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PERSPECTIVE

Prevention of Plaque Rupture: A New Paradigm of Therapy

James S. Forrester, MD

19 November 2002 | Volume 137 Issue 10 | Pages 823-833

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.

Author and Article Information

From Cedars-Sinai Medical Center, Los Angeles, California.

Requests for Single Reprints: James S. Forrester, MD, Division of Cardiology, Cedars-Sinai Medical Center, 8700 Beverly Boulevard, Los Angeles, CA 90048.

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