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How to Ablate Ventricular Tachycardia from the Left Ventricular Summit

Daniele Muser, MD; Jackson J. Liang, DO; Pasquale Santangeli, MD, PhD

Introduction

The left ventricular summit (LVS) is a complex anatomical region located at the epicardial base of the left ventricular outflow tract (LVOT) and is a common site of origin of idiopathic ventricular arrhythmias (VAs).¹ Given the proximity of major coronary vessels and a thick layer of epicardial fat at the region of the atrio-ventricular and interventricular grooves, catheter ablation of arrhythmic foci at this site may be challenging.² Effective ablation can be achieved from anatomically adjacent sites, such as the coronary venous system, the coronary cusp region, and/or the endocardial left ventricular (LV) or right ventricular (RV) outflow tracts. When ablation from adjacent sites is unsuccessful, alternative approaches such as epicardial or surgical ablation may be considered. In this chapter, we will discuss a practical approach to map and ablate VAs arising from the LVS.

Anatomic Landmarks

The region referred to as the LVS is a complex anatomical area representing the most superior aspect of the epicardial side of the left ventricular outflow tract (LVOT). More precisely, the LVS is a triangular region with the apex of the triangle constituted by the bifurcation of the left anterior descending (LAD) and the left circumflex (LCx) coronary arteries and the base represented by a line connecting the origin of the first septal perforator branch of the LAD and with the LCx.¹ The LVS is transected laterally by the great cardiac vein (GCV) at its junction with the anterior interventricular vein (AIV). In particular, the course of the GCV divides the region into 2 main areas of clinical interest: (1) a medial and more superior region (above the GCV), corresponding to the apex of the LVS, inaccessible to catheter ablation because of close proximity to the major coronary vessels and the presence of thick epicardial fat (inaccessible area); and (2) a more lateral and inferior region (below GCV), towards the base of the triangle, which may be suitable for catheter ablation due to its typical location remote from major coronary vessels and epicardial fat (accessible area) (Figure 37.1). The knowledge of the anatomic boundaries of this complex region and its spatial relationship with nearby structures is of fundamental value to understand the 12-lead ECG morphology of arrhythmias arising from this site and the potential strategies to approach them.³

Electrocardiographic Features

Based on the anatomy of this region, several specific ECG features may be helpful not only in predicting the site of origin from the LVS but also in differentiating a possible origin from the accessible or inaccessible region that can influence the best ablation approach.^1,4

Ventricular arrhythmias originating from the LVS typically show a right bundle branch block (RBBB) morphology with a positive concordance throughout the precordial leads or a left bundle branch block (LBBB) morphology with very early precordial transition. The axis is typically rightward and inferior. In particular, a dominant R wave in V₁ with a R/S ratio ≥ 2.0 is observed in up to 80% of cases when the ventricular arrhythmia originates from the accessible area of the LV summit.1 Patients with arrhythmia origin from the inaccessible area may infrequently (< 10% of the cases) present a LBBB pattern but still with a very early precordial transition (≤V₂).⁵ Another peculiar pattern, not frequently seen but highly specific for an epicardial LVS origin, is the “pattern break” in V₂, characterized by an abrupt loss of R wave in lead V₂ compared to V₁ and V₃. Such V₂ pattern break suggests an origin from the septal aspect of the LVS, a region anatomically known as the anterior interventricular sulcus, located opposite to the unipolar lead V₂ usually in close proximity to the proximal LAD before the takeoff of the first septal perforator branch.⁶ With regards to the frontal QRS axis, all arrhythmias originating from accessible epicardial LVS show a rightward inferior axis, which is reflected by a larger R-wave amplitude in lead III compared to lead II and a deeper Q wave in aVL compared to aVR (Figure 37.2A).¹ The epicardial origin is consistent with a slurring of the initial portion of the QRS complex reflecting delayed initial activation of the LV epicardium. Such delayed activation is indexed by the following quantitative measures: (1) time to earliest rapid deflection in precordial leads (pseudo-delta wave) ≥ 34 ms, (2) interval to peak of R wave in lead V₂ (intrinsicoid deflection time) ≥ 85 ms, (3) shortest interval to maximal positive or negative deflection divided by QRS duration (maximum deflection index) ≥ 0.55, and (4) time to earliest QRS nadir in precordial leads (shortest RS complex) ≥ 121 ms.^1,7–9

As stated above, LVS VAs can be addressed with catheter ablation either from adjacent structures (LCC, GCV, AIV) or directly from the epicardial surface (Figure 37.1). The distinction between accessible and inaccessible region is crucial because the likelihood of successful ablation of epicardial VAs arising from the inaccessible area is very low. Those LVS VAs that exhibit a RBBB pattern and deeper Q waves in aVL compared to aVR (especially in the presence of a QS pattern in lead I) are more likely to be suppressed with radiofrequency (RF) energy delivery within the GCV, AIV, or the accessible area of the LVS surface.1 For arrhythmias originating from the septal aspect LVS triangle, a direct epicardial approach is typically not possible due to the vicinity of major coronary vessels and epicardial fat. These arrhythmias can still be targeted from anatomically adjacent structures such as the LCC, and ECG predictors of successful ablation include a Q-wave ratio in aVL/aVR < 1.45 (reflecting the anatomic proximity between the GCV/AIV and the LCC) with a sensitivity of 89% and a specificity of 75%.⁵

Recently, the ECG features of LVS VAs arising from the accessible vs. inaccessible area have been further explored in a consecutive series of patients who underwent epicardial mapping and attempted ablation of LVS VAs after failed ablation attempts from adjacent structures, including the LVOT and RVOT, the coronary cusp region, and coronary venous system. In this series, the aVL/aVR Q-wave ratio was significantly greater in patients with successful epicardial ablation (2.63 ± 1.31) compared with that in the unsuccessful group (1.39 ± 0.58, P = 0.017). Moreover, an R-wave to S-wave ratio in lead V₁ greater than 2 and absence of initial q wave in V₁ were more prevalent in the successfully ablated group. Once again, these features reflect a more lateral site of origin of VAs in the “accessible area,” distant from the main coronary arteries.⁴

How to Map LVS VAs

The LVS can be reached directly by a percutaneous epicardial access; however, as mentioned, this approach has significant limitations. Because of the complex anatomy of this region, an accurate preprocedural analysis of the 12-ECG features of the arrhythmia is crucial to choose the most appropriate approach.

Due to significant anatomic variations between patients, the first step of the procedure should always be detailed anatomic reconstruction of the LVOT and RVOT, including the coronary cusp region, in order to define the attitudinal relationships between different structures and the anatomical distance between adjacent sites. A 3-dimensional (3D) anatomic map of the ventricles and outflow tracts can be reconstructed using different techniques such as intracardiac echocardiography (ICE), computed tomography (CT) or magnetic resonance imaging (MRI). The advantage of using ICE is the ability to perform a real-time reconstruction and immediate integration into the electroanatomic mapping system (CARTOSOUND Module, Biosense Webster, Diamond Bar, CA). This is superior to off-line techniques which, despite providing a high spatial resolution, may be affected by registration errors (need for reference points to merge the anatomical map with the 3D reconstruction) and do not allow for real time monitoring of mapping and ablation (Figure 37.3).

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