Journal
STROKE
Volume 39, Issue 11, Pages 3092-3095Publisher
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1161/STROKEAHA.108.517128
Keywords
atherosclerosis; carotid artery disease; inflammation; lipids; stroke
Categories
Funding
- Medinnova Foundation
- Eckbo's Foundation
- Novo Nordisk Foundation
- Danish Diabetes Association
- Danish Medical Research Council
- Rikshospitalet Medical Center
Ask authors/readers for more resources
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, beta-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. (Stroke. 2008; 39: 3092-3095.)
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available