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
Fisch S. On the Origin of Cardiac Pain: A New Hypothesis. Arch Intern Med. 1980;140(6):754–755. doi:10.1001/archinte.1980.00330180028016
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