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Treatment of Angina Pectoris by Electrical Stimulation of the Carotid-Sinus Nerves: Results in 17 Patients with Severe Angina
Journal article   Peer reviewed

Treatment of Angina Pectoris by Electrical Stimulation of the Carotid-Sinus Nerves: Results in 17 Patients with Severe Angina

Stephen E Epstein, G. David Beiser, Robert E Goldstein, David Redwood, Douglas R Rosing, Gerald Glick, Andrew S Wechsler, Morris Stampfer, Lawrence S Cohen, Robert L Reis, …
The New England journal of medicine, v 280(18), pp 971-978
01 May 1969
PMID: 4888077

Abstract

Radiofrequency carotid-sinus nerve stimulators implanted for treatment of incapacitating angina pectoris, unrelieved by intensive medical management, produced appreciable symptomatic improvement in 13 of 17 patients: nearly all episodes of angina were terminated by activation of the stimulator, and prophylactic use increased intensity and duration of exercise that could be performed. After long-term use exercise capacity was increased in many patients even when the stimulator was not activated. Two had no benefit, and two died. Prophylactic use during exercise lowered mean arterial pressure an average of 18 mm of mercury (p less than 0.001) in 13 of the 15 survivors, but heart rate was reduced by an average of only 4 beats per minute. The other two showed no hemodynamic response. The principal physiologic factor in the relief of angina appears to be a decrease in arterial pressure, which reduces a major determinant of myocardial oxygen consumption and re-establishes the balance between myocardial oxygen demands and supply. ANGINA pectoris results when myocardial oxygen requirements suddenly exceed the ability of a diseased coronary circulation to provide adequate amounts of oxygen, as may occur during periods of physical or emotional stress. Experimental studies have demonstrated that such increases in oxygen requirements are produced by increases in heart rate, systemic pressure and the inotropic state of the myocardium. 1 2 3 Conversely, a decrease in any of these factors will lower myocardial oxygen consumption (MVO 2 ), and will thereby tend to alleviate the ischemic pain. Since stimulation of the carotid-sinus nerves reflexly decreases sympathetic activity, 4 with consequent reductions in arterial pressure, heart . . .

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