Skip Navigation

European Heart Journal 2004 25(5):386-391; doi:10.1016/j.ehj.2003.12.026
Copyright © 2004 by the European Society of Cardiology.
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrow Search for citing articles in:
ISI Web of Science (12)
Right arrowRequest Permissions
Google Scholar
Right arrow Articles by Eriksson, A.-L.
Right arrow Articles by Ohlsson, C.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Eriksson, A.-L.
Right arrow Articles by Ohlsson, C.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Clinical research

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

Anna-Lena Erikssona, Stanko Skrtica, Anders Niklasona, Lillemor Mattsson Hulténc, Olov Wiklundc, Thomas Hednera and Claes Ohlssona,b,*

a Division of Clinical Pharmacology, Department of Internal Medicine, Sahlgrenska University Hospital, SE-413 45 Göteborg, Sweden
b Division of Endocrinology, Department of Internal Medicine, Sahlgrenska University Hospital, SE-413 45 Göteborg, Sweden
c Wallenberg Laboratory, Sahlgrenska University Hospital, SE-413 45 Göteborg, Sweden

* Corresponding author. Tel.: +46-31-3422873; fax: +46-31-821524
E-mail address: Claes.Ohlsson{at}medic.gu.se

Received 9 July 2003; revised 2 December 2003; accepted 24 December 2003

Abstract

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, ). 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, ). Serum levels of estradiol were increased () 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.

Key Words: Myocardial infarction • Estrogen • COMT • Polymorphism


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
 J. Clin. Endocrinol. Metab.Home page
L. Stolk, J. B. J. van Meurs, M. Jhamai, P. P. Arp, J. P. T. van Leeuwen, A. Hofman, F. H. de Jong, H. A. P. Pols, and A. G. Uitterlinden
The Catechol-O-Methyltransferase Met158 Low-Activity Allele and Association with Nonvertebral Fracture Risk in Elderly Men
J. Clin. Endocrinol. Metab., August 1, 2007; 92(8): 3206 - 3212.
[Abstract] [Full Text] [PDF]

Home page
 JAMAHome page
T. M. Morgan, H. M. Krumholz, R. P. Lifton, and J. A. Spertus
Nonvalidation of Reported Genetic Risk Factors for Acute Coronary Syndrome in a Large-Scale Replication Study
JAMA, April 11, 2007; 297(14): 1551 - 1561.
[Abstract] [Full Text] [PDF]


Disclaimer:
Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.