MTHFR polymorphism and risk of periprocedural myocardial infarction after coronary stenting

Background and aim Pro-thrombotic status and platelet hyperreactivity still represent an important challenge for periprocedural myocardial infarction (PMI) after coronary stenting. Hyperhomocysteinemia has been suggested to increase the risk of cardiovascular events. The genetic variant of methylenetetrahydrofolate reductase (MTHFR) 677 C > T has been associated to reduced function of the enzyme, thus inducing hyperhomocysteinemia. In our study we investigated whether MTHFR 677 C > T polymorphism is associated with increased risk of periprocedural MI in patients undergoing coronary stenting. Methods and results We included 778 patients undergoing PCI. Homocysteinemia and genetic status were assessed at admission for all patients. Myonecrosis biomarkers were dosed at intervals from 6 to 48 h, PMI was defined as CKMB increase by 3 times the ULN or 50% of pre-PCI value, periprocedural myonecrosis for troponin I increase by 3 times the ULN or by 50% of the baseline. As many as 521 patients carried the MTHFR-T allele. No difference was found for main demographical and clinical features nor for biochemistry parameters, but for higher rate of statins treatment ( p = 0.03) in T-carriers. Polymorphic patients displayed significantly higher levels of homocysteine ( p = 0.005), with additive effect of the mutated T-alleles. Angiographic and procedural features were similar according to genetic status. MTHFR677T was not associated with periprocedural myocardial infarction (adjusted OR = 0.97[0.67–1.4], p = 0.87) or myonecrosis (adjusted OR = 1.03[0.83–1.36], p = 0.82). Same results were found at subgroup analysis in higher-risk subsets of patients. Conclusion Our study showed that among patients undergoing PCI, MTHFR 677 C > T polymorphism is associated to higher homocysteine levels, but does not influence the risk of periprocedural myocardial infarction.