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(Stroke. 2008;39:3092.)
© 2008 American Heart Association, Inc.

Research Letters

Soluble CD36 in Plasma Is Increased in Patients With Symptomatic Atherosclerotic Carotid Plaques and Is Related to Plaque Instability

Aase Handberg, MD, DMSc; Mona Skjelland, MD; Annika E. Michelsen, MSc; Ellen Lund Sagen, BSc; Kirsten Krohg-Sørensen, MD, PhD; David Russell, MD, PhD; Arve Dahl, MD, PhD; Thor Ueland, PhD; Erik Øie, MD, PhD; Pål Aukrust, MD, PhD Bente Halvorsen, MSc, PhD

From the Department of Clinical Biochemistry (A.H.), Aarhus University Hospital, Aarhus, Denmark; and the Department of Neurology (M.S., D.R., A.D.), the Research Institute for Internal Medicine (A.E.M., E.L.S., T.U., P.A., B.H.), the Department of Thoracic and Cardiovascular Surgery (K.K.-S.), the Section of Endocrinology (T.U.), the Department of Cardiology (E.Ø.), and the Section of Clinical Immunology and Infectious Diseases (P.A.), Rikshospitalet Medical Center, University of Oslo, Oslo, Norway.

Correspondence to Bente Halvorsen, MSc, PhD, Research Institute of Internal Medicine, Rikshospitalet Medical Center, N-0027 Oslo, Norway. E-mail bente.halvorsen{at}rr-research.no

Background and Purpose— The risk for cardiovascular events is related to the composition and stability of an atherosclerotic plaque driven by inflammation and deposition of lipids. Scavenger receptors are a family of cell surface receptors involved in lipid uptake and inflammation. Recently, we found that soluble CD36 is increased in plasma from patients with diabetes strongly correlated with insulin resistance.

Methods— We tested whether soluble CD36 is a marker of plaque stability in patients with high-grade internal carotid stenoses (n=62). The patients were classified according to plaque symptomatology and plaque echogenicity on ultrasound examination.

Results— When patients were divided into 3 groups according to the latest clinical symptoms from plaques (ie, symptoms within the last 2 months [n=16], symptoms within the last 2 to 6 months [n=15], or asymptomatic [n=31]), the former group had significantly raised plasma levels of soluble CD36 as compared with the other 2 groups. In contrast, we found no differences in plasma levels of C-reactive protein, β-thromboglobulin, lipid parameters, or HbA1C between these groups. The patients with echolucent carotid plaques (n=20) tended to have higher soluble CD36 levels in plasma compared with those with echogenic/heterogenic plaque (n=39; P=0.087). By immunohistochemistry, CD36 was localized to macrophages-rich area of intima within the atherosclerotic lesion.

Conclusion— We propose that sCD36 may be a marker of plaque instability and symptomatic carotid atherosclerosis, possibly at least partly as a result of CD36 release to the circulation from the foam cells within the atherosclerotic lesion.

Key Words: atherosclerosis • carotid artery disease • inflammation • lipids • stroke

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