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Thrombogenesis in Acute Coronary Syndromes

Thrombogenesis in Acute Coronary Syndromes It is well‐established that intracoronary thrombosis, which may be associated with plaque fissure and enhanced coronary vasoconstriction, is the immediate cause of a sudden impairment of regional myocardial perfusion, which is transient in unstable angina and is, eventually, irreversible in acute myocardial infarction. It is also well‐known that increased platelet reactivity, increased procoagulant activity, and reduced endogenous fibrinolysis are risk factors for acute coronary events. Nevertheless, the primary causes responsible for sudden intracoronary thrombosis and for coronary vasoconstriction causing acute coronary syndromes are still largely speculative. Recent studies have shown activated inflammatory cells both in the coronary arterial wall and in the systemic circulation of patients with unstable angina. Furthermore, the intensity of the inflammatory response is correlated with an adverse prognosis. This inflammatory component may have important pathogenetic and prognostic roles because an outburst of inflammatory cytokines has the potential to increase the sensitivity of platelets to agonists, to turn the anticoagulant and vasodilator physiological properties of the endothelium into procoagulant and vasoconstrictor properties, and to cause plaque fissure by the release of proteolytic enzymes. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Journal of Interventional Cardiology Wiley

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References (53)

Publisher
Wiley
Copyright
Copyright © 1995 Wiley Subscription Services, Inc., A Wiley Company
ISSN
0896-4327
eISSN
1540-8183
DOI
10.1111/j.1540-8183.1995.tb00924.x
Publisher site
See Article on Publisher Site

Abstract

It is well‐established that intracoronary thrombosis, which may be associated with plaque fissure and enhanced coronary vasoconstriction, is the immediate cause of a sudden impairment of regional myocardial perfusion, which is transient in unstable angina and is, eventually, irreversible in acute myocardial infarction. It is also well‐known that increased platelet reactivity, increased procoagulant activity, and reduced endogenous fibrinolysis are risk factors for acute coronary events. Nevertheless, the primary causes responsible for sudden intracoronary thrombosis and for coronary vasoconstriction causing acute coronary syndromes are still largely speculative. Recent studies have shown activated inflammatory cells both in the coronary arterial wall and in the systemic circulation of patients with unstable angina. Furthermore, the intensity of the inflammatory response is correlated with an adverse prognosis. This inflammatory component may have important pathogenetic and prognostic roles because an outburst of inflammatory cytokines has the potential to increase the sensitivity of platelets to agonists, to turn the anticoagulant and vasodilator physiological properties of the endothelium into procoagulant and vasoconstrictor properties, and to cause plaque fissure by the release of proteolytic enzymes.

Journal

Journal of Interventional CardiologyWiley

Published: Dec 1, 1995

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