GENETIC POLYMORPHYSM IN THE GENE OF METHYLTETRAHYDROFOLATREDUCTAZA AND ITS IMPACT ON PLASMA HOMOCYSTEINE LEVEL AND ON LONG-TERM EFFECTS OF ACUTE MYOCARDIAL INFARCTION

Abstract

Hipergomocystenemia (HHC) is a significant risk factor for cardiovascular deseases. According to research in HHC incidence of acute myocardial infarction (AMI) increases by 3-4 times. There are hereditary and acquired causes of HHC. One of the reasons is the presence of inherited genetic polymorphisms in the MTHFR gene. According to research conducted by us, the level of homocysteine (HC) plasma at the time of admission was higher than the reference values in 75 % of cases (95 % CI: 60-86). On the 14th day of flow above the AMI level of HC reference values was observed in 73 % (95 % CI: 57-84) cases. The level of HC in patients with homozygous MTHFR gene polymorphism was significantly higher than in patients with heterozygous polymorphism, or without it on the first day of flow of AMI (p = 0.028), and on the 14th day course of acute myocardial infarction (p = 0.001.) In assessment of the long-term outcome after coronary flow AMI endpoints (development of re-infarction, unstable angina, stroke, repeat revascularization, death from CHD), there has been established a clear correlation between the presence of genetic polymorphisms in the MTHFR gene and the development of re-infarction (p = 0.04), the need to repeat revascularization (p = 0.003), the development of unstable angina (p = 0.001). In patients with homozygous polymorphism in the gene encoding MTHFR, re-infarction occurred more frequently (p = 0.021). These data suggest HHC, as one of the most important risk factors for AMI, as well as a higher level of HHC and more severe course of acute myocardial infarction in patients with the presence of polymorphisms in the MTHFR gene.