ATHEROSCLEROTIC PLAQUES IN HUMAN CORONARY ARTERIES
Keywords:
Atherosclerosis, lipids, stroke, inflammatory cells, plaque.Abstract
Atherosclerosis or coronary artery disease (CAD) is the most common form of cardiovascular disease (CVD) where the main component is lipid accumulation and inflammation of the large arteries, which eventually may lead to its clinical complications, myocardial infarction (MI) and stroke. As a disease of slow progression, clinically significant atherosclerosis occurs primarily in older individuals and, despite declining incidence in some countries, remains the leading cause of mortality worldwide. Atherosclerotic lesions are characterized by a lifetime long accumulation and transformation of lipids, inflammatory cells, smooth muscle cells, and necrotic cell debris in the intimal space underneath a monolayer of endothelial cells (ECs) that line the interior vessel wall. Typically, lesion growth can reduce blood flow in the lumen by >50% and may cause angina particularly during exercise or stress. Lesions can become unstable and rupture, particularly if they have fatty and inflammatory composition. If this occurs in the coronary arteries, it can result in a local clot that may completely obstruct the blood flow to cause an MI. Alternatively, the clot can escape the heart and travel to the brain where it may cause a stroke.
References
Davies M. J., Woolf N., Rowles P. M., Pepper J. Morphology of the endothelium over atherosclerotic plaques in human coronary arteries. Br Heart J. 1988 Dec;60(6):459–464. doi: 10.1136/hrt.60.6.459.
Driscoll D. M., Getz G. S. Extrahepatic synthesis of apolipoprotein E. J Lipid Res. 1984 Dec 1;25(12):1368–1379.
Eisenberg S., Friedman G., Vogel T. Enhanced metabolism of normolipidemic human plasma very low density lipoprotein in cultured cells by exogenous apolipoprotein E-3. Arteriosclerosis. 1988 Sep-Oct;8(5):480–487. doi: 10.1161/01.atv.8.5.480
Faggiotto A., Ross R., Harker L. Studies of hypercholesterolemia in the nonhuman primate. I. Changes that lead to fatty streak formation. Arteriosclerosis. 1984 Jul-Aug;4(4):323–340. doi: 10.1161/01.atv.4.4.323.
Fazio S., Yao Z., McCarthy B. J., Rall S. C., Jr Synthesis and secretion of apolipoprotein E occur independently of synthesis and secretion of apolipoprotein B-containing lipoproteins in HepG2 cells. J Biol Chem. 1992 Apr 5;267(10):6941–6945.
Gabuzda D. H., Hess J. L., Small J. A., Clements J. E. Regulation of the visna virus long terminal repeat in macrophages involves cellular factors that bind sequences containing AP-1 sites. Mol Cell Biol. 1989 Jun;9(6):2728–2733. doi: 10.1128/mcb.9.6.2728. [DOI]
Gordon V., Innerarity T. L., Mahley R. W. Formation of cholesterol- and apoprotein E-enriched high density lipoproteins in vitro. J Biol Chem. 1983 May 25;258(10):6202–6212.






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