[Participation of platelets in the progression of atherosclerosis].

The role of platelets in the early steps of atherosclerogenesis is controversial, but it is well established that platelets play a prominent part in arterial thrombosis, the leading event in the progression of atherosclerosis. Ulceration of the plaque breaks the endothelial cover, and induces blood to interact with the deeper components of the lesion, which leads to adhesion, activation and aggregation of platelets at the intimal breach. The resulting clump of platelets becomes a thrombus by further platelet accumulation and the addition of fibrin (through the triggering of the coagulation cascade). The thrombus has three possible fates. 1. It can grow by addition of successive layers of platelet, fibrin, white and red blood cells, until it eventually occludes the arterial lumen, often provoking an ischaemic event (such as a myocardial infarction). 2. At any time of its growth, the thrombus can be dislodged in whole or in part to cause arterial embolism. 3. The thrombotic material may become overgrown by endothelium and incorporated into the intima, becoming part of the atherosclerotic lesion and strongly contributing to the increase of its sclerotic as well as atheromatous (lipid) mass. Although the mechanisms of ulceration remain unclear, the resulting platelet activation leads to mural thrombosis and greatly contributes to the progression and complications of atherosclerosis. Available antiplatelet agents interfere favourably with the atherosclerotic process, but more efficient drugs will be designed when we better understand the mechanisms of ulceration and the influences that modulate the growth and fate of arterial thrombi.