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).
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.
C667T and A1298C polymorphisms of methylenetetrahydrofolate reductase gene and susceptibility to myocardial infarction: A systematic review and meta-analysis.
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%).
The results suggested that the C allele of the MTHFRA1298C polymorphism might be associated with the increased risk of MI for Europeans (CC vs. CA+AA: OR [95% CI]=1.37 [1.03-1.84], p(z)(-test)=0.033, p(heterogeneity)=0.668).
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).
To find the incidence of 677 C>T and 1298 A>C in MTHFR gene single nucleotide polymorphisms (SNPs) among the south Indian population, polymerase chain reaction and restriction fragment length polymorphism were employed among 152 patients with myocardial infarction and 167 controls.
Therefore in this study we investigated whether the eNOS and MTHFR gene polymorphisms is associated with myocardial infarction and stroke in patients with or without diabetes.
We report a case of myocardial infarction at a young age in a subject heterozygous for the G20210A prothrombin gene variant and homozygous for the C677TMTHFR polymorphism, who presented a strong family history of atherothrombosis.
We explored the association of homocysteine and its main genetic modulator methylenetetrahydrofolate reductase (MTHFR) 677C->T polymorphism with the development of MI <or=35 years of age.
We report a 42-year old woman with myocardial infarction and venous thrombosis in whom recognition of heterozygous MTHRF gene mutation, hyperhomocysteinemia, and protein C deficiency.
A stepwise forward selection procedure demonstrated that IPF1, MTHFR, and LPL genotypes significantly affected the prevalence of myocardial infarction.
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.
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).
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.
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.
We performed a MEDLINE search to identify published case-control and cohort studies correlating the factor V Leiden, prothrombin (PT) G20210A, and methylenetetrahydrofolate reductase (MTHFR) C677T (TT genotype) mutations with myocardial infarction, ischemic stroke, or peripheral vascular disease.