Coronary artery spasm. Multiple causes and multiple roles in heart disease.
Myocardial infarction and sudden cardiac death may be initiated by a sudden intense localized contraction of coronary artery smooth muscle. When this event occurs around a vulnerable eccentric lipid-filled plaque, rupture and extrusion of plaque contents and exposure of collagen occur. This may sometimes be a silent and self-limiting event; other times it leads to thrombus formation. A second wave of spasm due to accumulated platelet and inflammatory mediators may compound the contractile consequences of the initiating event. Spasm involves intrinsic smooth muscle cell electrical mechanisms, hyper-responsive cells, and multiple agonists that synergize their actions, and the involvement of each mechanism varies at different times in the sequence of vascular occlusion. Study of spasm requires vascular systems that adequately model coronary artery responses of the ageing human heart. As previously emphasized, tissues obtained postmortem, and when possible from recipients during heart transplants, must be integral to theory building, alongside animal models, despite the experimental limitations such tissues impose. A multidisciplinary approach, at all levels of vascular physiology and pharmacology, will be necessary to understand coronary motor activity and human heart disease.
Kalsner
S
S
Department of Physiology, City University of New York Medical School, New York City 10031, USA.
D000818:Animals; D003327:Coronary Disease / Q000209:etiology* / Q000503:physiopathology; D003328:Coronary Thrombosis / Q000209:etiology; D004730:Endothelium, Vascular / Q000503:physiopathology; D006801:Humans; D009131:Muscle, Smooth, Vascular / Q000503:physiopathology*; D009203:Myocardial Infarction / Q000209:etiology; D013035:Spasm / Q000209:etiology; D014662:Vasoconstrictor Agents / Q000009:adverse effects
D014662:Vasoconstrictor Agents