Background Acute myocardial infarction (AMI) is a leading cause of death and morbidity around the world. Although the association between thrombophilia and AMI is well-established, controversial data are present on the association between thrombophilic polymorphisms and AMI. The aim of this study was to investigate the association of three thrombophilic polymorphisms including factor V Leiden (FVL), MTHFRC677T (methylenetetrahydrofolate reductase), and Coagulation factor XIIIVal34Leu with AMI in East of Iran. Result There were no statistically significant differences between the patients and control groups in terms of the distributions of allelic and genotypic frequencies of FVL and FXIIIVal34Leu polymorphisms (P-value > 0.05). Subjects who carried CT genotype of MTHFR C677T polymorphism were at a 2.03-fold higher risk for AMI (P-value: 0.02, OR 1.76, 95% CI 1.07–2.75). Furthermore, patients with MTHFR 677CT (P-value < 0.001, β = - 0.90, 95% CI − 1.33, − 047) or 677CC (P-value < 0.001, β = - 1.04, 95% CI − 1.47, − 0.61) genotypes showed significantly Lower creatinine levels compared with patients having the MTHFR 677TT. No association was observed between the other remaining polymorphisms and AMI (P-value > 0.05). Conclusion Our findings showed that MTHFRC677T polymorphism could contribute to AMI susceptibility and increase creatinine levels in east Iran population. This was the first study to examine the association of these three polymorphisms with AMI in east Iran.
Neutrophil-lymphocyte (NLR), platelet-lymphocyte (PLR), eosinophil-lymphocyte (ELR), and monocyte-lymphocyte (MLR) ratios are systemic inflammatory markers related to myocardial infarction. The aim of this study is to investigate the association of Src homology 2-B adapter protein 3 (SH2B3) C784 T and methylenetetrahydrofolate reductase (MTHFR) C677 T polymorphisms (SNP) with systemic inflammatory markers and the severity of coronary artery disease (CAD) in 150 ST-elevation myocardial infarction (STEMI) patients. Single nucleotide polymorphisms were genotyped using the tetra-primer amplification refractory mutation system-polymerase chain reaction (T-ARMS-PCR) method. The inflammatory markers were calculated. An interventional cardiologist blinded to other data assessed the SYNTAX (SX) Score. Eosinophil and platelet counts were significantly higher in SH2B3 variants than in the wild type. Additionally, SH2B3 variants had significantly higher ELR than the wild type (.12 ± .19 vs .25 ± .34, p = .018). NLR, PLR, ELR, and MLR were considerably higher in MTHFR variants than in the wild type ( p < .05). The SX score was significantly higher in both SH2B3 C784 T (21.24 ± 8.90 vs 15.29 ± 9.40, p = .00) and MTHFR C677 T (20.34 ± 10.21 vs 16.08 ± 8.39, p = .00) variants when compared with wild type. In conclusion, these polymorphisms are associated with several markers of systemic inflammation as well as the severity of CAD.
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