| Titre : | Association between Estrogen receptor alpha gene variation and cardiovascular disease. (2003) |
| Auteurs : | Amanda-M SHEARMAN ; Ladrienne CUPPLES ; Serkalem DEMISSIE ; David-E HOUSMAN ; Richard-H KARAS ; Daniel LEVY ; Michael-E MENDELSOHN ; Inga PETER ; Christopher-H SCHMID ; Boston University School of Public Health. Department of Biostatistics. Boston. MA. USA ; Massachusetts Institute of Technology. Center for Cancer Research. Cambridge. USA ; Tufts New England Medical Center Specialized Center of Research in Ischemic Heart Disease. Boston. MA. USA ; Tufts New England Medical Center. Department of Medicine. Division of Clinical Care Research. Biostatistics Research Center. Boston. MA. USA ; Tufts New England Medical Center. Department of Medicine. Molecular Cardiology Research Institute. Boston. MA. USA |
| Type de document : | Article |
| Dans : | JAMA - Journal of the american medical association (vol. 290, n° 17, 2003) |
| Pagination : | 2263-2270 |
| Langues: | Anglais |
| Mots-clés : | Appareil circulatoire [pathologie] ; Homme ; Hérédité |
| Résumé : | [BDSP. Notice produite par INIST-CNRS R0xz6SO8. Diffusion soumise à autorisation]. Context : Estrogen and related hormone therapies activate estrogen receptors, which in turn regulate genes for several cardiovascular disease (CVD) risk factors. Relatively little is known, however, about the impact of genetic variation in estrogen receptor alpha (ESR1) on CVD risk. Objective To investigate whether the ESR1 c. 454-397T>C polymorphism is associated with CVD risk. Design, Setting, and Participants Prospective study of 1739 unrelated men and women from the population-based offspring cohort of the Framingham Heart Study, who were followed up from 1971 to 1998. Main Outcome Measures Total atherosclerotic CVD events, defined as recognized or unrecognized myocardial infarction (MI), angina pectoris, coronary insufficiency, intermittent claudication, coronary heart disease death, or atherothrombotic stroke (n=178) ; major atherosclerotic CVD, defined as recognized acute Ml, coronary insufficiency, coronary heart disease death, or atherothrombotic stroke (n=83) ; and recognized acute Ml (n=59). Results Twenty percent of participants (n=352) were homozygous for the ESR1 c. 454-397C allele. After adjustment for covariates (age, sex, body mass index, hypertension, diabetes mellitus, total cholesterol, high-density lipoprotein cholesterol, and cigarette smoking), the CC genotype was significantly associated with major atherosclerotic CVD, with an odds ratio of 2.0 (95% confidence interval [Cl], 1.3-3.2 ; P=004) compared with individuals with the CT or TT genotypes. Participants with the CC genotype had 3.0-fold greater odds of Ml (95% Cl, 1.7-5.2 ; P<. 001) compared with those with the CT or TT genotype. The results remained significant when analyses were restricted to men ; too few women had events to study them separately. Conclusions Individuals with the common ESR1 c. 454-397CC genotype have a substantial increase in risk of Ml. Whether ESR1 c. 454-397T>C is causally related to Ml risk or in linkage disequilibrium with 1 or more causal variants remains to be deter-mined. These findings support the importance of estrogen receptors in CVD susceptibility, especially in men. Estrogen receptor variation also has potential to explain recent conflicting data regarding the effects of hormone therapy on CVD susceptibility in women. |
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