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Previous Volume 349:2316-2325 December 11, 2003 Number 24 Next

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ABSTRACT

Background Intraplaque hemorrhage is common in advanced coronary atherosclerotic lesions. The relation between hemorrhage and the vulnerability of plaque to disruption may involve the accumulation of free cholesterol from erythrocyte membranes.

Methods We stained multiple coronary lesions from 24 randomly selected patients who had died suddenly of coronary causes with an antibody against glycophorin A (a protein specific to erythrocytes that facilitates anion exchange) and Mallory's stain for iron (hemosiderin), markers of previous intraplaque hemorrhage. Coronary lesions were classified as lesions with pathologic intimal thickening, fibrous-cap atheromas with cores in an early or late stage of necrosis, or thin-cap fibrous atheromas (vulnerable plaques). The arterial response to plaque hemorrhage was further defined in a rabbit model of atherosclerosis.

Results Only traces of glycophorin A and iron were found in lesions with pathologic intimal thickening or fibrous-cap atheromas with cores in an early stage of necrosis. In contrast, fibroatheromas with cores in a late stage of necrosis or thin caps had a marked increase in glycophorin A in regions of cholesterol clefts surrounded by iron deposits. Larger amounts of both glycophorin A and iron were associated with larger necrotic cores and greater macrophage infiltration. Rabbit lesions with induced intramural hemorrhage consistently showed cholesterol crystals with erythrocyte fragments, foam cells, and iron deposits. In contrast, control lesions from the same animals had a marked reduction in macrophages and lipid content.

Conclusions By contributing to the deposition of free cholesterol, macrophage infiltration, and enlargement of the necrotic core, the accumulation of erythrocyte membranes within an atherosclerotic plaque may represent a potent atherogenic stimulus. These factors may increase the risk of plaque destabilization.

Source Information

From the Department of Cardiovascular Pathology, Armed Forces Institute of Pathology, Washington, D.C. (F.D.K., A.P.B., D.K.W., A.F., R.K., R.V.); the Cardiac Unit, Department of Internal Medicine, Massachusetts General Hospital, Boston (H.K.G., L.J.G., M.H., A.V.F.); the Department of Pathology, University of Maryland, Baltimore (D.R.F.); the Section of Experimental Atherosclerosis, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Md. (H.S.K.); and Drexel University College of Medicine, Philadelphia (J.N.).

Address reprint requests to Dr. Virmani at the Department of Cardiovascular Pathology, Armed Forces Institute of Pathology, Bldg. 54, Rm. 2005, 6825 16th St., Washington, DC 20306-6000, or at virmani{at}afip.osd.mil.

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