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Circulation. 2001;103:3142-3149

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(Circulation. 2001;103:3142.)
© 2001 American Heart Association, Inc.


Clinical Cardiology: New Frontiers

Evaluation of the Culprit Plaque and the Physiological Significance of Coronary Atherosclerotic Narrowings

Morton J. Kern, MD; Bernhard Meier, MD

From the Department of Internal Medicine, Division of Cardiology, Saint Louis University Health Sciences Center, Saint Louis, Mo (M.J.K.), and the Division of Cardiology, Swiss Cardiovascular Center Bern, University Hospital, Bern, Switzerland (B.M.).

Correspondence to Morton J. Kern, MD, Director, J.G. Mudd Cardiac Catheterization Laboratory, Saint Louis University Health Sciences Center, 3635 Vista Avenue at Grand Blvd, St. Louis, MO 63110. E-mail kernm@slu.edu


Key Words: plaque • atherosclerosis • imaging


*    Introduction
 
Clues to the identification of a plaque as dangerous (ie, vulnerable to sudden activation and/or rupture) before it becomes the culprit of a major, potentially life-threatening event currently must be gleaned from studies examining plaques after the fact.1 2 Although the risk of a given plaque causing a cardiac event, in particular a myocardial infarction, is closely related to the severity of luminal narrowing (complete occlusions excepted), it is incorrect to focus exclusively on the most conspicuous stenoses, that is, the angiographically significant (>70% diameter narrowing) lesions that compete with a larger number of nonsignificant (<50% diameter narrowing) and, at times, inapparent lesions. Because the aggregate risk of rupture associated with many nonsignificant lesions (each with an admittedly lower individual potential) exceeds that of the fewer significant lesions, a myocardial infarction will more likely originate from a nonsignificant lesion.3

In addressing atherosclerotic plaques, coronary interventionists strive to achieve the following 2 primary therapeutic goals: (1) the elimination of angina and (2) the prevention of myocardial infarction and death. The first goal may be readily achieved with revascularization, either by percutaneous coronary interventions (PCI) or coronary bypass surgery. Methods to identify and neutralize a vulnerable plaque before it produces a coronary occlusion are new and as-yet unproven, and the therapeutic approaches in some cases are highly controversial.4

To these ends, the interventionist is handicapped when relying solely on contrast angiography to identify fine details of coronary artery disease because lumenology has an inherent inability to evaluate the vessel wall, atherosclerotic plaque dimensions, . . . [Full Text of this Article]




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