This review summarizes the pathophysiology of ventricular tachycardia in post-infarction cardiomyopathy and the contemporary practice of catheter ablation.
Monomorphic ventricular tachycardia (VT) in patients with post-infarction cardiomyopathy (CMP) is caused by reentry through slowly conducting tissue with in areas of myocardial scar. The use of implantable cardioverter-defibrillators (ICDs) has helped to decrease the risk of arrhythmic death in patients with post-infarction CMP, but the symptomatic and psychological burden of ICD shocks remains significant. Experience with catheter ablation has progressed substantially in the past 20 years, and is now routinely used to treat patients with post-infarction CMP who experience VT or receive ICD therapy. Depending on the hemodynamic tolerance of VT, a variety of mapping techniques may be used to identify sites for catheter ablation, including activation and entrainment mapping for mappable VTs, or substrate mapping for unmappable VTs. In this review, we discuss the pathophysiology of VT in post-infarction CMP patients, and the contemporary practice of catheter ablation.
Nazer et al. (Wed,) studied this question.
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