| Pathophysiology of coronary artery disease. | |
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MedLine Citation:
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PMID: 8653652 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Atherogenic risk factors provoke chronic injury to the endothelium in certain parts of the arterial tree leading to dysfunctional endothelium. Lipid accumulation, macrophage formation, and smooth muscle cell proliferation are key events in the initial slow progression of atherosclerotic lesions (phase 1). If extracellular lipid accumulation predominates, atherosclerotic process progresses into a more clinically relevant, advance lipid-rich lesion (phase 2)--the pathogenic basis for plaque rupture and thrombus formation. Small plaque fissures and mural thrombus formation may be responsible for the rapid, clinically silent progression of lesions (phase 3). Plaque rupture with large thrombus formation may be responsible for acute coronary syndromes (phase 4). Alternatively, if smooth muscle cell proliferation and collagen matrix synthesis predominate, atherosclerotic lesions may progress into advanced, stable sclerotic lesions (phase 5). |
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Authors:
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A Fernández-Ortiz; V Fuster |
Publication Detail:
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Type: Journal Article; Review |
Journal Detail:
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Title: Clinics in geriatric medicine Volume: 12 ISSN: 0749-0690 ISO Abbreviation: Clin. Geriatr. Med. Publication Date: 1996 Feb |
Date Detail:
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Created Date: 1996-07-31 Completed Date: 1996-07-31 Revised Date: 2007-11-15 |
Medline Journal Info:
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Nlm Unique ID: 8603766 Medline TA: Clin Geriatr Med Country: UNITED STATES |
Other Details:
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Languages: eng Pagination: 1-21 Citation Subset: IM |
Affiliation:
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San Carlos University Hospital, Complutense University, Madrid, Spain. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Aged Coronary Artery Disease / etiology, physiopathology* Coronary Disease / etiology, physiopathology Humans Risk Factors |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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