C667T and A1298C polymorphisms of methylenetetrahydrofolate reductase gene and susceptibility to myocardial infarction: A systematic review and meta-analysis.
A stepwise forward selection procedure demonstrated that IPF1, MTHFR, and LPL genotypes significantly affected the prevalence of myocardial infarction.
Case-control and prospective studies of association between MTHFR 677C-->T variant and myocardial infarction, coronary artery occlusion, or both; 80 studies were included.
For all MTHFR genotypes combined, the OR for MI in the lowest quartile of folate (<5.4 nmol L-1) compared with the highest quartile (>10.4 nmol L-1) was 3.0 (95% CI 1.7, 5.1).
For all MTHFR genotypes combined, the OR for MI in the lowest quartile of folate (<5.4 nmol L-1) compared with the highest quartile (>10.4 nmol L-1) was 3.0 (95% CI 1.7, 5.1).
Functional variants of angiotensin-1-converting enzyme (ACE), beta-fibrinogen, plasminogen activator inhibitor-1, methylenetetrahydrofolate reductase, glycoprotein Illa, and many apolipoprotein genes are considered excellent candidate risk factors for MI.
Further, in contrast to reports from other investigators, we found little evidence for association of a C677T polymorphism in the 5,10-methylenetetrahydrofolate reductase gene, the angiotensin-I-converting enzyme 1 insertion/deletion polymorphism, a 4G/5G polymorphism in the serine/cysteine proteinase inhibitor-clade E-member 1 gene, the factor V Leiden mutation, the G20210A factor II mutation, a -455G>A polymorphism in the beta-fibrinogen gene, the cys112arg/arg158cys apolipoprotein E gene polymorphism, a gly460trp polymorphism in the alpha-adducin gene, and a -629C>A polymorphism in the cholesteryl ester transfer protein gene with risk of MI.
Genetic typing found him to be homozygous for a mutation in the methylenetetrahydrofolate reductase (MTHFRA1298C) gene, which, in the presence of additional thrombophilic factors, may have increased his risk of myocardial infarction.
Genetic typing found him to be homozygous for a mutation in the methylenetetrahydrofolate reductase (MTHFR A1298C) gene, which, in the presence of additional thrombophilic factors, may have increased his risk of myocardial infarction.
None of the 9 polymorphisms of genes encoding proteins involved in coagulation (G-455A beta-fibrinogen: OR, 1.0; CI, 0.8 to 1.2; G1691A factor V: OR, 1.1; CI, 0.6 to 2.1; G20210A factor II: OR, 1.0; CI, 0.5 to 1.9; and G10976A factor VII: OR, 1.0; CI, 0.8 to 1.3), platelet function (C807T glycoprotein Ia: OR, 1.1; CI, 0.9 to 1.3; and C1565T glycoprotein IIIa: OR, 0.9; CI, 0.8 to 1.2), fibrinolysis (G185T factor XIII: OR, 1.2; CI, 0.9 to 1.6; and 4G/5G plasminogen activator inhibitor type 1: OR, 0.9; CI, 0.7 to 1.2), or homocysteine metabolism (C677Tmethylenetetrahydrofolate reductase: OR, 0.9; CI, 0.8 to 1.1) were associated with an increased or decreased risk of myocardial infarction.
Of the chosen polymorphisms, two (Leu125Val PECAM1 and A1/A2 FVII) are related to myocardial infarction and two (C677TMTHFR and 5A/6A MMP3) to advanced stenosis in arterial vessels (> 75%).
Our data show that 9p21.3 locus and MTHFR gene polymorphisms could influence long-term prognosis of recurrent hard cardiac events in patients who underwent the first MI.
Overall, significant association was found between MTHFRC677T polymorphism and risk of MI when all studies pooled with fixed-effects model for TT vs. CT (OR = 1.183, 95% CI: 1.076-1.300).
Several recent studies evaluated a possible effect of the prothrombotic polymorphisms such as 5,10 methylenetetrahydrofolate reductase (MTHFR) nt 677C --> T, factor V (F V) nt 1691G --> A (F V Leiden), and factor II (F II) nt 20210 G --> A on the risk of myocardial infarction.
The aim was to analyze the relationship between the C677T and A1298C polymorphisms of MTHFR, Hcy levels, and prothrombotic biomarkers in pulmonary embolism (PE) and acute myocardial ischemia (AMI).