| CHAPTER | ||
| 37 | Epicardial Mapping and Ablation of Premature Ventricular Complexes | |
| David F. Briceño, MD; David S. Frankel, MD |
INTRODUCTION
Premature ventricular complexes (PVCs) are a frequent cause of disturbing symptoms, including palpitations, lightheadedness and decreased exercise tolerance. Additionally, when frequent enough, PVCs can cause a PVC-mediated cardiomyopathy.1 Further, frequent PVCs can worsen a preexisting cardiomyopathy.2 Thus treatment of PVCs is often warranted. Generally, β-blockers and calcium-channel blockers are considered first-line treatment, despite modest rates of success. Class 1C anti-arrhythmic drugs are often more effective, though their use in the setting of structural heart disease is generally discouraged.3 Class III antiarrhythmic drugs are limited by need for inpatient initiation and more significant side effects. Catheter ablation is therefore an important treatment for PVCs, with generally superior efficacy in comparison to medications.4 When antiarrhythmic drugs are ineffective, not tolerated, or not desired by the patient, catheter ablation should be offered.5
The most common PVC sites of origin include the right ventricular outflow tract (RVOT), left ventricular outflow tract (LVOT), and papillary muscles. Within the LVOT, the left ventricular summit (LVS) is increasingly recognized as an important epicardial PVC site of origin.6 In this chapter, we describe our approach for mapping and ablation of ventricular arrhythmias arising from the LVS.
LEFT VENTRICULAR SUMMIT ANATOMY
As originally described by McAlpine, the LVS is the most superior portion of the LV epicardium.7 It is bounded by the bifurcation of the left main coronary artery into the left anterior descending (LAD) and left circumflex (LCx) coronary arteries (Figure 37.1).8 The relationship of coronary arteries and veins is variable. In the majority of cases, the anterior interventricular vein (AIV) originates leftward of and runs adjacent to the LAD. The great cardiac vein (GCV) typically crosses the LCx, forming the triangle of Brocq and Mouchet, composed by the intersections of the LAD, LCx, and GCV.6 The LVS can be divided into two regions: a medial and more superior region, close to the apex of the triangle, which is inaccessible to catheter ablation because of immediate proximity to the major coronary arteries and extensive epicardial fat (inaccessible area), and a more lateral and inferior region, toward the base of the triangle, which may be suitable for catheter ablation (accessible area).8
ELECTROCARDIOGRAPHIC CHARACTERISTICS
Several ECG criteria have been proposed to identify an epicardial site of origin for ventricular arrhythmias.8,9 LVS PVCs either have a right bundle branch block (RBBB) configuration in lead V1 or a left bundle branch block (LBBB) configuration with early precordial transition (V3 or earlier). The axis is always inferior.6 Importantly, there is generally a pattern break in lead V2, with more net negativity than leads V1 or V3, given that the LVS is anatomically opposite to lead V2.10 Ventricular arrhythmias (VAs) originating from the “inaccessible region” uniformly have a LBBB pattern, larger R-wave amplitude in the inferior leads, and absence of an S wave in leads V5–V6.8
Other general criteria suggesting an epicardial site of origin for ventricular arrhythmias relate to a more slurred QRS complex, including: (1) time to earliest rapid deflection in the precordial leads (pseudodelta wave) ≥ 34 ms; (2) interval to peak of R wave in lead V2 (intrinsicoid deflection) ≥ 85 ms; (3) time to earliest QRS nadir in the precordial leads (shortest RS complex) ≥ 121 ms; and (4) maximum deflection index ≥ 0.55.11,12
Figure 37.1 Left ventricular summit anatomy. This computer tomographic image depicts the anatomy of the left ventricular summit (LVS). The LVS is a triangular region of the LV epicardium with the apex at the bifurcation of the left main (LM) into the left anterior descending (LAD) and left circumflex (LCx) coronary arteries, and the base formed by an arc connecting the first septal perforator branch (SP) of the LAD with the LCx (white dotted line and arrows). The LVS is bisected by the great cardiac vein (GCV), dividing it into inaccessible (blue dotted lines) and accessible (yellow dotted lines) areas. Reprinted with permission from Santangeli et al., Circ Arrhythm Electrophysiol. 2015;8:337–343. doi:10.1161/CIRCEP.114.002377
MAPPING AND ABLATION
The LVS is one of the most challenging PVC sites of origin to safely and successfully ablate. Santangeli et al.13 reported the outcomes of percutaneous epicardial mapping and ablation of VAs arising from the LVS and the ECG features associated with success. They found that epicardial ablation was only successful in 22% acutely, with a long-term arrhythmia-free survival of 17%. PVCs that could be successfully ablated from the epicardium had a Q-wave ratio in leads aVL/aVR > 1.85, R/S wave ratio in lead V1 > 2, and lack of initial q wave in lead V1, all suggesting a more leftward site of origin.
Given the low likelihood of success with epicardial ablation of LVS PVCs, the preferred initial approach is to map the coronary venous system (CVS), which typically provides the best access to epicardial PVCs.6,8
Mountantonakis et al.14
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