| Abstrakt: |
Abstract: An attempt was made to determine the relationship between the characteristics of electrical activity of the hypertrophied myocardium of rats at the cellular level and at the level of the whole heart after a one-month left ventricular pressure overload. Such an animal model has already been demonstrated to be highly resistant to epinephrine-induced arrhythmias. Since severe ventricular arrhythmias often occur in patients with cardiac hypertrophy, ventricular vulnerability might depend on some electrophysiological characteristics of the heart related to the stage of hypertrophy. Using the "floating" microelectrode technique, the computed characteristics of cardiac transmembrane action potentials (AP) of the left and right epicardium cells were compared in situ to computed characteristics of the electrocardiograms in anaesthetized control rats (group C) and in rats with left ventricular hypertrophy (group H) induced by a one-month suprarenal constriction of the abdominal aorta. The aortic pressure overload caused a significant (p< 0.001) and marked increase in AP duration of left ventricular cells: APD 30 and APD 80 were 29 ±3 ms and 89 ±6 ms, respectively, in group H and 14 ±1 ms and 53 ±2 ms in group C. The same modifications were observed in right ventricular cells when right hypertrophy was present. Simultaneous electrocardiograms exhibited a significant (p<0.01) prolongation of P-R, Q-S and T duration and T wave flattening in group H (63 ±2 ms, 32 ±3 ms, 109 ±5 ms and 0.25 ±0.03 mV as compared with 53 ±1 ms, 20 ±1 ms, 88 ±2 ms and 0.40 ±0.04 mV in group C). After a one-month aortic overload in rats, both left and right ventricles are hypertrophied and have the same electrophysiological characteristics: in this model, at this stage of hypertrophy, some factors favouring ventricular arrhythmias are missing. The corresponding flattening of the T wave in the ECG might be of clinical relevance. |
