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“It is ironic and instructive that in the age of cellular and molecular biology, great advances in our understanding of the pathophysiology of cardiovascular disease continue to be made by pathologists who perform meticulous and imaginative studies”—Heistad.1
Acute coronary syndromes, including unstable angina, myocardial infarction, and sudden ischaemic death, are a leading cause of morbidity and mortality in the Western world. Current pharmacological and mechanical (angioplasty, bypass surgery, stenting) interventions have been effective, but treatment can be improved with more potent pharmacologic strategies based on an understanding of the underlying pathogenic processes. Critical steps in the development of acute coronary syndromes are the disruption of atherosclerotic plaque and the superimposed formation of the platelet-rich thrombus.2
ATHEROSCLEROTIC PLAQUE DESTABILISATION
Atherosclerotic plaques differ widely in the relative content of major constituents: collagen, proteoglycans, intracellular lipid, and extracellular lipid, even within a single individual. Predominance of collagen and proteoglycans results in fibrous plaques that are more common in patients with stable coronary artery disease and have accordingly been designated as “stable” plaques (fig 1). Lipid-rich or “vulnerable” …
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