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Prevention of plaque rupture: a new paradigm of therapy
1Division of Cardiology, Cedars-Sinai Medical Center, Los Angeles, California 90048, USA.
Insights
Acute coronary syndromes result from unstable atheroma rupture. New insights into plaque instability
Area of Science:
- Cardiovascular Medicine
- Cell Biology
- Pathology
Background:
- Acute coronary syndromes (ACS), including unstable angina and myocardial infarction, stem from the rupture of unstable coronary atheromatous plaques.
- Unstable plaques are characterized by a large lipid core, abundant inflammatory cells, and a thin fibrous cap, and may be asymptomatic before rupture.
Purpose of the Study:
- To identify the cellular processes underlying unstable plaque formation.
- To propose novel therapeutic strategies based on understanding plaque cell biology.
Main Methods:
- Histologic examination of unstable plaques to identify key features.
- Review of recent cell biology research on plaque instability.
- Development of therapeutic strategies targeting identified cellular processes.
Main Results:
- The cellular mechanisms driving the development of unstable plaque's characteristic features have been elucidated.
- New therapeutic targets include endothelial passivation, LDL reduction, LDL oxidation inhibition, and anti-inflammatory strategies.
Conclusions:
- Understanding the cell biology of plaque instability offers promising new therapeutic avenues for ACS.
- Targeting these pathways could lead to significant reductions in ACS morbidity and mortality, building on recent advances.
Abstract:
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.
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