Relief of Angina Pectoris by Electrical Stimulation of the Carotid-Sinus Nerves

Abstract

BECAUSE angina pectoris is a consequence of inadequate myocardial oxygenation, ideal therapy for this incapacitating symptom would be directed toward both increasing coronary blood flow and decreasing myocardial oxygen requirements. In the setting of severe coronary-artery disease, however, the ability of the coronary vascular bed to dilate is limited so that methods designed to decrease myocardial oxygen requirements may provide a more fruitful approach. Recent experimental studies have demonstrated that these oxygen requirements are directly related to the heart rate, to the inotropic state of the myocardium and to the intraventricular pressure, which is a reflection of the intramyocardial wall . . .