作者: Kaj Winther , Steen Elkjær Husted , Hans Kræmmer Nielsen , Jørn Dalsgaard Nielsen
DOI: 10.1007/978-94-009-1577-0_10
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摘要: Two major hypotheses to explain the pathogenesis of atherosclerotic disease — thrombogenic and lipid hypothesis have dominated in past century. The theory was postulated by Rokitansky, who 1844 described intimai thickening resulting from fibrin deposition with subsequent organization fibroblast accumulation. He deduced that deposit derived arterial blood, reviving idea dyscrasia, which had been popular antiquity [1]. proposed Virchow 1856, observed atherosclerosis located subendothelial layer, therefore could not be surface deposits [2]. Both theories integrated into one single multifactorial involves common step endothelial dysfunction as a reponse injury developed Ross [3]. One or more risk factors (hyperlipidemia, smoking, obesity, hypertension, diabetes etc.) plus local such shear stress are hypothesized contribute development lesions.