Abstract
Propranolol, a beta-adrenergic receptor site blocking agent, is an effective means of treating over 70 per cent of patients with angina pectoris due to coronary artery disease. Through reductions in contractility and heart rate the oxygen requirement of the myocardium is decreased. Inhibition of the response to circulating catecholamines and sympathetic nervous stimulation is achieved. The tachycardia response to exercise is blunted. This retards circulatory adjustments and the hemodynamic setting associated with pain is reached more slowly. Nitrites are synergistic by achieving a reduction in peripheral vascular resistance and contractility. Several unanswered questions remain before these drugs can receive unqualified recommendation in angina pectoris. 1. 1. Is there a reduction in coronary flow that is inappropriate for the reduction in myocardial metabolism? 2. 2. Does the drug reduce collateral vessel development and flow in coronary artery disease? 3. 3. Does chronic oral use of the drug place the patient at a disadvantage if a myocardial infarction results in hypotension or shock? 4. 4. Is there a direct toxic effect on the myocardium? 5. 5. Will other drugs of this class prove to be equally effective yet have fewer side effects?
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