MINI-SYMPOSIUM
Pathological changes in the coronary arteries in the acute coronary syndromes
Department of Pathology AZ-Middelheim Antwerp, and the department of Pharmacology University of Antwerp, Belgium
Correspondence to:
Correspondence to:
Dr Mark Kockx
Department of Pathology AZ-Middelheim Antwerp, Belgium; kockx@histogenex.com
Keywords: acute coronary syndromes; coronary arteries
| The first 150 words of the full text of this article appear below. |
"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 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
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