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The membrane of the red blood cell hides constituents that are lipid rich and can bind to macrophage scavenger receptors, thus posing the challenging hypothesis that erythrocytes contribute to atheroma formation in coronary arteries
In atherosclerotic disease, proliferation of smooth muscle cells, matrix synthesis, and lipid accumulation narrows the lumen. Thrombus formation may be superimposed on mature plaques by rupture or superficial erosion of the atherosclerotic lesion1 leading to unstable angina and myocardial infarction. The three determinants of a plaque's vulnerability to rupture are the size of the atheromatous core, the thickness of the fibrous cap covering the core, and inflammation within the cap.
The size of the atheromatous core seems critical for the stability of the plaque. Postmortem studies revealed larger atheromatous cores in lesions that rupture compared with lesions that have an intact surface or in atheromas with a thin cap (vulnerable plaque).2 Furthermore, Davies and colleagues3 found a relation between core size and the occurrence of plaque rupture. They identified a threshold for rupture prone atherosclerotic plaques when the core occupied more than 40% of the atherosclerotic lesion. The consistency of the core also seems important for plaque stability. Liquid cholesteryl esters soften while crystalline cholesterol stiffens the atheroma. If temperature increases, as with inflammation,4 the core gets softer resulting in less stability. Virmani and colleagues reported a higher percentage of area occupied by the cholesterol cleft in sections with plaque rupture than in thin cap atheromas.2 The atheromatous core is rich in extracellular lipid, avascular, and the only cells are macrophages that are …