Association between platelet glycoprotein Ib-alpha and myocardial infarction: results of a pilot study performed in male and female patients from Sicily.

Myocardial infarction (AMI) is a complex multifactorial disorder. Platelet adhesion and thrombosis are pivotal events in the development of atherosclerotic lesions. Occlusive thrombus is almost exclusively initiated by plaque rupture and adhesion of platelets to subendothelial von Willebrand factor (vWf) by its specific platelet receptor, the alpha-chain of glycoprotein (GP) Ib-IX-V complex of the human platelet-specific antigens (HPA). Two polymorphisms have been reported in the sequence of GPIb-alpha. The first, a C/T transition at nucleotide 1018 results in an amino acid dimorphism (Thr/Met) at residue 145 of GPIb-alpha, which is located within the vWF-binding domain of the receptor. The second is a T/C polymorphism in the Kozak sequence at position -5 from the initiator ATG. This affects the receptor density on the platelet surface. We assessed 1018 C/T and -5 T/C Kozak polymorphisms to see whether they are associated with AMI in homogeneous populations of Sicilian patients with AMI. To this end, we have analyzed the distribution of 1018 C/T and -5 T/C Kozak polymorphisms in 105 young Sicilian patients (<46 years) and 110 healthy age-related controls, by PCR-SSP and PCR-RFLP. Our results demonstrate no significant differences in the frequency of 1018 C/T and -5 T/C Kozak polymorphism between patients with AMI and controls. Stratifying by gender, there is no difference between male and female patients and control data. Thus, our results indicate that the HPA-2 polymorphisms are not associated with an increased risk for AMI at early onset (< 46 years) both in men and in women.