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REVIEW

Vulnerable Plaque: Pathobiology and Clinical Implications

Iftikhar J. Kullo, MD; William D. Edwards, MD; and Robert S. Schwartz, MD

15 December 1998 | Volume 129 Issue 12 | Pages 1050-1060

Purpose: To review the pathobiology and clinical implications of vulnerable coronary atherosclerotic plaques and to discuss the identification of vulnerable plaques and mechanisms of plaque stabilization.

Data Sources: English-language articles in the MEDLINE database that were published from 1966 to the present, identified by using the terms atherosclerotic plaque, myocardial revascularization, and plaque stabilization. Selected references cited in identified articles were reviewed.

Study Selection: Experimental, clinical, and basic research studies related to coronary atherosclerotic plaques.

Data Synthesis: Rupture at the site of a vulnerable atherosclerotic plaque is the most frequent cause of acute coronary syndromes. Typically, such plaque does not cause high-grade stenosis and has a large lipid core and a thin fibrous cap that is often infiltrated by inflammatory cells. Mechanical stresses contribute to plaque vulnerability, and certain triggers may cause plaque disruption directly. The most important consequence of plaque rupture is thrombosis. No method reliably identifies plaques prone to rupture. The reduction of coronary events by lipid-lowering agents despite only modest luminal changes suggests that these agents have a plaque-stabilizing effect. Surgical or percutaneous revascularization does not address the basic biology of coronary atherosclerosis and therefore may have little effect on plaque vulnerability.

Conclusions: Improved understanding of the biology of atheromatous plaques has led to the concept of plaque vulnerability. Identification and stabilization of vulnerable plaques are important new directions in the treatment of coronary atherosclerosis. The relative benefits of aggressive medical therapy aimed at plaque stabilization should be compared with those of revascularization in the management of chronic coronary artery disease.

Author and Article Information

From the Mayo Clinic and Mayo Foundation, Rochester, Minnesota.
Grant Support: In part by the Mayo Foundation Clinician-Investigator Training Program (Dr. Kullo) and by the Minnesota affiliate of the American Heart Association (Dr. Kullo).
Requests for Reprints: Iftikhar J. Kullo, MD, Mayo Clinic, 200 First Street SW, Rochester, MN 55905.
Current Author Addresses: Drs. Kullo, Edwards, and Schwartz: Mayo Clinic, 200 First Street SW, Rochester, MN 55905.

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