Experimental and clinical cardiology · 2009
The effects of renovascular hypertension on repolarization of ventricular epicardium.
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Krandycheva Valeria V, Kharin Sergey N, Azarov Jan E, Shmakov Dmitry N
Аннотация
BACKGROUND AND OBJECTIVE: Alterations in the recovery sequence of hypertrophied myocardium favour the development of cardiac arrhythmias. The aim of the present study was to investigate apex-to-base and interventricular heterogeneities in the duration of epicardial ventricular repolarization in rats with renovascular hypertension.
METHOD: Renovascular hypertension was induced in six Wistar rats by constricting the left renal artery for one month. Six sham-operated Wistar rats served as normotensive controls. Epicardial mapping was performed using 32 unipolar leads distributed over the apex and base of the heart ventricles under sinus rhythm. Activation-recovery intervals (ARIs) were calculated from electrograms.
RESULTS: The ratio of left ventricular weight to body weight was increased in hypertensive rats compared with controls. In control rats, ARIs at the base of both ventricles were shorter than those at the apex. In hypertrophied hearts, ARIs were prolonged on both the left and right ventricular epicardium. Heterogeneous prolongation was observed via reduced apex-to-base differences in ARIs and increased interventricular differences, with a trend toward increasing dispersion of ARIs. In rats with renovascular hypertension, nonuniform prolongation of epicardial ARIs on both ventricles and the changes in the ARI distribution resulted in a reduction of the repolarization time gradient between the ventricles.
CONCLUSION: Nonuniformly prolonged ARIs across the ventricular epicardium and the interventricular electrical inhomogeneity in rats with renovascular hypertension should be considered when interpreting the T wave alterations together with the reduction of the transmural and apex-to-base repolarization gradients.
METHOD: Renovascular hypertension was induced in six Wistar rats by constricting the left renal artery for one month. Six sham-operated Wistar rats served as normotensive controls. Epicardial mapping was performed using 32 unipolar leads distributed over the apex and base of the heart ventricles under sinus rhythm. Activation-recovery intervals (ARIs) were calculated from electrograms.
RESULTS: The ratio of left ventricular weight to body weight was increased in hypertensive rats compared with controls. In control rats, ARIs at the base of both ventricles were shorter than those at the apex. In hypertrophied hearts, ARIs were prolonged on both the left and right ventricular epicardium. Heterogeneous prolongation was observed via reduced apex-to-base differences in ARIs and increased interventricular differences, with a trend toward increasing dispersion of ARIs. In rats with renovascular hypertension, nonuniform prolongation of epicardial ARIs on both ventricles and the changes in the ARI distribution resulted in a reduction of the repolarization time gradient between the ventricles.
CONCLUSION: Nonuniformly prolonged ARIs across the ventricular epicardium and the interventricular electrical inhomogeneity in rats with renovascular hypertension should be considered when interpreting the T wave alterations together with the reduction of the transmural and apex-to-base repolarization gradients.