Polymorphic Ventricular Tachycardia—Part I: Structural Heart Disease and Acquired Causes

Abstract Polymorphic ventricular tachycardia (PMVT) is an unusual ventricular tachyarrhythmia. Perhaps its most unique characteristic is a continuously evolving QRS morphology. Although the most common substrate for PMVT is structural heart disease, the prevalence of sudden cardiac death in the population without structural heart disease is even greater, and the absence of a myocardial substrate would suggest that PMVT is the anticipated cause of sudden cardiac death in this population as well. Mechanistically, PMVT is distinct from ventricular fibrillation. It appears to be a condition of abnormal repolarization and resultant cellular heterogeneities, and the principles of triggering and reentry have been demonstrated to govern its initiation and maintenance. The “channelopathies”—a growing category of inherited or acquired conditions that predispose to PMVT and sudden cardiac death—present a fascinating challenge with potentially dire consequences as there are few indicators of their existence except for subtle, if any, electrocardiographic changes. The ever-expanding number of pharmaceuticals that affect ion channel function further magnifies this risk.