Hypotension, Nitroglycerin, and Acute Myocardial Infarction

IT IS widely recognized that hypotension may lead to serious consequences in the patient suffering an acute myocardial infarction. The fear of hypotension is amply justified and originates, in large part, from the poor outcome in patients who develop cardiogenic shock. Under these circumstances hypotension is a result of pump failure due to massive myocardial damage, but the diminished arterial pressure itself undoubtedly plays a causal role in the usually lethal cycle characterized by diminished coronary perfusion pressure, greater ischemic injury, more severe hypotension, etc. In addition, any baroreceptormediated increase in heart rate and myocardial contractility (cauised by the reduction in arterial pressure) would tend to raise myocardial oxygen demand and thereby further augment the ischemic insult. These considerations understandably have focused the physician's attention on the prompt treatment of hvpotension and the avoidance of any drugs that may reduce blood pressure in patients with acute myocardial infarction. An interesting paradox exists, however, insofar as most of us accept the dogma that the decrease in blood pressure produced by vasodilators (in particular, nitroglycerin) is potentially lethal in the patient with acute myocardial infarction, but almost invariably benefits the patient with angina pectoris. The relief afforded by nitroglycerin to the patient with angina pectoris has been well documented. The concept that nitroglycerin is deleterious during acute myocardial infarction, however, has been untested until very recently. Surprisingly enough, rather than supporting the clinical bias against the use of nitroglycerin during acute myocardial infarction, these recent studies suggest that, under certain circumstances, vasodilators may exert beneficial effects. For example, Franciosa and coworkers showed hemodynamic improvement in some patients with depressed cardiac output during acute myocardial infarction after administration of the vasodilator nitroprusside,' and Gold et al. reported similar results following administration of nitroglycerin to patients with long-standing cardiac decompensation consequent to myocardial infarction.2 However, hemodynamic improvement is not necessarily indicative of reduced ischemic injury since the peripheral or reflex effects of a vasodilator could improve the net pumping performance of the heart at a time when the degree of ischemic injury of the involved portion of myocardium is unchanged or even increased. To assess more directly the effects of nitroglycerin