Does intravenous propranolol alter myocardial mechanics, energetics, and hemodynamic functions in subjects with and without coronary atherosclerosis?
Intravenous propranolol acutely decreases myocardial oxygen demand and mechanical effort, providing a physiological mechanism for its efficacy in treating angina pectoris.
The success of propranolol in treating the symptoms of angina pectoris has raised questions about the effects of beta-adrenergic blockade on the hemodynamic functions, myocardial mechanics, energetics, and metabolic functions. Five milligrams of propranolol was given intravenously to 27 human subjects, 18 with and nine without angiographically proven coronary atherosclerosis. The drug produced a decrease in externally measured indices of myocardial mechanical effort and consequently a fall in myocardial oxygen demands. The hemodynamic changes and resultant increases in myocardial oxygen consumption and coronary flow during supine leg exercise were also attenuated. Propranolol produced different changes in myocardial arteriovenous oxygen extraction depending upon whether the coronary circulation was normal or diseased. Although the data suggest that coronary vasoconstriction occurred in patients with atherosclerotic lesions, no significant change in myocardial lactate exchange was noted after administration of propranolol. Beta-adrenergic blockade caused a decline in cardiac filling pressures and volumes at the dose level used in this study, presumably by decreasing venous return.
Wolfson et al. (Wed,) studied this question.