title: Association between the low activity genotype of catechol-O-methyltransferase and myocardial infarction in a hypertensive population.
abstract: OBJECTIVE
  Estrogens regulate several biological processes involved in the pathogenesis of myocardial infarction. Catechol-O-methyltransferase (COMT) is a key enzyme in the degradation of estrogens. There is a functional polymorphism in the COMT gene (Val158Met), affecting the activity of the enzyme. We investigated if the low activity genotype of COMT is associated with an altered risk of myocardial infarction.
  
  
  RESULTS
  In a prospectively followed hypertensive cohort we identified 174 patients who suffered a myocardial infarction during the study and compared them to 348 controls from the same cohort. The COMT polymorphism and serum levels of sex hormones were analysed. Patients homozygous for the low activity COMT genotype had a decreased risk of myocardial infarction compared to those with the high activity genotype, odds ratio 0.65 (95% CI 0.44-0.97, p=0.033 ). The protective effect of the low activity genotype was most evident among older patients (> 58 years of age), odds ratio 0.43 (95% CI 0.23-0.79, p=0.006 ). Serum levels of estradiol were increased ( p=0.006 ) in males with the low activity genotype.
  
  
  CONCLUSIONS
  Our findings suggest that the low activity COMT genotype is protective against myocardial infarction. One may speculate that the altered estrogen status could be involved in this effect.
authors.affiliation: Division of Clinical Pharmacology, Department of Internal Medicine, Sahlgrenska University Hospital, SE-413 45 Göteborg, Sweden.
authors.forename: Anna-Lena
authors.initials: AL
authors.lastname: Eriksson
authors.forename: Stanko
authors.initials: S
authors.lastname: Skrtic
authors.forename: Anders
authors.initials: A
authors.lastname: Niklason
authors.forename: Lillemor Mattsson
authors.initials: LM
authors.lastname: Hultén
authors.forename: Olov
authors.initials: O
authors.lastname: Wiklund
authors.forename: Thomas
authors.initials: T
authors.lastname: Hedner
authors.forename: Claes
authors.initials: C
authors.lastname: Ohlsson
mesh_terms: D000806:Angiotensin-Converting Enzyme Inhibitors / Q000627:therapeutic use*; D002216:Captopril / Q000627:therapeutic use*; D016022:Case-Control Studies; D002394:Catechol O-Methyltransferase / Q000235:genetics*; D005260:Female; D005838:Genotype; D006801:Humans; D006973:Hypertension / Q000188:drug therapy / Q000235:genetics*; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000201:enzymology / Q000235:genetics*; D011110:Polymorphism, Genetic; D011446:Prospective Studies
chemical_list: D000806:Angiotensin-Converting Enzyme Inhibitors; D002216:Captopril; D002394:Catechol O-Methyltransferase