title: Myocardial infarction marker levels are influenced by prothrombin and tumor necrosis factor-α gene polymorphisms in young patients.
abstract: Polymorphisms 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 -308G/A and pro-thrombin (FII) 20210G/A polymorphisms on the laboratory parameters of young patients affected by AMI. Results indicated that TNF -308A positive genotype frequencies were increased in these patients and that a genetically determined higher production of TNF-α 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 TNFα 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.
authors.affiliation: Department of Biopathology and Medical and Forensic Biotechnology, University of Palermo, Italy. loredana.vaccarino@unipa.it
authors.forename: Loredana
authors.initials: L
authors.lastname: Vaccarino
authors.forename: Silvana
authors.initials: S
authors.lastname: Vitale
authors.forename: Marco
authors.initials: M
authors.lastname: Caruso
authors.forename: Marisa
authors.initials: M
authors.lastname: Palmeri
authors.forename: Letizia
authors.initials: L
authors.lastname: Scola
authors.forename: Manuela
authors.initials: M
authors.lastname: Bova
authors.forename: Calogero
authors.initials: C
authors.lastname: Caruso
authors.forename: Maria Fatima
authors.initials: MF
authors.lastname: Massenti
authors.forename: Francesco
authors.initials: F
authors.lastname: Vitale
authors.forename: Salvatore
authors.initials: S
authors.lastname: Novo
authors.forename: Domenico
authors.initials: D
authors.lastname: Lio
authors.forename: Giusi Irma
authors.initials: GI
authors.lastname: Forte
mesh_terms: D000328:Adult; D000367:Age Factors; D015415:Biomarkers / Q000097:blood; D052279:Creatine Kinase, MB Form / Q000096:biosynthesis; D005340:Fibrinogen / Q000096:biosynthesis; D005787:Gene Frequency; D020022:Genetic Predisposition to Disease; D005838:Genotype; D006801:Humans; D007249:Inflammation / Q000235:genetics; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000235:genetics* / Q000378:metabolism; D020641:Polymorphism, Single Nucleotide; D011516:Prothrombin / Q000235:genetics*; D014336:Troponin / Q000096:biosynthesis / Q000235:genetics; D014409:Tumor Necrosis Factor-alpha / Q000096:biosynthesis / Q000235:genetics*; D055815:Young Adult
chemical_list: D015415:Biomarkers; D014336:Troponin; D014409:Tumor Necrosis Factor-alpha; D011516:Prothrombin; D005340:Fibrinogen; D052279:Creatine Kinase, MB Form