Atherosclerotic vascular disease is the leading cause of death in the United States and much of the industrialized world and is rapidly gaining the same dubious distinction in the developing world (1). Atherosclerosis involves the development of a plaque composed of variable amounts of connective tissue matrix (collagen, proteoglycans, glycoseaminoglycans), vascular smooth muscle cells, lipoproteins, calcium, inflammatory cells (chiefly monocyte-derived macrophages, T lymphocytes, and mast cells) and new blood vessels (neoangiogenesis). The precise etiology and pathogenesis of atherosclerosis are incompletely understood but an emerging paradigm suggests that atherosclerosis may reflect a chronic inflammatory response to vascular injury caused by a variety of agents that activate or injure endothelium, or promote lipoprotein infiltration, lipoprotein retention, and lipoprotein oxidation (2). © 2006 Humana Press Inc.
CITATION STYLE
Shah, P. K. (2006). Pathogenesis of atherosclerosis. In Essential Cardiology: Principles and Practice: Second Edition (pp. 409–418). Humana Press. https://doi.org/10.1007/978-1-59259-918-9_22
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