(Circulation. 2002;106:760.)
© 2002 American Heart Association, Inc.
Editorial |
From the Department of Cardiovascular Medicine, The Cleveland Clinic Foundation, Cleveland, Ohio.
Correspondence to Stephen G. Ellis, MD, Sones Cardiac Catheterization Laboratories, Department of Cardiovascular Medicine, The Cleveland Clinic Foundation, 9500 Euclid Ave, F-24, Cleveland, Ohio, 44195. E-mail elliss@ccf.org
Key Words: Editorials coronary disease plaque ultrasonics imaging
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
In this issue of Circulation, Rioufol et al1 describe the presence of multiple ruptured atherosclerotic coronary plaques in patients presenting with an acute coronary syndrome (ACS). With the use of intravascular ultrasound (IVUS), the authors systematically examined proximal portions of the entire coronary tree in 24 patients. Ruptured plaques were found at the culprit lesion in 9 patients (37.5%) but, more importantly, distant from the culprit lesion in 19 patients (79%). These additional ruptured plaques were frequently multiple, located in a vessel different from the culprit vessel in 70% of patients and in 2 vessels not related to the acute event in 12% of patients. Both culprit lesions and additional ruptured plaques were characterized by positive remodeling. The authors proceeded with coronary stent placement at the culprit lesion site in 19 patients (86%) and, on the basis of angiographic and IVUS criteria (minimum luminal diameter <1.5 mm, minimum luminal cross-sectional-area <4 mm2), at additional sites in 16 patients (72%).
See p 804
It is important to consider these findings in the context of the recent literature. Traditional diagnostic criteria of lesion significance define focal, hemodynamically significant plaques that cause acute or chronic impairment of coronary blood flow. These lesions are identified by selective coronary angiography. However, it is well known from angiographic studies that most myocardial infarctions occur at sites that previously caused only mild-to-moderate luminal stenosis.2 In histological studies of patients with coronary artery disease who died suddenly, the plaque at the culprit lesion site shows evidence
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