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platelet monolayer forms at the site of the disrupted plaque agonists promote platelet activation(collagen, ADP, epinephrine, serotonin) platelet cross-linking and aggregation thromboxane A 2  (a potent local vasoconstrictor) is released Factors VII and X are activated, ultimately leading to the conversion of prothrombin to thrombin, which then converts fibrinogen to fibrin conformational change in the glycoprotein IIb/IIIa receptor  further platelet activation and potential resistance to fibrinolysis develops ,[object Object],[object Object],high affinity for amino acid sequences on soluble adhesive proteins  (fibrinogen - can bind to two different platelets simultaneously
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Clinical Presentation
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ST- Segment Elevation Myocardial Infarction

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