ABSTRACT
Hyperhomocysteinemia has recently been identified as a risk for coronary artery disease [CAD]. Some genetic variants such as C677T polymorphism are postulated in this regard. We studied the relation between hyperhomocysteinemia and the above genetic variant and the risk of CAD and also the number of involved vessels. In total, there were 90 patients: 45 with angiographically documented CAD and 45 with the clinical manifestations of CAD but negative angiography. The blood homocystein level was measured using the ELISA and C677T polymorphism using the PCR method. The homocystein level was significantly higher in the case group [p value=0.00], but it did not show any correlation between its level and the extent of CAD. The case group was more homozygote in C677T allele but again it had no relation to the extent of CAD. Hyperhomocysteinemia acts as a CAD risk factor and whilst its presence increases the risk, it does not predict the extent of it
ABSTRACT
Aggregation is the final step in activation of platelets and is mediated by presentation of GPIIb/IIIa receptors on the platelet membrane that bands to fibrinogen and von Willebrand's factor. There are common mutations in GPIII structure that can change the behavior of the molecule and may change the pattern of interaction between platelets and injured endothelium, thus they can have prognostic impact in coronary artery disease [CAD] and acute coronary syndrome. In some large trials, persons homozygous for the PIA2 allele had a greater chance of coronary stenosis and myocardial infarction [MI] than heterozygotes or non-carriers, but other studies did not confirm this association. This is the first study of PIA polymorphism in Iran and is aimed to find a possible association of this mutation and CAD in the Iranian population. In this case-control study, we chose 200 patients who underwent diagnostic coronary angiography between 2005 and 2006 in Hamedan, Iran. In these patients HPIa genotype determination was done using PCR method. We found no significant association of coronary artery stenosis and PIA2A2 or P1A1A2 genotypes in our patients, p value > 0.05. However, there was a significant association between possession of P1A2 allele and occurrence of CAD in patients more than 50 years of age, p value 0.045. Variations in P1A phenotype do not seem to have an association with ischemic heart disease, but the P1A2 allele may have a role in the development of atherosclerosis and MI in persons more than 50 years of age