| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 2925637 | Heart Rhythm | 2006 | 8 Pages |
BackgroundLeft ventricular hypertrophy (LVH) is associated with an increased risk of death, vulnerability to ventricular arrhythmia, and multiple electrophysiological abnormalities.ObjectivesThe 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.MethodsRabbits 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.ResultsThe duration of action potentials was prolonged in the LVH group compared with the control group in both male (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 APD90 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 APD90 Epi and APD90 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, APD90 was greater in males 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 males and females, respectively; P<.05). In addition, while control rabbits did not show induction of arrhythmias, an enhanced susceptibility to ventricular arrhythmia was seen in LVH male rabbits (6/8 male vs. 1/7 female LVH rabbits; P<.05).ConclusionWe conclude that the electrical remodeling associated with LVH inverted the gender-dependent differences, with male 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.
