Myocardial infarction marker levels are influenced by prothrombin and tumor necrosis factor-α gene polymorphisms in young patients

Abstract

a b s t r a c tPolymorphisms of genes encoding key factors for the control and activation of inflammatory response and coagulation cascade regulation may play a role in genetic susceptibility to acute myocardial infarction (AMI). This study sought to analyze the effect of TNF À308G/A and pro-thrombin (FII) 20210G/A polymorphisms on the laboratory parameters of young patients affected by AMI. Results indicated that TNF À308A positive genotype frequencies were increased in these patients and that a genetically determined higher production of TNF-a is associated in young subjects to a more severe cardiac damage as depicted by higher levels of troponin, Creatine kinase-MB Isoenzyme (mCK-MB) and a significant increased plasma fibrinogen levels. Similar and probably additive effects on might have a genetically determined increased production of pro-thrombin even if no significant differences in genotype frequencies of pro-thrombin (FII) 20210G/A polymorphisms were observed in this study. All together these results, indicating the relationship among genetically determined TNFa and FII production and increased levels of tissue damage markers of AMI, suggest that a complex genetic background, might be involved in susceptibility to AMI in young men influencing the extension and severity of the disease.

Prothrombin G20210A (rs1799963) polymorphism increases myocardial infarction risk in an age-related manner: A systematic review and meta-analysis

“…Substantive studies over the past decade have been making efforts to unmask the correlation between the G20210A SNP and MI. However, previous conflicting reports failed to draw a consistent conclusion, thereby making the association between the G20210A SNP and MI elusive 8 , 10 , 18 , 19 , 25 – 27 , 37 – 39 . The variance may result from different study designs and distinct ethnic backgrounds of subjects.…”

Association between TNF-α rs1800629 polymorphism and the risk of myocardial infarction: A meta-analysis

“…Of the 147 initially identified studies, 12 publications with 13 case-control studies were included in our analysis (Herrmann et al, 1998;Padovani et al, 2000;Koch et al, 2001;Tobin et al, 2004;Bennet et al, 2006;Hou et al, 2009;Ghaderian et al, 2011;Zeybek et al, 2011;Chu et al, 2012;Szabó, 2013;Vaccarino et al, 2013;Biswas et al, 2014). Figure 1 shows a detailed flowchart of the selection process.…”

“…Of those studies, one was a multiple-center study, and consisted of two case-control studies (Herrmann et al, 1998), while all others were single-center studies. Three studies investigated acute myocardial infarction (AMI) patients only (Ghaderian et al, 2011;Vaccarino et al, 2013;Biswas et al, 2014), while the other 10 case-control studies included mixed patients at varying stages of the disease (old, recent, or acute). All studies reported the genotype frequencies of cases and controls.…”

“…In the selection of control subjects, 8 studies were population-based (Herrmann et al, 1998;Padovani et al, 2000;Koch et al, 2001;Bennet et al, 2006;Chu et al, 2012;Vaccarino et al, 2013;Biswas et al, 2014), and 5 were hospital-based (Tobin et al, 2004;Hou et al, 2009;Ghaderian et al, 2011;Zeybek et al, 2011;Szabó et al, 2013). The genotype distributions of the controls in the 9 studies (Herrmann et al, 1998;Padovani et al, 2000;Koch et al, 2001;Tobin et al, 2004;Bennet et al, 2006;Hou et al, 2009;Chu et al, 2012;Vaccarino et al, 2013) were in accordance with the HWE, while that of the remaining 4 studies deviated from the HWE (Ghaderian et al, 2011;Zeybek et al, 2011;Szabó et al, 2013;Biswas et al, 2014). Table 1 presents the major characteristics of the 13 case-control studies.…”

Effects of coagulation factors and inflammatory cytokines on development of acute myocardial infarction in patients younger than 60 years

“…Although great improvements have been achieved in the diagnosis and treatment of AMI, the short-and long-term mortality rates in AMI patients still remain high [3,4]. In addition, the onset age of AMI is becoming increasingly low [5,6]. Therefore, it is of great significance to investigate the pathogenesis of AMI in patients younger than 60 years.…”