Abstract

The aim of this study was to characterize the effects of valsartan on ventricular tachycardia or fibrillation (VT/VF) after myocardial infarction (MI). Rabbits in the MI and valsartan (VAL) groups were subjected to median sternotomy followed by left coronary artery ligation. MI was induced among the rabbits and the VAL rabbits were given VAL orally for 12 weeks. VT/VF episodes, as well as monophasic action potentials (MAPs) were recorded. Transient potassium efflux from the myocytes isolated from the border zone of the infarcts in the left ventricular wall was recorded. In the MI group, the action potential at 90% repolarization (APD₉₀) in the ventricular myocytes was prolonged after MI. However, in the VAL group, no significant difference was observed between the APD₉₀ before MI and at 12 weeks after VAL treatment. The transmural dispersion of repolarization (TDR) was increased after MI. The increase in TDR was reversed by VAL. The density transient outward potassium current (Ito) was lower in the MI group than in the sham-operated (SHAM) and VAL groups, respectively. However, no significant difference was observed between the SHAM group and the VAL group. VAL reduces electrophysiologic heterogeneity. VAL reverses the abnormal ionic flux during the plateau of the action potential.

Key words: Myocardial infarction (MI), monophasic action potential duration, transient outward potassium current, patch clamp, valsartan (VAL).