Gender differences in electrical remodeling and susceptibility to ventricular arrhythmias in rabbits with left ventricular hypertrophy

Background Left ventricular hypertrophy (LVH) is associated with an increased risk of death, vulnerability to ventricular arrhythmia, and multiple electrophysiological abnormalities. Objectives The purpose of the present study was to determine the gender-dependent differences in electrical remodeling and the susceptibility to ventricular arrhythmias in a rabbit model of renovascular hypertension. Methods Rabbits of both sexes underwent unilateral renal artery banding and contralateral nephrectomy or were placed in the control group. Data are expressed as mean +/- standard error of the mean. Results The duration of action potentials was prolonged in the LVH group compared with the control group in both mate (123 +/- 2.4 ms and 151 +/- 2.3 ms vs. 180 +/- 5.1 ms and 196 +/- 3.1 ms for action potential duration [APD](90 Epi) and APD(90 Endo) of control [n=5] and LVH rabbits [n=8], respectively; P<.05) and female rabbits (131 +/- 1.9 ms and 166 +/- 2.0 ms vs. 156 +/- 4.2 ms and 175 +/- 2.2 ms for APD(90 Epi) and APD(90 Endo) of control [n=5] and LVH rabbits [n=7], respectively; P<.05). Moreover, the gender-dependent differences in repolarization were opposite to those seen under control conditions. In LVH rabbits, APD(90) was greater in mates than in females. The changes induced in APD lead to a greater transmural dispersion of repolarization (38 +/- 6.6 ms vs. 19 +/- 6.5 ms for mates and females, respectively; P<.05). In addition, white control rabbits did not show induction of arrhythmias, an enhanced susceptibility to ventricular arrhythmia was seen in LVH mate rabbits (6/8 mate vs. 1/7 female LVH rabbits; P<.05). Conclusion We conclude that the electrical remodeling associated with LVH inverted the gender-dependent differences, with mate rabbits now exhibiting action potentials with Longer durations both in the endocardial and epicardial surface of the Left ventricle, increased dispersion of repolarization, and increased vulnerability to ventricular arrhythmia induction.