Rosenson R S, Lowe G D
Department of Medicine, Rush-Presbyterian-St. Luke's Medical Center, Chicago, IL 60612, USA.
Atherosclerosis. 1998 Oct;140(2):271-80. doi: 10.1016/s0021-9150(98)00144-0.
Atherosclerotic plaque rupture and erosions precipitate thrombus formation and may lead to an acute ischemic syndrome. Lipids and lipoproteins modulate the expression and/or function of thrombotic, fibrinolytic and rheologic factors, and thereby influence hemostasis and potential tissue damage resulting from vascular injury. Triglyceride-enriched lipoproteins are accompanied by elevations in factor VII clotting activity, plasminogen activator inhibitor (PAI-1) and viscosity of blood and plasma. Low density lipoprotein (LDL) promotes platelet activation and tissue factor expression and LDL levels correlate with levels of vitamin K dependent coagulation factors and fibrinogen. Conversely, LDL inhibits tissue factor pathway inhibitor (TFPI) which limits activation of the extrinsic coagulation pathway. High density lipoprotein (HDL) has anti-atherothrombotic properties that result from inhibition of platelet and erythrocyte aggregation, reduced blood viscosity and suppression of tissue factor activity and PAI-1 activity and antigen levels. The effects of lipids and lipoproteins on hemostasis and rheology may have important implications for the clinical sequelae following plaque disruption and erosion.
动脉粥样硬化斑块破裂和糜烂会促使血栓形成，并可能导致急性缺血综合征。脂质和脂蛋白可调节血栓形成、纤维蛋白溶解和流变学因子的表达及功能，从而影响止血以及血管损伤导致的潜在组织损伤。富含甘油三酯的脂蛋白伴随着凝血因子VII凝血活性、纤溶酶原激活物抑制剂（PAI-1）以及血液和血浆粘度的升高。低密度脂蛋白（LDL）促进血小板活化和组织因子表达，且LDL水平与维生素K依赖性凝血因子和纤维蛋白原水平相关。相反，LDL抑制组织因子途径抑制剂（TFPI），而TFPI可限制外源性凝血途径的激活。高密度脂蛋白（HDL）具有抗动脉粥样硬化血栓形成特性，这源于其对血小板和红细胞聚集的抑制、血液粘度降低以及组织因子活性、PAI-1活性和抗原水平的抑制。脂质和脂蛋白对止血和流变学的影响可能对斑块破裂和糜烂后的临床后遗症具有重要意义。
