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Emanuel J. Cohen, MD
Los Angeles

JAMA. 1970;212(12):2122.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

To the Editor:—

The clinical study of angina pectoris reveals that all cardiovascular signs are signs of sympathetic overactivity, such as tachycardia, increase of blood pressure, arterial hypertonia, or increase of myocardial demands. The sympathetic system also exerts a coronary vasodilation action. The overactivity of the sympathetic system in angina pectoris explains why the drugs useful here are sympatholytics or antiadrenergics and the new treatments of this disease (propranolol hydrochloride and the electric stimulation of the carotid sinus) provide the same action.

The good results published by Wasserman in 1928 through mechanical stimulation of the carotid sinus have been amply confirmed.¹ The carotid sinus stimulation may have resulted in a decrease of the sympathetic activity or in an increase of vagal activity.² Wasserman wondered how it is possible to reduce the anginal pain when the resultant vagal stimulation produces a coronary vasoconstriction.

The explanation is that the vagal . . . [Full Text PDF of this Article]

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