The rupture or fissuring of a coronary atherosclerotic plaque and subsequen
t thrombosis is considered the key event in the pathogenesis of unstable an
gina and myocardial infarction. Although plaque disruption frequently occur
s during the evolution of atherosclerosis, only a minority of ruptured plaq
ues develop thrombosis. The content and procoagulant activity of tissue fac
tor in human coronary atherosclerotic plaques varies widely, and different
studies confirm that it is higher in the plaques extracted from patients wi
th unstable angina, myocardial infarction or histologic/angiographic eviden
ce of coronary thrombosis than in those taken from patients with stable ang
ina or uncomplicated coronary lesions. Variations in tissue factor content
and activity may be responsible for the different thrombotic responses to h
uman coronary atherosclerotic plaque rupture. (C) 2000 Published by Elsevie
r Science B.V. All rights reserved.