Arthur C. Fox, MD; Richard I. Levin, MD
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Current Author Addresses: Drs. Fox and Levin: Cardiology Section, New York University School of Medicine, 550 First Avenue, New York, NY 10016.
Fox A., Levin R.; Ruptured Plaques and Leaking Cells: Cost-Effectiveness in the Diagnosis of Acute Coronary Syndromes. Ann Intern Med. 1999;131:968-970. doi: 10.7326/0003-4819-131-12-199912210-00011
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Published: Ann Intern Med. 1999;131(12):968-970.
Acute coronary syndromes arise when an atherosclerotic plaque becomes unstable. The cap develops either superficial erosions with overlying thrombus or, more commonly, deep fissures that cause the plaque to swell with clotted blood and encroach on the arterial lumen. Plaques become unstable when the fibrous matrix surrounding the lipid core is attenuated by the action of cytokines from T lymphocytes, which inhibit the synthesis of the matrix, and by metalloproteinases from activated macrophages, which degrade the matrix. The cause of the initial surface breach of the weakened cap may be chemical, caused by reactive oxygen species, or mechanical, caused by focal stresses. The consequent growing fault may reach the plaque center; the resulting acute eruption of the lipid core amplifies local thrombosis. Abrupt occlusion of an artery unprotected by recruitable collaterals leads to acute regional ischemia. Complete and persistent occlusion produces myocardial infarction. Partial occlusion or occlusion that waxes and wanes results in unstable angina. Plaques can be multiple or single, regress, develop recurrent instability, or remain dormant for years (1-3). Study of the unstable plaque thus resembles volcanology and plate tectonics; the detection of clinical and biological markers of plaque instability, ischemia, and infarction is like seismography.
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Cardiology, Emergency Medicine, Acute Coronary Syndromes, Coronary Heart Disease.
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Print ISSN: 0003-4819 | Online ISSN: 1539-3704
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