INTRODUCTION

The subendocardium is at greater risk for necrosis during myocardial infarction. Compared to the subepicardium, it is subject to greater wall stress, has higher metabolic requirements, and is perfused by coronary vasculature that is more susceptible to decreases in perfusion pressure. Many factors modify the pattern of necrosis, including collateral vessels, microvascular obstruction, intramyocardial hemorrhage and reperfusion.¹ Thus, although evidence of subendocardial infarction is the rule in patients with post-infarction ventricular tachycardia (VT), the subepicardial extent of the infarct is variable, ranging from none to extensive. The majority of patients with VT from prior myocardial infarction have reentry circuits that can be targeted with endocardial ablation. In patients who have failed endocardial ablation and have been selected to go on to have epicardial mapping (10–13% of post-infarct patients in some studies), up to 75% have a VT abolished with epicardial ablation.^2–6 However, these patients are selected for recurrent VT despite endocardial ablation and a favorable consideration of the risk/benefit of an epicardial procedure. In one series of 444 patients, epicardial mapping was performed in only 13%; and in one-third of patients, a desirable epicardial target was not identified; epicardial ablation abolished at least one VT in 6% of patients overall.² This is likely a substantial underestimate of the number of VT patients with epicardial arrhythmia substrate. More recent substrate-guided ablation approaches, some including patients who have not failed endocardial ablation, find abnormal electrograms on the epicardium in two-thirds of patients.^7,8 It is clear that some abnormal areas of conduction can be targeted from either the epicardium or the endocardium.^8,9 Others cannot be adequately ablated from the endocardium.

Epicardial mapping and ablation is an important consideration in this population with a benefit that must be weighed against the risk of complications. Unfortunately, the electrocardiogram (ECG) of VT is not a reliable marker of the need for epicardial versus endocardial ablation in patients with ischemic cardiomyopathy. It nonetheless does provide useful insights into the likely reentry circuit location and substrate characteristics.

RELATION BETWEEN EXITS AND REENTRY CIRCUITS IN INFARCT-RELATED VT

Infarct-related monomorphic VT (MMVT) is usually due to reentry through regions of myocardial scar containing surviving myocyte bundles with diminished cell coupling and interstitial fibrosis that promote slow conduction and non-uniform refractory periods creating the conditions for reentry.^10,11 These reentry circuits can be conceptualized as having isthmuses (also referred to as channels) that traverse portions of the infarct region.^12,13 These are relatively small masses of muscle that do not contribute to the surface ECG. The QRS is inscribed when the wavefront emerges from the exit of an isthmus that is often along the border of the infarct region and propagates away, depolarizing a sufficient amount of myocardium to create the onset of the QRS (Figure 21.1). The wavefront then returns to the entrance of the isthmus by propagating through one or more loops along the border of the infarct (outer loop) or through another channel (inner loop). Some isthmuses are defined by fixed conduction block, such as the mitral or aortic valve annulus, or fibrous tissue in the scar. Reentry circuit paths can also be defined by functional conduction block, or wavefront collision.^14,15

The location of the reentry circuit exit is an important determinant of the QRS morphology. There are several reasons that the QRS morphology can be misleading as a guide to the exit (Figure 21.1). The exit from the circuit can be deep within the scar, remote from the border of the infarct. Exits can also be broad, funnel-shaped areas that are difficult to interrupt.¹⁶ The circuit can be in the endocardium, but the exit may be on the epicardium, or vice versa.¹⁷ Ablation in the exit region therefore may change the VT QRS but fail to interrupt VT. Changes in propagation outside the scar as the wavefront spreads across the myocardium can also potentially alter the QRS morphology. This may manifest as block occurs in conducting loops or with variable use of the Purkinje system to activate portions of the ventricle. Although 3D mapping of post-infarct circuits is not possible in humans, mapping of the endocardium and epicardium support the existence of three-dimensionally complex reentry circuits.^11,12 Application of these considerations to a theoretical 3D circuit that involves the endocardium and epicardium is shown in Figure 21.1. A circuit can involve the epicardium and have an epicardial exit, but be ablated from the endocardium (Figure 21.1, Panels A and B).¹⁶ Alternatively the same circuit might be interrupted with epicardial ablation (Figure 21.1, Panel C). Depending on wall thickness, these lesions may interrupt only a part (e.g., the entrance or exit) of an isthmus, leaving a part that may connect to other pathways forming other reentry circuits. If the ventricular wall is sufficiently thin to allow a transmural lesion, ablation on either the epicardium or endocardium may be sufficient to completely abolish conduction through the isthmus. Recent studies of CT imaging have found that reentry circuits may tend to occur in thin infarct areas (only a few mm thick), where ablation from either the endocardium or epicardium may be likely.⁹

Reentry circuits can also be largely determined by functional block, as in the figure-eight type of circuits that are seen in the subepicardium of 3- to 5-day infarcts in canine models, and more recently investigated in other infarct models.^15,18,19

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