ST-segment elevation myocardial infarction (STEMI) results from a complete coronary obstruction by an acute thrombosis secondary to atherosclerotic plaque rupture or erosion. The subsequent exposure of collagen and von Willebrand factor leads to local vasoconstriction and platelet activation; this phenomenon is self-sustained by continuous interplatelet recruitment with expression of glycoprotein IIb/IIIa and the local release of thromboxane A2, adenosine diphosphate and thrombin. The resulting platelet plug - the first step of the physiological haemostasis process - then catalyses thrombin formation allowing fibrinogen molecules to polymerise into a fibrin mesh – the clot framework - enabling its growth and stabilisation.
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