Propranolol in Angina Pectoris

Abstract

To the Editor:— The anginal pains in pheochromocytoma raises the question of the mechanism of this pain during the release of sympathetic neurohormones (epinephrine and norepinephrine) which are coronary dilators. These adrenergic neurohormones produce at the same time an increase in myocardial demands (the catabolic action of the sympathetic) to a greater degree than is met by the increased blood supply. The insufficient increase of blood supply related to the myocardial needs is also the cause of angina pectoris in patients with coronary artery disease. This catabolic action of the sympathetic nervous system and the insufficient increase in blood supply are signs of sympathetic overactivity, but other cardiovascular signs of angina pectoris are related to this overactivity such as tachycardia, increase of blood pressure, and arterial hypertonia. Overactivity of the sympathetic in anginal attacks explains why drugs useful here are sympatholytics, including the beta-adrenergic blocking agent, propranolol hydrochloride. This explains