlier studies,8 and in the 2.5% to 15% range in more recent single-center studies with selected cohorts and influenced by underlying heart disease.9,10 Clinical presentation of IEVAs is similar to that of VAs originating from the RVOT, with patients usually suffering from palpitation, chest pain, and shortness of This work was partially supported by Wenzhou Municipal Science and Technology Commision (Grant No. Y2008086). Disclosures: None. Address for correspondence: Prof. Jia-Feng Lin, M.D., Department of Cardiology, Second Affiliated Hospital of Wenzhou Medical College, Wenzhou 325000, 109 Xueyuan Road, Wenzhou Zhejiang, China. Fax: 86-577-88832693; E-mail: [email protected].
Manuscript received 25 May 2015; Revised manuscript received 18 June 2015; Accepted for publication 8 July 2015. doi: 10.1111/jce.12756
breath and less commonly syncope.11 Symptoms tend to be more pronounced during exercise and emotional stress. In electrocardiogram evaluation, most IEVA patients present with incessant or consecutive PVCs, and occasionally nonsustained VT, which might precipitate tachycardia mediated cardiomyopathy that is reversible after catheter ablation. Although the prognosis of idiopathic VAs is relatively good with most patients having a benign course, there are rare cases of VAs arising from RVOT that evolve into polymorphic VT or occasionally into ventricular fibrillation.12 It is therefore important to exclude potential malignant VAs among patients with idiopathic VAs who are admitted to the hospital with unexplained syncope. It is well known that most idiopathic VAs can be eliminated by radiofrequency catheter ablation (RFCA) at the endocardium, which is not successful in those of LVOT epicardial origin13-15 sharing a perivascular origin, usually located at the transitional area from the great cardiac vein to the anterior interventricular vein or sporadically the middle cardiac vein.8,9,16,17 As reported by most authors and in our experience, most IEVAs can be completely ablated through the coronary venous system (CVS), and the remaining through a percutaneous or transthoracic approach.18,19 In this article, we review previous studies on IEVAs and focus on their mechanism, distinctive ECG morphology of different origin sites, and catheter ablation through the CVS. Mechanism of IEVAs Idiopathic VAs are usually caused by triggered activity or automaticity of normal cardiomyocytes,20 while VAs in patients with underlying heart disease are scar mediated and present as macroreentrant arrhythmias around the scar and
Chen and Lin Catheter Ablation of Idiopathic Epicardial Ventricular Arrhythmias
1161
Figure 1. Schematic view of the coronary sinus system, the distal great cardiac vein (GCV) divided into 2 regions (DGCV1 and DGCV2). AIV: anterior interventricular vein; CS: coronary sinus; DGCV1: epicardium of anterolateral wall of mitral annulus; DGCV2: AIV opening proximal end; EDGCV: extended tributary of the distal great cardiac vein; LVOT: left ventricular outflow tract; MA: mitral annulus; MCV: middle cardiac vein; RVOT: right ventricular outflow tract; SCV: small cardiac vein; TA: tricuspid annulus. (Modified from Li Yue-Chun: International journal of cardiology; from Li Ji-Wu: International journal of cardiology.) For a high quality, full color version of this figure, please see Journal of Cardiovascular Electrophysiology’s website: www.wileyonlinelibrary.com/journal/jce
surviving myocytes.21,22 Lerman et al.23 found that the most prevalent form of idiopathic RVOT VAs, which present as frequent PVCs, ventricular couplets, or nonsustained VT usually at rest, is cAMP-mediated triggered activity and delayed after-depolarizations (DADs); these also are described as adenosine-sensitive VAs. IEVAs, a subtype of LVOT VAs,24 have the same electrophysiological and pharmacologic properties as RVOT VAs, such as inability to be concealed or manifest entrainment, and inducibility by programmed stimulation, burst pacing or isoproterenol infusion. Therefore, these VAs appear to share the same underlying mechanism and should be regarded as a single entity originating from different sites. The underlying mechanism of triggered activity has been demonstrated to be cAMP-stimulated intracellular calcium overload, with subsequent Na+ /Ca2+ exchanger function enhancement and inward current increase leading to DADs, and eventually to VT or PVCs.25-27 Thus, lowering stimulated intracellular cAMP levels with adenosine or vagus nerve stimulation terminates triggered activity and eliminates ventricular arrhythmia. Anatomical Considerations of CVS A systematic understanding of IEVAs originating from the CVS requires a thorough understanding of CVS anatomy. Use of coronary venography by retrograde injection of contrast medium into the coronary sinus usually allows clear visualization of the architecture of this system throughout various radiographic projections (anteroposterior, left and right anterior oblique, and lateral).28,29 The coronary venous tree presents greater variation than the coronary artery one; however, it commonly comprises the coronary sinus, and great, middle and small cardiac veins.30 The coronary sinus, which is located around the atrioventricular groove in close association with the left circumflex artery, runs along the posterior and lateral part of the mitral valve and ends in the right atrium. After crossing the posterior interventricular sulcus, it directly continues as the great cardiac vein (GCV) that runs around the anterior and lateral portions of the mitral valve, and turns anteriorly along the outer surface of the anterobasal left ventricular outflow, beneath the left atrium and the aortic valve cusp. The distal GCV continues as the anterior interventricular vein (AIV),
which runs parallel to the left anterior descending coronary artery. The middle cardiac vein, also known as the inferior interventricular vein, starts at the apex of the heart adjacent to the posterior descending artery, lies in the inferior interventricular sulcus and eventually empties into the coronary sinus. The aforementioned veins, constituting the left CVS, are by far the most important venous network of the heart, practically draining approximately three-quarters of coronary blood flow. The remaining venous return, which usually empties into the coronary sinus through the cardiac small vein, occasionally may infuse blood flow directly into the right atrium. The cardiac small vein runs along the atrioventricular groove in the epicardial surface of the right ventricle. In some patients, coronary venous angiography also shows a distinct branch located distal to the transitional area between the GCV and the AIV, which is known as the extended tributary of the distal great cardiac vein (EDGCV). A small left atrial vein named Marshall (or Marshall ligament) is the remnant of the embryonic left superior cardinal vein and runs diagonally on the posterior left atrial surface.31 Marshall vein (or ligament) drains into the coronary sinus at the point where the great cardiac vein turns into the coronary sinus; according to the study by El-Maasarany et al.,29 15% of patients have a well-developed Vieussens valve at this site that might preclude ablation catheter advancement because of a decrease in GCV diameter. Moreover, there is also a small folded tissue known as Thebesian valve at the ostium of the coronary sinus, which might occasionally be an obstacle to catheterization.32,33 The architecture of the coronary sinus system is shown in Figure 1. The anatomic structure of the CVS provides unique access to the left ventricular epicardium with minimal injury and is currently used for drug delivery, placement of left ventricular leads in cardiac resynchronization therapy, stem cell treatment for heart failure or ischemic heart disease, and increasingly for catheter ablation of various arrhythmias.30,34,35 Electrocardiographic Characteristics of IEVAs Although epicardial VTs had been reported, no ECG criteria to predict an epicardial origin of VTs had been described until Berruezo et al.36 analyzed the ECG
1162
Journal of Cardiovascular Electrophysiology
Vol. 26, No. 10, October 2015
characteristics of 14 consecutive patients with VTs that were unsuccessfully ablated via an endocardial approach. Three variables, namely pseudo delta wave (PdW), intrinsicoid deflection time (IDT), and RS complex duration time, emerged as high sensitivity and specificity significant predictors of an epicardial origin. Subsequently, Daniels et al.8 introduced a new variable, the maximum deflection index (MDI), to identify epicardial VTs with remote origin relative to the aortic sinus of Valsalva; MDI ࣙ0.55 indicated such an origin with a sensitivity of 100% and specificity of 98.5%. However, Yamada et al.37 posited that a delayed MDI was less reliable for discriminating endocardial from epicardial VTs arising from the great cardiac vein or anterior interventricular cardiac vein because of preferential conduction or intramural origin. Other variables and algorithms38,39 to predict epicardial foci are summarized in (Table 1). Recently, our study10 suggested that IDT >70 ms and MDI >0.54 strongly predict idiopathic VTs arising from the CVS. However, inconsistent with previous studies, no significant differences in PdW time were found among VTs originating in the epicardial region adjacent to the transitional area from the GCV to the AIV, right ventricular endocardial outflow tract, aortic sinus of Valsalva or left ventricular endocardium. Heterogeneity in baseline clinical characteristics among patients in other studies with underlying heart disease might be responsible for the differing results.40 Idiopathic VTs arising from a different epicardial region manifest different ECG morphology (Table 2). A large number of epicardial VTs can be ablated within CVS, which as mentioned above mainly can be divided into GCV, middle cardiac vein, and AIV, with rarely a small EDGCV located distal to the origin of AIV.10 The inconsistent presence of the latter vein among patients might underlie the lack of reports of idiopathic VTs originating from the region adjacent to EDGCV and of distinctive ECG characteristics before publication of our study. Generally, most IEVAs that originate from the CVS present with left or right bundle-branch block morphology with slurring R wave; R wave transition zone in precordial leads earlier than V3 ; with or without S(s) wave in leads V5 or V6 ;9,41 and on the frontal plane leads, most with an inferior axis with rS, R, qr complex in lead I and QS complex in lead aVR/aVL. With some exceptions, IEVAs ablated from within the proximal coronary sinus or middle cardiac vein are characterized by left superior axis; deeply negative deltoid wave caused by the lower spatial location in frontal plane; and activation wave deviated from the inferior leads.42 Moreover, previous studies described the ECG features of VTs ablated from within the left coronary veins, however, without detailed distinction of QRS morphology of VTs originating at different sites within the CVS. Our studies documented differential ECG characteristics of VAs arising originating from the distal GCV, AIV and EDGCV.10 VTs originating from distal GCV have S wave in leads V5 –V6 without S wave in lead V1 , and precordial transition zone always earlier than V1 . The PdW time of VTs originating at the distal CGV is significantly longer than that of VTs from AIV and EDGCV because the distal GCV is located at the lateral left ventricular wall and much more time is required by VTs originating at this site to activate the entire heart. The area of the distal GCV can be further subdivided into 2 regions with distinctive ECG characteristics (Fig. 2). AIV is located more anteriorly than the distal GCV, and
VTs originating at AIV show rS wave in lead V1 and no s wave in leads V5 –V6 ; greater r wave amplitude in lead V1 than V2 is unique to VTs of AIV origin. Both of the sites present rS and qr in lead I. The anatomic location of EDGCV is distal to AIV and close to the septum, and more rightward and posterior than distal CGV, which results in higher R wave in lead I and shorter PdW time, an Rs pattern in lead V1 , and R wave in leads V5 –V6 . However, target sites of IEVAs determined by detailed electrophysiological examination are not always in accord with those inferred from surface ECG because clockwise or counterclockwise rotation, displacement of ECG electrodes, or movement of diaphragm may alter the intrathoracic position of the heart, thereby influencing QRS morphology. In summary, VTs of CVS origin present distinctive ECG patterns. Analysis of ECG morphology and use of algorithms or variables allow one to predict possible sites of origin of IEVTs before mapping and to establish an optimal strategy for catheter ablation. Catheter Ablation Although antiarrhythmic agents partly attenuate VAs, they are not devoid of side effects. Recently, RFCA has become an increasingly favored option because of its high efficacy in the treatment of idiopathic VAs with a low incidence of complications. Epicardial ablation by percutaneous approach is required for more than 30% of epicardial VAs in postinfarction patients and in those with nonischemic cardiomyopathy; however, several potential risks including pericardial bleeding, injury to the esophagus, vessels, and/or phrenic nerve or pericarditis limit the utilization of epicardial access.18 Epicardial fat in some patients also is a potential barrier to pacing and catheter ablation. Because most idiopathic epicardial VAs are of perivascular origin and usually adjacent to a coronary vein, CVS provides a safer, more convenient, and minimally invasive access to the ventricular epicardial regions, especially to the transition area between the GCV and the AIV. Previous investigators had achieved pace mapping and earliest ventricular activation of VTs from within the CVS; however, ablation was not attempted because of safety concerns and technical challenges.47,48 In 1997, Stellbrink et al.16 published a case report of idiopathic ventricular tachycardia originating from the left ventricular free wall; and after failing to completely ablate it through the left ventricular endocardium, they finally eliminated it by transcoronary venous catheter ablation within coronary sinus and its branch, therefore providing a new approach for ablating epicardial VT. Similarly, Obel et al.46 described a group of patients with idiopathic epicardial outflow tract VT that was successfully eliminated in all cases by ablation within the distal great coronary vein, demonstrating that epicardial VAs can be successfully and safely ablated within the different sites of CVS. More recently, in a study of 27 consecutive patients, Baman et al.9 found that idiopathic epicardial VAs were acutely eliminated within the CVS in 20 of 27 (74%) patients. These studies and our more recent ones show a high success rate, with epicardial VAs being eliminated in almost all patients through a coronary venous approach.10,37,49 However, Steven et al.50 reported only 6 of 14 (43%) patients in whom initially successful ablation was achieved from the GCV; longterm success rate decreased because of PVC recurrence. The
Chen and Lin Catheter Ablation of Idiopathic Epicardial Ventricular Arrhythmias
1163
TABLE 1 Sensitivity, Specificity, Positive Predictive Value, and Negative Predictive Value of Different ECG Variables and Algorithms in Predicting the Epicardial Origin of Idiopathic VAs in Different Studies Underlying Disease
ECG Variables
Berruezo et al. [36]
Ischemic/dilated
Ito et al. [38] Daniels et al. [8] Yamada et al. [37]
Idiopathic Idiopathic Idiopathic
PdW ࣙ34 milliseconds IDT ࣙ85 milliseconds RS ࣙ121 milliseconds aVR/aVL >1.4 Or S ࣙ1.2 mV* MDI ࣙ0.55 RS >121 milliseconds MDI >0.55 Inferior q waves PdW ࣙ75 milliseconds MDI ࣙ0.59 q wave in lead I IDT >70 milliseconds MDI >0.54 IDT ࣙ70 milliseconds MDI ࣙ0.54
Vall`es et al. [43]
NICM
Li et al. [10]
Idiopathic
Li et al. [64]
Idiopathic
Sensitivity 83 87 76 86 100 67 67 88#
Specificity
PPV
95 90 85 97 98.5 69 82 88#
83.33 83.33 90.0 83.3
NA NA NA 75 NA 33 46 NA
95.83 97.22 94.3 96.2
97.18 97.22 81.8 86.2
NPV NA NA NA 99 NA 90 91 NA
76.92 83.33 97.1 95.3
NICM = nonischemic cardiomyopathies; PPV = positive predictive value; NPV = negative predictive value; pseudo delta wave; IDT = intrinsicoid deflection time; RS = RS complex duration; MDI = maximum deflection index; aVR/aVL = the Q wave amplitude in aVL to aVR; S = the S wave amplitude in V1; NA = not available; *a step in the ECG algorithm; # sensitivity and specificity of the algorithm including the 4 steps. TABLE 2 ECG Characteristics of Idiopathic Epicardial Ventricular Arrhythmias Arising from the Coronary Sinus System QRS Complex Morphology Origin GCV DGCV1 DGCV2 AIV EDGCV Crux pCS MCV
QRS Axis
Transition Zone
Ⅰ
Ⅱ/Ⅲ/aVF
aVR
aVL
V1
V2 –V3
V4
V5 –V6
References
Inferior Inferior Inferior Inferior
