作者: Solomon Fisch
DOI: 10.1001/ARCHINTE.1980.00330180028016
关键词: Ventricular wall 、 Medicine 、 Pathophysiology 、 Anesthesia 、 Cardiac nerve 、 Cardiology 、 Cardiac pain 、 Angina 、 Pericardium 、 Myocardial ischemia 、 Internal medicine 、 Coronary disease
摘要: Current theory states that cardiac pain arises when myocardial anoxia stimulates nerve endings. Discrepancies between facts and this were reviewed by James, 1 who points out "even in those patients with proved coronary disease classical angina pectoris, the true pathophysiologic basis remains a mystery." The accepted has these drawbacks: (1) it does not explain why 20% to 60% of infarctions are painless or silent 2 ; (2) requires heart possess intravisceral sensitivity, unlike any other encapsulated organs similar innervation; (3) mechanism noncoronary pectoris 3 (4) relief despite closure grafts (bypass "sham") without improvement stress tests cardiodynamics. 4 My new hypothesis circumvents difficulties proposing ischemia, necrosis, anoxia, metabolic derangement lead abnormal ventricular wall motion, which, coupled