Association of C677T MTHFR and G20210A FII prothrombin polymorphisms with susceptibility to myocardial infarction

Abstract

Abstract. Myocardial infarction (MI) is a common complex pathology, localized in the main leading causes of mortality worldwide. It is the result of the interaction of genetic and environmental factors. The aim of the present study was to investigate the potential association of C677T 5,10-methylenetetrahydrofolate reductase (MTHFR) (rs1801133) and G20210A factor II prothrombin (FII) (rs1799963) polymorphisms with the susceptibility of MI. Following extraction by the standard salting-out procedure, DNA samples of 100 MI patients and 182 apparently healthy controls were genotyped by polymerase chain reaction-restriction fragment length polymorphism using Hinf I and HindIII restriction enzymes, respectively. The results show a significant association of the G20210T FII polymorphism with the MI risk. The frequencies of the heterozygote genotype GA, homozygous mutated AA and the G20210A allele was higher among patients compared to controls (GA: 59 vs. 5.5%, P<0.001; AA: 10 vs. 0%, P=0.003; and 20210A: 39.5 vs. 2.7%, P<0.003), suggesting that this polymorphism may be a potential genetic marker for MI. No significant association was observed between the C677T MTHFR and MI occurrence, and there was more heterozygote CT in the patient group compared to the controls. As a multifactorial disease, the development of MI may be the result of numerous factors that influence synergistically its occurrence.Thus, further studies are merited to try to better assess these associations (gene-gene and gene-environment interactions).

Risk factors profile of young and older patients with myocardial infarction

“…If the above polymorphism is combined with casual smoking, the risk is increased 22-fold (95% CI: 9.192-66.517) 71 . Hmimech et al showed that polymorphisms G20210A of prothrombin [FII] gene -even if there is a single or double copy of the 20210A allele-is highly associated with premature MI 73 .…”

MTHFR gene polymorphisms and susceptibility to myocardial infarction: Evidence from meta-analysis and trial sequential analysis

“…The remaining 143 manuscripts were screened and assessed based on the full text for eligibility. Eventually, 66 studies for C677T and 18 studies for A1298C qualified for quantitative analysis [21] , [29] , [30] , [31] , [32] , [33] , [34] , [35] , [36] , [37] , [38] , [39] , [40] , [41] , [42] , [43] , [44] , [45] , [46] , [47] , [48] , [49] , [50] , [51] , [52] , [53] , [54] , [55] , [56] , [57] , [58] , [59] , [60] , [61] , [62] , [63] , [64] , [65] , [66] , [67] , [68] , [69] , [70] , [71] , [72] , [73] , [74] , [75] , [76] , [77] , [78] , [79] , [80] , [81] , [82] , [83] , [84] , [85] , [86] , [87] , [88] , [89] , [90] , [91] , [92] , ...…”

Polymorphisms of candidate genes determining the clinical and hemostasiological characteristics of endocarditis of various etiology

“…Нарушение фолатного цикла способствует гипергомоцистеинемии, что может приводить к гиперкоагуляции и формированию тромботических масс на сердечных клапанах [20,21]. Ген MTR кодирует аминокислотную последовательность фермента метионинсинтазы -одного из ключевых ферментов обмена метионина, катализирующего образование метионина из гомоцистеина путем его реметилирования.…”