DISPERSION OF VENTRICULAR ACTIVATION AND REFRACTORINESS IN PATIENTS WITH IDIOPATHIC DILATED CARDIOMYOPATHY

Sudden death, primarily from ventricular arrhythymias, accounts for up to 50% of deaths among patients with congestive heart failure.(1) The pathophysiologic basis for this high prevalence of sudden death remai ns poorly understood. Recently, prolongation of the action potential d uration has been reported in myocardial cells and tissue isolated from failing animal and human hearts.(2,3) Inhomogeneous prolongation of t he action potential can predispose to increased dispersion of ventricu lar recovery, which may provide a substrate for ventricular arrhythmia s Abnormalities of cardiac conduction may exaggerate the dispersion of recovery and contribute to vulnerability to arrhythmias.(6) We hypoth esized that the electrophysiologic substrate in patients with an idiop athic dilated cardiomyopathy (LDC) is characterized by increased condu ction times and refractoriness, resulting in prolonged total recovery times (TRT). The purpose of our study was to test this hypothesis by c omparing the rates and spatial dispersion of ventricular activation an d refractoriness in IDC patients and controls.