The imbalance of coagulation and fibrinolysis in coronary heart disease and its relation to traditional risk factors

Abstract

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