ISSN:
1435-1803
Keywords:
Coronary vasomotion
;
myocardial stunning
;
quantitative coronary angiography
;
endothelial stunning
;
PTCA
Source:
Springer Online Journal Archives 1860-2000
Topics:
Medicine
Notes:
Abstract The term “stunned” moycardium describes a dysfunction of the myocardium which may persist for hours, days or even weeks after restoration of coronary blood flow following thrombolysis, percutaneous transluminal coronary angioplasty (PTCA) or aorto-coronary bypass grafting (7, 9). The “stunned” myocardium is characterized — despite marked dyskinesis — by near, normal levels of myocardial perfusion and normal or even enhanced oxygen consumption (2), probably due to higher oxygen requirements of the contractile elements. Thus, a mismatch between function and flow exists which has been recognized to be a characteristic finding of the “stunned” myocardium. However, coronary reperfusion may result in an attenuation of the endothelial response to coronary vasodilators such as acetylcholine, bradykinin, etc. (3). It is well established that prolonged myocardial ischemia is associated with irreversible myocardial damage and profound structural and functional derangements of the coronary microvasculature which may persist even if perfusion is restored (1). Local vasoactive substances such as the endotheliumdependent relaxing factor (EDRF) also play an important role in the regulation of myocardial perfusion. EDRF is a potent vasodilator which is released from the coronary endothelium but is reduced in patients with atherosclerotic plaques or hypercholesterolemia (=endothelial dysfunction). Since there are shear-stress dependent flow receptors, EDRF is released proportionally to coronary flow, i.e., the higher the flow the larger the artery and vice versa. However, flow regulation is dependent on several factors such as perfusion pressure, peripheral resistance, sympathetic activation, oxygen saturation, metabolic factors etc. EDRF is synthetized in the endothelial cells and is rapidly broken down during ischemia by superoxide radicals which inactivate EDRF and, thus, decrease flow induced vasodilation (6). Neutrophil aggregation may further contribute to this process by the release of proteolytic enzymes which can convert oxygen to superoxide anions, i.e., oxygen free radicals. These radicals may injure the endothelium when generated in large amounts such as during ischemia (4) and may sensitize the smooth vasculature to contraction by alpha-adrenergic mechanisms (8).
Type of Medium:
Electronic Resource
URL:
http://dx.doi.org/10.1007/BF00797902
Permalink
