The Use of Nitroprusside in the Treatment of Acute Myocardial Infarction

Abstract

In 15 patients with acute myocardial infarction, intravenous infusion of the potent vasodilator, nitroprusside, produced an average 50% fall in the elevated left ventricular filling pressure and a modest reduction in arterial pressure (average, 15.5%) without a change in heart rate. Careful dose adjustment in several patients resulted in a significant fall in left ventricular filling pressure with little or no change in arterial pressure. Cardiac output consistently rose during nitroprusside infusion in patients with clinical signs of left ventricular failure or shock and low control cardiac output, whereas output changed little on those patients with normal cardiac index. A fall in pressure time per minute as well as the fall in left ventricular filling pressure indicated a reduction in myocardial oxygen consumption during the vasodilator infusion. Drug infusion was usually accompanied by subjective improvement, including relief of dyspnea and of chest pain, and reduction in ventricular irritability. These data suggest, that vasodilator therapy, by reducing left ventricular afterload, can improve left ventricular performance in patients with acute myocardial infarction. Such treatment may be a rational approach to the management of patients with heart failure, pulmonary edema, or early shock. 1 Commentary Until the publication of this manuscript, little attention was given to the reduction of the peripheral vascular resistance as a method of improving left ventricular function in patients with acute myocardial infarction. The concern about using vasodilators were either that reducing blood pressure will decrease coronary blood flow or because physicians were concerned that a decrease in blood pressure was associated with clinical deterioration. However, Dr Cohn and his colleagues hypothesized that increases in blood pressure in a failing ventricle is harmful and therefore a control decrease in blood pressure may be expected to decrease left ventricular filling pressure. This is the reason why they used nitroprusside in infusion rates between 30 lg ⁄min and 150 lg ⁄min to control blood pressure in these patients and demonstrated a striking fall in left ventricular filling pressure with very little decrease in blood pressure. They also caution that if patients are hypotensive, one should be careful. In this manuscript, the authors put forth a possible mechanism for why nitroprusside may be beneficial to these patients in decreasing left ventricular afterload more than left ventricular preload. In addition, they suggested that compared with inotropic agents, using nitroprusside in patients with acute myocardial infarction reduced left ventricular oxygen consumption. Finally, the authors conclude that nitroprusside may be beneficial in patients with acute pulmonary edema and those with heart failure or early shock. The next historical vignette will discuss the use of nitroprusside in the treatment of refractory heart failure.