Figure 9.
Role of platelet activation in vascular tissue repair and atherothrombosis. The intensity and duration of the haemostatic response to coronary plaque erosion or rupture is controlled by a local balance between stimuli to platelet activation and counter-regulatory thromboresistance mechanisms (e.g. endothelial prostacyclin synthesis) of the vessel wall and fibrinolysis. Increased thromboxane A2–dependent platelet activation, in concert with impaired endothelial thromboresistance mechanisms (e.g. because of non-steroidal anti-inflammatory drug use), may favour uncontrolled progression towards vascular occlusion over physiological tissue repair and plaque healing