Cardiac pain has long been of clinical interest, but not until the past decade has it been subjected to laboratory investigation. Although Allbutt's1theory of the aortic origin of angina pectoris was once widely accepted, recent experimental evidence strongly points toward the cardiac origin of pain. Sutton and Lueth2have shown that compression by means of a ligature on coronary vessels in the unanesthetized dog results in pain characteristic of angina pectoris. Their studies have been confirmed by White, Garrey and Atkins3and by Katz and his associates.4All these authors have agreed that the fundamental mechanism initiating pain is a chemical factor produced by impaired coronary circulation. In essence, this contention is the basis of Lewis'5theory that myocardial ischemia is the cause of cardiac pain. From the aforementioned studies it is generally inferred that the mechanical factor is of secondary importance in producing