INTRODUCTION

Endocardial sinus rhythm ventricular activation in the absence of disease is well understood. The rapidly conducting His-Purkinje system is tasked with fast, smooth, and synchronous distribution of the activating wavefront from the septum to both ventricular free walls to allow for optimally coordinated mechanical systole. This pattern is susceptible to disruption by both confluent and diffuse fibrosis as well as by His-Purkinje disease.^1–3

Transmural and epicardial sinus rhythm ventricular activation are less well characterized, both in health and disease. A number of factors clearly influence this activation pattern, including:

1.the absence of a rapidly conducting Purkinje network on the epicardium,

2.marked heterogeneity in wall thickness and fiber architecture, both between and within each ventricle, and

3.the variable distribution of fibrosis in cardiomyopathies that display intramural and epicardial scarring as part of their phenotype.

This sinus rhythm activation pattern potentially has important implications for the configuration and characteristics of ventricular tachycardia (VT) circuits. Reentrant VT arising in post-myocardial infarction scar is predominantly an arrhythmia based in the endocardium, being confined to that region by confluent layers of subendocardial infarct scar. Irrespective of the substrate location, this can be inferred for any given scar-related VT when entrainment mapping places all circuit components in the endocardium and finds only remote bystander sites in the epicardium. The key component of the post-infarct substrate that allows for this apparent compartmentalization of the endocardium is the confluent sheet-like nature of the myocardial infarct scarring process.

In the setting of the nonischemic cardiomyopathies, the substrate is usually more diffuse with interstitial and replacement fibrosis seen in a characteristic basal, periannular distribution and potentially transmurally throughout the thickness of the ventricular wall. There are, however, some characteristic nonischemic myocardial diseases that may exhibit confluent layered epicardial (or intramural) scarring, including Chagas disease, specific subtypes of myocarditis, and arrhythmogenic right ventricular cardiomyopathy (ARVC). The latter in particular can form large sheets of layered scar overlying the thin-walled right ventricle.

POTENTIAL FOR EPICARDIAL COMPARTMENTALIZATION DURING SCAR-RELATED VT

The potential effects of such a pattern of layered epicardial substrate are demonstrated in the reentrant VT depicted in Figure 18.1. This patient with ARVC had basal periannular right ventricular (RV) low voltage and a large confluent sheet of epicardial scar with low voltage and widespread isolated late potentials. The clinical VT was induced and entrainment mapping showed that all tested endocardial substrate sites were remote from the active circuit, while all isthmus sites could be demonstrated to lie on the epicardium. During this VT, the RV endocardium was passively activated, while the epicardium containing the entire reentrant circuit was effectively compartmentalized off. This is essentially the inverse of the situation generally seen with most post-infarct VT where the epicardium is passively activated.

The normal sequence of left ventricular (LV) depolarization starts at the Purkinje myocyte interface on the left side of the interventricular septum. In the RV, depolarization commences from the distal right bundle branch (inside the moderator band) as it arborizes throughout its RV apical insertion, eventually distributing the propagating wavefront back towards the basal annular region.4

Relative to this typical endocardial sequence, epicardial activation may theoretically proceed in two possible ways (Figure 18.2).

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