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(Stroke. 2005;36:2337.)
© 2005 American Heart Association, Inc.
Editorials |
From the Department of Radiology, Erasmus MC-University Medical Center Rotterdam, Rotterdam, The Netherlands.
Correspondence to Aad van der Lugt, MD, PhD, Department of Radiology, Erasmus MC-University Medical Center Rotterdam, Dr. Molewaterplein 40, 3015 GD, Rotterdam, The Netherlands. E-mail a.vanderlugt@erasmusmc.nl
Key Words: atherosclerosis MRI
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
See related article, pages 25072516
Atherosclerosis remains a major cause of death in industrialized countries. Our understanding of the natural course of the disease and of the effects of intervention is mainly based on autopsy studies and on studies in animal models. This has primarily been because of the lack of good tools to image plaque components in vivo. Indeed, even in animal studies, analysis of plaque components has occurred for the most part ex vivo by histologic sections and dedicated staining techniques. In vivo visualization of the atherosclerotic plaque and its components (calcifications, fibrocellular tissue, lipid core, hemorrhage, and thrombus), particularly in humans, will further elucidate the disease process and the effect of various types of interventions, and subsequently will have important clinical implications.
The severity of stenosis in the carotid artery is a well-known predictor of cerebral infarction and is currently the main parameter used in deciding between carotid intervention (endarterectomy or stent placement) and pharmacologic intervention. Plaque morphology is considered an additional, independent predictor of cerebral infarction: plaques containing a necrotic lipid core covered by a thin fibrous cap (known as unstable or vulnerable plaque) are prone to rupture,1,2 releasing thromboembolic particles to the brain. Therefore, noninvasive, in vivo assessment of plaque components in the carotid artery would be useful in therapy determination.
Carotid stenosis of a severity that warrants surgical or endovascular treatment is found in 10 to 20% of all patients with transient ischemic attack (TIA) or ischemic stroke. Atrial fibrillation occurs in 5%
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