Experimental induction of spasm, sudden progression of organic stenosis and intramural hemorrhage in the epicardial coronary arteries.
Pathogenesis of the so-called "heart attack" still remains to be elucidated. The links between stable effort angina and unstable or acute myocardial infarction, and between asymptomatic and spontaneous angina are all missing. In medicine presently, pathophysiology of ischemic heart disease is considered a consequence of i) the progression of atherosclerotic narrowing of the coronary artery, and ii) dynamic and transient obstruction (coronary spasm), but these mechanisms are traditionally believed to be unrelated. This article demonstrates various experimental evidence indicating that these two mechanisms are related. And, this review article describes how to produce experimental coronary spasm in the presence of atherosclerosis, similar to that seen in patients with variant angina, and that coronary spasm can produce sudden progression of coronary atherosclerotic obstruction due to intramural hemorrhage. Establishment of various animal models to elucidate mechanisms related to various stages of ischemic heart disease are needed.
Nakamura
M
M
Research Institute of Angiocardiology, Faculty of Medicine, Kyushu University, Fukuoka, Japan.
D000788:Angina Pectoris, Variant / Q000503:physiopathology*; D000818:Animals; D003327:Coronary Disease / Q000503:physiopathology*; D003329:Coronary Vasospasm / Q000503:physiopathology; D003331:Coronary Vessels / Q000503:physiopathology*; D004195:Disease Models, Animal; D006632:Histamine / Q000494:pharmacology; D005996:Nitroglycerin / Q000494:pharmacology; D012701:Serotonin / Q000494:pharmacology; D013552:Swine
D012701:Serotonin; D006632:Histamine; D005996:Nitroglycerin