Kefah H Ali¹, Nagwan A Sabek^1,, Loaa A Tag Eldeen¹, Emad F Ismail¹, Gamela Nasr²

Background: Hyperhomocysteinemia and platelet glycoprotein GpIIIa polymorphism had been identified as risk factors for coronary atherosclerosis. The methylenetetrahydrofolate reductase MTHFR C677T variant has been shown to influence homocysteine metabolism, the interaction of plasma tHcy with other conventional risk factors remain uncertain in the clinical setting of acute myocardial infarction (AMI). The present study aimed to examine whether the MTHFR and platelet glycoprotein IIIa polymorphisms were associated with increased risk of (MI) in Egyptian patients. Subjects and Method: 150 newly diagnosed MI patients and 50 healthy matched subjects were recruited into this study, genotyping of the MTHFR C677T and GpIIIa 1565 A¹/A² polymorphisms were carried out by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) technique, plasma tHcy, and folic acid levels were estimated. Results: Fasting plasma total Hcy levels were significantly higher in MI patients than controls (P <0.05), folate levels were significantly lower in MI patients than controls (P <0.05), no significant differences were observed in the MTHFR C677T and GpIIIa genotypes frequencies between MI patients and controls (P > 0.05). The frequency of the MTHFR C allele was 80.6 % and 76 % in MI patients and controls respectively and did not differ significantly between the two groups (P > 0.05). The frequency of risk allele, GpIIIa, PIA² was significantly higher in MI patients compared to controls (p<0.05), plasma tHcy level was significantly higher and folate level was significantly lower in MI patients carrying MTHFR CC and GPIIIa PIA²A²genotypes. Conclusions: In this population, the both risk alleles of MTHFR and GpIIb/IIIa polymorphisms had no major effect on the MI incidence, they were associated with higher homocysteine levels. A gene-environment interaction might increase the risk indirectly by elevating tHcy, especially when folate intake was low, our findings might support that MTHFR and GpIIb/IIIa polymorphisms as risk factors for MI.

Myocardial infarction (MI), homocysteine (tHcy), folate, methylenetetrahydrofolate reductase (MTHFR), Glycoprotein (GP) IIb/IIIa