Vasodilator Therapy of Myocardial Infarction

Recent interest in pharmacologic interventions to alter the course of acute myocardial infarction has led to the consideration of arterial pressure and systemic vascular resistance as factors controlling left ventricular function. In the first 24 hours after the onset of symptoms, the circulatory pattern of extensive transmural acute myocardial infarction is characterized by increased left ventricular end-diastolic pressure, reduced stroke volume and normal or even elevated arterial pressure.1 Maintenance of the arterial pressure in the face of a reduction in cardiac output implies an increase in peripheral resistance that may, in part, represent the vascular consequence of activation of the . . .