Lassila R
Wihuri Research Institute, Helsinki, Finland.
Eur Heart J. 1993 Dec;14 Suppl K:94-7.
Atherosclerosis is an inflammatory reaction to accumulated extracellular lipid in the arterial intima. Evidence from pathological studies indicate that there is constant deposition and lysis of fibrin within the atherosclerotic arterial wall. In patients with stable peripheral atherosclerosis, the functional severity of the disease is associated with circulating fibrinogen and degradation of cross-linked fibrin reflecting procoagulant activity in the blood-vessel wall interface, or in the wall itself. In atheromas the fibrinolytic activity is connected to macrophages, which can assemble in the plasminogen-plasmin system and generate plasmin-mediated pericellular proteolysis in tissues with inflammation. Plasmin capable of activating collagenase may therefore be a candidate for plaque rupture. The nature of the exposed vascular tissue, the inflammatory state, tissue-factor dependent thrombin generation and the degree of matrix degradation regulate platelet reactivity. Little is yet known about platelet adhesive functions in proteolyzed collagens that are the underlying substrate where platelets deposit during plaque rupture, the triggering event for thrombosis. Research in these areas is likely to improve the understanding of the thrombogenicity of atheromas when the tissue is suddenly exposed to blood.
动脉粥样硬化是对动脉内膜中细胞外脂质积聚的一种炎症反应。病理研究证据表明，在动脉粥样硬化动脉壁内存在纤维蛋白的持续沉积和溶解。在稳定的外周动脉粥样硬化患者中，疾病的功能严重程度与循环纤维蛋白原以及反映血管壁界面或血管壁本身促凝活性的交联纤维蛋白降解有关。在动脉粥样硬化斑块中，纤维蛋白溶解活性与巨噬细胞有关，巨噬细胞可聚集在纤溶酶原 - 纤溶系统中，并在炎症组织中产生纤溶酶介导的细胞周蛋白水解。因此，能够激活胶原酶的纤溶酶可能是斑块破裂的一个因素。暴露的血管组织的性质、炎症状态、组织因子依赖性凝血酶生成以及基质降解程度调节血小板反应性。关于血小板在蛋白水解胶原蛋白中的黏附功能知之甚少，而蛋白水解胶原蛋白是斑块破裂时血小板沉积的潜在底物，也是血栓形成的触发事件。当组织突然暴露于血液中时，这些领域的研究可能会增进对动脉粥样硬化斑块血栓形成倾向的理解。
