The injury-vasospasm hypothesis of ischemic heart disease, revisited.
The injury-vasospasm hypothesis of IHD was discussed in relation to coronary artery autoregulation and the anoxic-feedback mechanism. Observations in the recent literature, not usually attributed to spasm, were examined in light of this phenomenon. This includes reperfusion models of experimental AMI, the association of AMI with myocarditis, and findings in AMI and SCD as necrotic microlesions, prodromata, and epicardial arterial plaque rupture and hemorrhage. The disparity between the severity of coronary disease and the occurrence of the various types of IHD suggest that atherosclerosis itself does not precipitate attacks of chest pain. It was emphasized that plaque rupture due to spasm might help induce CAT. With exercise, the possible importance of the autoregulatory system was explored in the prevention and induction of AMI and SCD, and the improvement of AP. The role of spasm in IHD should be defined.
D000787:Angina Pectoris / Q000209:etiology; D000818:Animals; D001157:Arterial Occlusive Diseases / Q000150:complications*; D003327:Coronary Disease / Q000209:etiology*; D003331:Coronary Vessels / Q000503:physiopathology*; D003645:Death, Sudden / Q000209:etiology; D004285:Dogs; D006801:Humans; D006940:Hyperemia / Q000150:complications; D000860:Hypoxia / Q000150:complications; D009203:Myocardial Infarction / Q000209:etiology; D009205:Myocarditis / Q000150:complications; D005082:Physical Exertion; D013927:Thrombosis / Q000209:etiology