On the Origin of Cardiac Pain

Abstract

Current theory states that cardiac pain arises when myocardial anoxia stimulates cardiac nerve endings. Discrepancies between facts and this theory were reviewed by James,¹ who points out that "even in those patients with proved coronary disease and classical angina pectoris, the true pathophysiologic basis remains a mystery." The accepted theory has these drawbacks: (1) it does not explain why 20% to 60% of myocardial infarctions are painless or silent²; (2) it requires the heart to possess intravisceral sensitivity, unlike any other encapsulated organs with similar innervation; (3) it does not explain the mechanism of noncoronary angina pectoris³; and (4) it does not explain the relief of angina despite closure of grafts (bypass "sham") or without improvement in stress tests or cardiodynamics.⁴ My new hypothesis circumvents these difficulties by proposing that myocardial ischemia, necrosis, anoxia, or metabolic derangement lead to abnormal ventricular wall motion, which, coupled with