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Prevention of plaque rupture: a new paradigm of therapy

Acute coronary syndromes--unstable angina, myocardial infarction, and sudden cardiac death--are caused by acute disruption of an unstable coronary atheroma. Unstable plaques have three histologic characteristics: a large lipid core, many inflammatory cells, and a thin fibrous cap. Because the unstab... Full description

Journal Title: Annals of internal medicine 19 November 2002, Vol.137(10), pp.823-33
Main Author: Forrester, James S
Format: Electronic Article Electronic Article
Language: English
Subjects:
ID: E-ISSN: 1539-3704 ; PMID: 12435220 Version:1
Link: http://pubmed.gov/12435220
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recordid: medline12435220
title: Prevention of plaque rupture: a new paradigm of therapy
format: Article
creator:
  • Forrester, James S
subjects:
  • Coronary Artery Disease -- Prevention & Control
ispartof: Annals of internal medicine, 19 November 2002, Vol.137(10), pp.823-33
description: Acute coronary syndromes--unstable angina, myocardial infarction, and sudden cardiac death--are caused by acute disruption of an unstable coronary atheroma. Unstable plaques have three histologic characteristics: a large lipid core, many inflammatory cells, and a thin fibrous cap. Because the unstable plaque is not necessarily obstructive, it may cause no symptoms before rupture. The cellular processes that lead to the characteristic histologic features of unstable plaque have recently been identified. This new understanding of the cell biology of plaque instability suggests new therapeutic strategies: passivation of the endothelium, reduction of low-density lipoprotein (LDL) in the vessel wall by decreasing serum LDL levels or accelerating reverse cholesterol transport, inhibition of LDL oxidation, inhibition of inflammatory cytokine expression, and inhibition of thrombus formation. Although the morbidity and mortality resulting from acute coronary disease have been reduced by more than 50% over the past 30 years, it is reasonable to anticipate further reductions of similar magnitude in the decade ahead.
language: eng
source:
identifier: E-ISSN: 1539-3704 ; PMID: 12435220 Version:1
fulltext: fulltext
issn:
  • 15393704
  • 1539-3704
url: Link


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descriptionAcute coronary syndromes--unstable angina, myocardial infarction, and sudden cardiac death--are caused by acute disruption of an unstable coronary atheroma. Unstable plaques have three histologic characteristics: a large lipid core, many inflammatory cells, and a thin fibrous cap. Because the unstable plaque is not necessarily obstructive, it may cause no symptoms before rupture. The cellular processes that lead to the characteristic histologic features of unstable plaque have recently been identified. This new understanding of the cell biology of plaque instability suggests new therapeutic strategies: passivation of the endothelium, reduction of low-density lipoprotein (LDL) in the vessel wall by decreasing serum LDL levels or accelerating reverse cholesterol transport, inhibition of LDL oxidation, inhibition of inflammatory cytokine expression, and inhibition of thrombus formation. Although the morbidity and mortality resulting from acute coronary disease have been reduced by more than 50% over the past 30 years, it is reasonable to anticipate further reductions of similar magnitude in the decade ahead.
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titlePrevention of plaque rupture: a new paradigm of therapy
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abstractAcute coronary syndromes--unstable angina, myocardial infarction, and sudden cardiac death--are caused by acute disruption of an unstable coronary atheroma. Unstable plaques have three histologic characteristics: a large lipid core, many inflammatory cells, and a thin fibrous cap. Because the unstable plaque is not necessarily obstructive, it may cause no symptoms before rupture. The cellular processes that lead to the characteristic histologic features of unstable plaque have recently been identified. This new understanding of the cell biology of plaque instability suggests new therapeutic strategies: passivation of the endothelium, reduction of low-density lipoprotein (LDL) in the vessel wall by decreasing serum LDL levels or accelerating reverse cholesterol transport, inhibition of LDL oxidation, inhibition of inflammatory cytokine expression, and inhibition of thrombus formation. Although the morbidity and mortality resulting from acute coronary disease have been reduced by more than 50% over the past 30 years, it is reasonable to anticipate further reductions of similar magnitude in the decade ahead.
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