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Association between the low activity genotype of catechol-O-methyltransferase and myocardial infarction in a hypertensive population

Eriksson, Anna-Lena, 1971 (author)
Gothenburg University,Göteborgs universitet,Institutionen för invärtesmedicin,Institute of Internal Medicine
Skrtic, Stanko, 1970 (author)
Gothenburg University,Göteborgs universitet,Institutionen för invärtesmedicin,Institute of Internal Medicine
Niklason, Anders, 1960 (author)
Gothenburg University,Göteborgs universitet,Institutionen för invärtesmedicin,Institute of Internal Medicine
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Mattsson Hultén, Lillemor, 1951 (author)
Gothenburg University,Göteborgs universitet,Wallenberglaboratoriet,Wallenberg Laboratory
Wiklund, Olov, 1943 (author)
Gothenburg University,Göteborgs universitet,Wallenberglaboratoriet,Wallenberg Laboratory
Hedner, Thomas, 1949 (author)
Gothenburg University,Göteborgs universitet,Institutionen för invärtesmedicin,Institute of Internal Medicine
Ohlsson, Claes, 1965 (author)
Gothenburg University,Göteborgs universitet,Institutionen för invärtesmedicin, Avdelningen för internmedicin,Institute of Internal Medicine, Dept of Medicine
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 (creator_code:org_t)
2004
2004
English.
In: Eur Heart J. ; 25:5, s. 386-91
  • Journal article (peer-reviewed)
Abstract Subject headings
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  • AIM: 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. METHODS AND 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.

Keyword

Angiotensin-Converting Enzyme Inhibitors/*therapeutic use
Captopril/*therapeutic use
Case-Control Studies
Catechol O-Methyltransferase/*genetics
Female
Genotype
Humans
Hypertension/drug therapy/*genetics
Male
Middle Aged
Myocardial Infarction/enzymology/*genetics
Polymorphism
Genetic
Prospective Studies

Publication and Content Type

ref (subject category)
art (subject category)

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