Beneficial electrophysiologic effects of nitroglycerin during acute myocardial infarction

Abstract

Nitroglycerin reduces ischemic injury after experimental coronary occlusion. To determine whether it also has the potential of protecting the heart against the development of serious ventricular arrhythmias, the effects of nitroglycerin on electrical stability of acutely ischemic myocardium were determined in open chest dogs. Electrical stability of the ventricle was assessed by measuring ventricular fibrillation threshold before and after acute myocardial ischemia was produced by occlusion of the left anterior descending coronary artery. Ventricular fibrillation threshold was measured in a random manner under conditions of nonischemia, ischemia, ischemia plus nitroglycerin, and simultaneous infusion of phenylephrine to maintain mean systemic arterial pressure at control levels. Heart rate was kept constant at 120 beats/min by destruction of the atrioventricular node and use of ventricular pacing. In the absence of ischemia ventricular fibrillation threshold was 77 ± 5 milliamperes (ma), a value unaffected by either nitroglycerin or phenylephrine. After 6 minutes of acute myocardial ischemia, ventricular fibrillation threshold was reduced to 30 ± 6 ma ( P <0.01). When nitroglycerin was infused at a rate of 200 μg/min (with a reduction in arterial pressure of 24 percent), ventricular fibrillation threshold after 6 minutes of acute ischemia increased from 30 ± 6 to 55 ± 3 ma ( P < 0.005). Restoration of arterial pressure by phenylephrine during infusion of nitroglycerin further raised the ventricular fibrillation threshold to 75 ± 6 ma, a value identical to that present in nonischemia. Thus, nitroglycerin enhances electrical stability of the heart during experimental acute myocardial ischemia, an effect probably related to reduction of ischemic injury. Since the ventricular fibrillation threshold increases even further after arterial pressure is restored to control levels, this beneficial electrophysiologic effect is probably caused by some action of nitroglycerin other than reduction in myocardial oxygen consumption mediated by decreased afterload.