Effect of gallopamil on electrophysiologic abnormalities and ventricular arrhythmias associated with left ventricular hypertrophy in the feline heart

Left ventricular hypertrophy increases vulnerability to ventricular fibrillation. To determine whether calcium channel blockade protects against ventricular arrhythmia in left ventricular hypertrophy, we studied the effects of gallopamil, a potent and specific calcium channel antagonist, in 37 cats undergoing aortic banding (group 1, n = 28) or a sham procedure (group 2, n = 9). Each cat underwent serial echocardiography and was studied after the development of left ventricular hypertrophy, defined as an increase of at least 30% in left ventricular posterior wall thickness. After baseline electrophysiologic testing, animals received gallopamil (70 μg/kg loading dose followed by 2.5 μg/kg/min infusion) ( n = 19) or a control infusion of saline solution ( n = 18), and testing was repeated. There was no significant difference between groups 1 and 2 in baseline excitability thresholds intraventricular conduction times, ventricular effective refractory periods, or monophasic action potential durations. Thresholds for induction of ventricular fibrillation were lower in group 1 than in group 2, and only in group 1 was ventricular fibrillation inducible during programmed stimulation. This altered vulnerability was associated with a significantly greater dispersion of excitability thresholds, ventricular effective refractory periods, and monophasic action potential durations. Gallopamil did not change baseline measurements except for prolonging sinus cycle length and atrioventricular conduction time. Ventricular fibrillation thresholds were similar to pretreatment values (12.3 ± 2 vs 11.9 ± 3 mA; p = NS) as were dispersion of excitability thresholds (0.45 ± 0.17 vs 0.49 ± 0.14 mA; p = NS), ventricular effective refractory periods (30.5 ± 9 vs 33.6 ± 12 msec; p = NS), and monophasic action potential durations (27.5 ± 11 vs 28.2 ± 14 msec; p = NS). A similar percentage of animals in group I were inducible by programmed stimulation before and after treatment with gallopamil ( 11 14 vs 8 12 ; p = NS ). Thus calcium channel blockade, even with a potent agent, does not protect against susceptibility to ventricular arrhythmia caused by left ventricular hypertrophy.