Repolarization abnormalities and arrhythmogenesis in hypertrophic myocardium.

Left ventricular hypertrophy (LVH) is accompanied by specific changes of the cellular electrophysiology, which are potentially arrhythmogenic, mainly prolongation of action potential duration due to down-regulation of several K channels. Moreover, transmural dispersion of repolarization due to presence of cell types with different repolarization properties within the ventricular wall plays an essential role in the development of transmural functional reentry responsible for the maintenance of ventricular tachycardia (VT), once it has been initiated. Experimental evidence has been provided that phase 2 early afterdepolarizations (EAD) can be generated from hypertrophied left ventricular wall in the absence of action potential duration (APD) prolonging agents. Phase 2 EADs could be associated with malignant "R on T" extrasystoles, initiating polymorphic VT. Unfortunately, the abnormalities of ventricular repolarization are not always revealed on surface electrocardiogram (ECG) and when present they have a low predictive power for occurrence of life-threatening arrhythmias and sudden cardiac death. In order to reveal signs of repolarization heterogeneities not apparent from 12-lead ECG analysis, we studied body surface potential maps in a group of patients with LVH due to valvular aortic stenosis. The similarity index was significantly lower and the late repolarization deviation index was significantly higher in patients than in normal subjects. These findings suggested a higher than normal degree of heterogeneities of repolarization in LVH patients, not detected by the usual ECG analysis.