Remodeling of ventricular repolarization in experimental right ventricular hypertrophy

To understand electrophysiological mechanisms that underlie the progression of compensated right ventricular hypertrophy (RVH) to heart failure, the purpose of the study was to evaluate remodeling of ventricular repolarization in connection with hemodynamic abnormalities and vulnerability of the heart ventricles to arrhythmias in RVH rats with pulmonary arterial hypertension (PAH) and heart failure.

PAH followed by heart failure was induced by monocrotaline in adult female Wistar rats. Unipolar epicardial electrograms and cardiac hemodynamic parameters were recorded in situ. Vulnerability to ventricular arrhythmias was measured as the threshold dose of aconitine required to produce sustained ventricular tachycardia. Histological examination of the heart ventricles was performed. Activation-recovery intervals (ARIs) and ARI dispersions were used as indices of durations and heterogeneity of repolarization respectively to assess ventricular repolarization.

The development of compensated RVH was characterized by the dramatic prolongation of repolarization against the less expressed increase in repolarization heterogeneity, whereas the dramatic increase in repolarization heterogeneity against the less expressed but inhomogeneous prolongation of repolarization occurred in the progression of compensated RVH to heart failure. These changes increased vulnerability of the failing heart but not the compensated heart to aconitine-induced ventricular arrhythmias.