EDITORIAL

The erythrocyte: a new player in atheromatous core formation

G Pasterkamp¹, R Virmani²

¹ Experimental Cardiology Laboratory, Utrecht Medical Center and the Interuniversity Cardiology Institute of the Netherlands, Utrecht, The Netherlands
² Department of Cardiovascular Pathology, Armed Forces Institute of Pathology, Washington DC, USA

Correspondence to:
Correspondence to:
Dr G Pasterkamp, Experimental cardiology Laboratory, Utrecht Medical Center, Room G02-523, 3584 CX Utrecht, the Netherlands;
g.pasterkamp@hli.azu.nl

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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

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Keywords: erythrocyte; atheroma core formation; atherosclerotic disease

The first 150 words of the full text of this article appear below.

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 . . . [Full text of this article]

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