title: [Relation of HLA antigens and myocardial infarction].
abstract: OBJECTIVE
  Genetic predisposition and chronic inflammation play the leading role in the early stages and in the development of atherosclerosis. Previous studies have shown that substantial amounts of T-lymphocytes are present in both early fatty lesions and advanced fibrous lesions in humans. This observation suggests that HLA antigens may be used as genetic markers for the tendency to coronary artery disease. The aim of our study was to investigate the relation of atherosclerosis and HLA antigens in patients with acute myocardial infarction.
  
  
  METHODS
  Thirty consecutive patients with acute myocardial infarction (15 male, 15 female, aged 54+/-8 years) and 30 subjects (15 male, 15 female, aged 52+/-7 years) without evidence of coronary artery disease--according to physical, fundoscopic, electrocardiographic and radiological examination--were enrolled to the study. Histocompatibility antigens (HLA-AB, -DR, -DQ) were studied with lymphocytotoxicity method.
  
  
  RESULTS
  Age, gender, smoking, alcohol consumption, frequency of obesity and diabetes mellitus were similar between the two groups. In patients with myocardial infarction frequency of hypertension, family history and hyperlipidemia were significantly higher than the controls (p < 0.0003, p < 0.0001, p < 0.01 respectively). Frequency of HLA antigens in patients and in controls was 50% and 23% for HLA-A2, 63% and 20% for HLA-DQ4 and 90% and 50% for HA-DQ7. Logistic regression analysis revealed a significant relation with the disease and the presence of these antigens (p = 0.02, p = 0.02 and p = 0.03 respectively).
  
  
  CONCLUSIONS
  It is concluded that in the Turkish population presence of HLA-A2, HLA-DQ4 ve HLA-DQ7 (3) may be used as genetic markers for the tendency to coronary artery disease.
authors.affiliation: Istanbul Universitesi Cerrahpaşa Tip Fakültesi Kardiyoloji Anabilim Dali.
authors.forename: Y
authors.initials: Y
authors.lastname: Doğan
authors.forename: D
authors.initials: D
authors.lastname: Ural
authors.forename: N
authors.initials: N
authors.lastname: Domaniç
authors.forename: E
authors.initials: E
authors.lastname: Yilmaz
mesh_terms: D000328:Adult; D000368:Aged; D016022:Case-Control Studies; D003324:Coronary Artery Disease / Q000235:genetics* / Q000276:immunology; D004562:Electrocardiography; D005260:Female; D005819:Genetic Markers; D020022:Genetic Predisposition to Disease; D006680:HLA Antigens / Q000032:analysis*; D015789:HLA-A2 Antigen / Q000032:analysis; D006683:HLA-DQ Antigens / Q000032:analysis; D006801:Humans; D016015:Logistic Models; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000235:genetics* / Q000276:immunology; D014421:Turkey; D044465:White People / Q000235:genetics
chemical_list: D005819:Genetic Markers; D006680:HLA Antigens; D015789:HLA-A2 Antigen; D006683:HLA-DQ Antigens