The resultant exposure of thrombogenic suben-dothelial vessel wall constituents such as collagen, laminin, fibronectin and von Willebrand factor leads to platelet adhesion and activation at these sites. Platelets adhere to and are fixed to the vessel wall by these proteins. Successive recruitment of new platelets together with activation of the coagula-tion cascade at the thrombus surface increase the size of the thrombus, which may become occlusive. According to the current consensus, platelets play a central role in atherogenesis. Repeated cycles of vessel wall injury and inflammation, accompanied by platelet activation, thrombus formation and release of platelet-derived growth factors, lead to the formation of complex atherosclerotic plaques.
Ischemic stroke occurs when arteries supplying blood to the brain are blocked by thrombi or emboli.
Arteries affected by cerebral thrombosis are usually damaged by atherosclerosis, while emboli can arise from cardiac, pe-ripheral or cerebral sources. It is possible to intervene in this process of platelet activation and recruitment by inhibiting the action of aggregating substance. The effectiveness of platelet aggregation inhibitors in reducing the number of ischemic events in patient at risk indicates the clinical significance of platelets in the process of atherothrombosis.