Effects of nifedipine on conduction delay during ventricular myocardial ischemia and reperfusion.
Nifedipine has been suggested to have more potent slow channel blocking action than other agents of this type. However, its use in the treatment of cardiac arrhythmias has been limited. Electrophysiologic studies on AV conduction have shown that nifedipine lacks any significant effect. However, the action of the drug on intraventricular conduction has not been investigated with regard to its potential in the treatment of ventricular arrhythmias especially during ischemia. Therefore, the effects of nifedipine on conduction delay during ischemia and reperfusion were assessed in the present study. Sixteen dogs (eight control and eight nifedipine-treated dogs) were used. Transmural electrodes were positioned in normal, ischemic, and reperfused tissue, and at the border of these segments. The left anterior descending artery was initially ligated below the second diagonal branch (first ligation) and 30 minutes later below the first diagonal branch (second ligation); the second ligation was released 30 minutes later. Conduction of electrically induced premature impulses from the midwall of the left ventricle was recorded at epicardial and endocardial sites. Conduction delay was measured from the stimulus artifact to the first high-frequency deflection in each zone in the anterograde (base to apex) and retrograde (apex to base) directions. Intravenous nifedipine 0.1 mg/kg was given over 10 minutes immediately after the first ligation. Nifedipine slightly decreased the magnitude of conduction delay in the ischemic myocardium at 15 minutes of ischemia, which corresponded with the peak plasma nifedipine level. However, conduction delay throughout the remainder of the study was essentially unaltered by nifedipine. In conclusion, though nifedipine may improve ischemic myocardial metabolism, infarct size, and hemodynamics, the effect on the electrophysiologic parameters affecting conduction was insignificant. This lack of any further deterioration in conduction in the ischemic and reperfused tissue by the drug further attests to its safety during acute myocardial ischemia.