Platelet adhesion and aggregation have been found to have a major role in acute coronary syndromes. Large clinical trials have confirmed the benefit of antiplatelet therapy in the prevention and reduction of cardiac events associated with acute coronary syndromes. Inhibition of platelet aggregation by blocking the glycoprotien IIb/IIIa receptor on the platelet surface decreases the risk of thrombotic corornary occlusions in patients undergoing coronary angioplasty. Platelet glycoprotien IIIa polymorphism PI AI/A2 is an important inherited risk factor for coronary thrombosis and stent thrombosis. PLA2 may be linked to another, as yet unidentified risk factor. Two linked and silent platelet polymorphisms in their glycoprotien Ia gene have been shown to be associated with an effect on platelet collagen receptor density. A four fold variation of the platelet receptor density of the collagen receptor glycoprotien Ia/IIa was found correlating with platelet function to adhere to collagen typeI and type III. The molecular basis of two silent polymorphisms at position 807C/T and 873G/A on the glycoprotien Ia gene was identified: individuals with low receptor densities are homozygous for the G allele, whereas individuals homozygous for the 807T/873A allele have high receptor densities.