Effect of an intravenous angiotensin-converting enzyme inhibitor on the electrophysiologic features of normal and hypertrophied feline ventricles.

Left ventricular hypertrophy is associated with an increased risk of ventricular arrhythmia and multiple electrophysiologic abnormalities that normalize with regression of hypertrophy. For patients who have hypertension, treatment with angiotensin-converting enzyme (ACE) inhibitors produces regression of hypertrophy and a reduction in ventricular arrhythmia. It is unclear whether the reduction in ventricular arrhythmia associated with ACE inhibitor therapy is due to regression of hypertrophy alone, a direct antiarrhythmic effect of ACE inhibition, or both. We performed electrophysiologic studies in normal cats and cats with fixed left ventricular hypertrophy before and after acute intravenous administration of trandolopril. Trandolopril produced a small, consistent prolongation of monophasic action potential duration in normal and hypertrophied ventricles although this prolongation did not reach statistical significance. Trandolopril had no significant effect on effective refractory period, inducibility of arrhythmia, or ventricular fibrillation threshold in normal or hypertrophied ventricles. These data suggest that the reduction in arrhythmia associated with ACE inhibitors is not caused by a direct electrophysiologic effect but is more likely caused by regression of hypertrophy.