Abstract

Scar-mediated ventricular tachycardia (VT) is a recognized cause of morbidity and mortality in patients with ischemic cardiomyopathy and other cardiomyopathies such as nonischemic cardiomyopathy, arrhythmogenic right ventricular cardiomyopathy, and cardiac sarcoidosis. Implantable cardioverter-defibrillator (ICD) therapy improves survival but does not prevent the onset of recurrent VT or associated morbidity from ICD shocks. While randomized controlled trials have demonstrated advantages of scar-mediated VT ablation in comparison with antiarrhythmic drugs, procedural success has remained overall modest at between 50% and 70%. Standard scar-mediated VT ablation has relied on the use of activation and entrainment mapping during sustained VT to identify critical isthmuses for ablation. Substrate-based approaches have emerged as options to address hemodynamically unstable VT and have focused on identifying electrograms characteristic of critical isthmuses (eg, late potentials, local abnormal ventricular activities, conducting channels) within dense scar during sinus rhythm. Scar homogenization, a more recent approach, relies minimally on mapping and focuses on complete substrate modification. Core isolation, on the other hand, another recent development, relies heavily on mapping to identify regions within scar that are “cores” for arrhythmogenicity and then concentrates ablation to these areas. At this time, scar-mediated VT ablation appears to be at a crossroads wherein evolving substrate-based approaches are exploring whether to rely less or increasingly more on mapping. This review will therefore discuss the evolution of substrate-based, scar-mediated VT ablation and in the process try to answer whether there is still a role for mapping.

Highlights

  • Ventricular tachycardia (VT) following myocardial infarction is established as a recognized cause of morbidity and mortality

  • Despite the substantial progress in our understanding of scar-mediated VT and the use of increasingly sophisticated mapping systems and ablation catheters, the success of scar-mediated VT ablation has remained modest and is reported to be between 50% and 70% in most studies. This has led to a reexamination of the standard approach for scar-mediated VT ablation that has traditionally relied on identifying the critical isthmuses for the reentrant VT circuits utilizing activation and entrainment mapping

  • Entrainment was first described in 1977 by Waldo et al.[12] as a pacing maneuver performed during sustained arrhythmic episodes that resulted in transient capture without arrhythmia termination and which has since been instrumental in establishing our understanding of the mechanism of reentry

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Summary

Introduction

Is observed in the case of other cardiomyopathies such as nonischemic cardiomyopathy (NICM), arrhythmogenic right ventricular (RV) cardiomyopathy (ARVC), and cardiac sarcoidosis. Despite the substantial progress in our understanding of scar-mediated VT and the use of increasingly sophisticated mapping systems and ablation catheters, the success of scar-mediated VT ablation has remained modest and is reported to be between 50% and 70% in most studies This has led to a reexamination of the standard approach for scar-mediated VT ablation that has traditionally relied on identifying the critical isthmuses for the reentrant VT circuits utilizing activation and entrainment mapping. Reentry was established early on as the primary mechanism for monomorphic VT in patients with prior myocardial infarction.[9] While abnormal automaticity accounts for up to 10% of monomorphic VT in ischemic heart disease, reentry is the predominant arrhythmic mechanism and involves slow conduction zones within areas of myocardial scar These slow conduction zones are composed of surviving myocytes that form strands of viable tissue, sometimes measuring only a single cell thick in diameter, within electrically inert fibrotic tissue that acts to protect the slowed conduction within these channels. These protected, slow, abnormally conducting channels within scar are the critical isthmuses for the maintenance of reentry VT and constitute targets for scar-mediated VT ablation

Activation mapping
Entrainment mapping
Linear ablation
Local abnormal ventricular activity ablation
Scar dechanneling
Scar homogenization
Core isolation
Nonischemic cardiomyopathy
Arrhythmogenic right ventricular cardiomyopathy
Cardiac sarcoidosis
Epicardial ablation
Deep intramural ablation
Future innovations
Findings
Conclusions
Full Text
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