Propranolol in the Treatment of Acute Myocardial Infarction

a substantial decrease in myocardial contractility. This was reflected by a fall i cardiac index (average of 0.6 L/min/M2, P < 0.001) and of arterial mean pressure (average of 16 mm Hg, P < 0.001) with little change in systemic vascular resistance. Decrease in cardiac index was due mainly to decrease in stroke volume. Heart rate, not strikingly increased at the control state in the majority of patients, decreased an average of 7 beats/min (P < 0.001). Pulmonary wedge pressure rose an average of 2 mm Hg (P < 0.05). It remained unchanged or decreased in three patients. These varying but small changes in wedge pressure in the presence of decreased contractility may be related to improved left ventricular compliance, produced by propranolol. Propranolol markedly improved myocardial metabolism. Arterial coronary sinus oxygen difference decreased an average of 0.72 ml/100 ml (P < 0.001); coronary sinus oxygen tension increased an average of 2 mm Hg. Myocardial lactate production shifted to extraction (average of -8% to 14%) or the rate of lactate extraction increased (average of 20% to 29%). Coronary blood flow decreased an average of 13 ml/100 g/min (P < 0.001). Both decrease in mean aortic pressure and decrease in myocardial oxygen requirements probably contributed to the fall in coronary blood flow. The finding, that myocardial metabolism improved, suggests that reduction in myocardial oxygen demand outweighed the decrease in coronary blood flow. None of the 20 patients developed left ventricular failure or other complications related to beta-adrenergic blockade. Severe chest pain, unresponsive to conventional therapy in four patients, was relieved by propranolol. These findings demonstrate that acutely administered propranolol improves myocardial oxygenation in patients with uncomplicated acute infarction without endangering perfusion of other vital organs.