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Arteriosclerosis, Thrombosis, and Vascular Biology
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Published Online
on August 12, 2004

Arteriosclerosis, Thrombosis, and Vascular Biology. 2004
Published online before print August 12, 2004, doi: 10.1161/01.ATV.0000142373.72662.20
A more recent version of this article appeared on October 1, 2004
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Submitted on March 12, 2004
Accepted on July 30, 2004

Finding Vulnerable Atherosclerotic Plaques. Is It Worth the Effort?

Mohammad Madjid ; Alireza Zarrabi ; Silvio Litovsky ; James T. Willerson ; and Ward Casscells *

From the Department of Internal Medicine/Division of Cardiology (M.M., A.Z.) and Department of Pathology (S.L.), School of Medicine, University of Texas-Houston Health Science Center and Texas Heart Institute, Houston, Tex; the Department of Internal Medicine and President of the University of Texas Health Science Center at Houston (J.T.W.), Medical Director, Texas Heart Institute, and Chief of Cardiology at St. Luke’s Episcopal Hospital, Houston, Tex; the Department of Medicine (Cardiology) and Public Health (W.C.), Vice President of Biotechnology, School of Medicine, University of Texas-Houston Health Science Center, and Associate Director of Cardiology Research Texas Heart Institute/St. Luke’s Episcopal Hospital, Houston, Tex, and Division of Cardiology/Department of Internal Medicine, Medical School, The University of Texas Health Science Center at Houston, The Texas Heart Institute at St. Luke’s Episcopal Hospital, and President Bush Center for Cardiovascular Health at Memorial Hermann Hospital, Houston, Tex.

* To whom correspondence should be addressed. E-mail: s.ward.casscells{at}uth.tmc.edu.

Abstract--Techniques to identify and treat vulnerable plaques are the focus of enormous research. Some have questioned the benefit of locating individual vulnerable plaque in a multifocal disease. On autopsy, it is found that most deaths are caused by thrombotic occlusion of a single plaque; simultaneous occurrence of 2 occlusive thrombi is rare, but a second vulnerable plaque is common, particularly in acute myocardial infarction (MI). Angiographic progression is poorly predicted by risk factors, and angiographic progression is a weak predictor of MI or death. Intravascular ultrasonography (intravascular ultrasound [IVUS]) studies find plaque rupture in most MI patients and in approximately half with unstable angina, but in only a minority of patients with stable angina. IVUS identifies a second vulnerable plaque in many patients with unstable angina, and in most MI patients. Angioscopy reveals a very low incidence of a second vulnerable plaque compared with angiography and IVUS, but identifies additional yellow plaques in many patients with stable angina and in most patients with unstable angina or MI. Using thermography catheters and a temperature cutoff of 0.1°C, approximately half the patients with stable angina have >1 hot lesion; however, if the cutoff is 0.2°C, only {approx}15% have a second hot lesion. New imaging techniques may detect additional characteristics of plaques and new predictive models may assess the risk of vulnerable plaques and patients. This approach enables physicians to "buy time" by application of local therapies until systemic therapies stabilize plaques. This may also reduce the risk in subjects in whom systemic therapies do not work.




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