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      Estrogen Receptor Dinucleotide (TA) Polymorphism Does Not Predict Premature Myocardial Infarction in Caucasian Women

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          In this association study, we tested the hypothesis whether the estrogen receptor gene dinucleotide (TA) polymorphism is a risk factor for premature myocardial infarction in Caucasian women. We also investigated the relationships between estrogen receptor gene dinucleotide (TA) polymorphism and serum lipid levels. One-hundred and forty-one women with premature myocardial infarction were compared with healthy women. Cases and controls did not demonstrate a statistically significant difference in distribution of the estrogen receptor dinucleotide (TA) gene polymorphism alleles. Neither could we demonstrate the length of the dinucleotide (TA) repeats of the estrogen gene to be associated with premature myocardial infarction in Caucasian women. Subjects with larger alleles (both alleles of ≧19 repeats) did not differ in serum lipid levels (total, LDL, HDL cholesterol and triglycerides) from subjects with other genotypes. We may conclude that in Caucasian women the length of the dinucleotide (TA) repeat in the regulatory region of the α-estrogen receptor gene is neither associated with premature myocardial infarction nor with serum lipid levels.

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          Estrogen-receptor polymorphisms and effects of estrogen replacement on high-density lipoprotein cholesterol in women with coronary disease.

          Sequence variants in the gene encoding estrogen receptor alpha (ER-alpha) may modify the effects of hormone-replacement therapy on levels of high-density lipoprotein (HDL) cholesterol and other outcomes related to estrogen treatment in postmenopausal women. We characterized 309 women with coronary artery disease who were enrolled in the Estrogen Replacement and Atherosclerosis trial with respect to eight previously described and two newly identified ER-alpha polymorphisms, and we examined the association between these polymorphisms and the response of HDL cholesterol and other lipids to treatment with estrogen alone or estrogen plus progestin. After adjustment for age, race, diabetes status, body-mass index, smoking status, alcohol intake, and frequency of exercise, the 18.9 percent of the women who had the IVS1-401 C/C genotype (i.e., with C on both chromosomes in intervening sequence 1 at position 401 before exon 2) had an increase in the HDL cholesterol level with hormone-replacement therapy that was more than twice the increase observed in the other women (13.1 mg per deciliter vs. 6.0 mg per deciliter, P for treatment-by-genotype interaction = 0.004); this effect was limited to changes in the HDL subfraction 3 (HDL3) (P for interaction=0.04). Similar patterns of response were observed for three other highly linked ER-alpha intron 1 polymorphisms close to the IVS1-401 site (range of P values for interaction = 0.07 to 0.005). The pattern of increased response of HDL cholesterol in women with the IVS1-401 C/C genotype was evident in both the women receiving estrogen and those receiving estrogen plus progestin, was preserved across racial and ethnic groups, and was significant among women who were compliant with the study medication (P<0.001). Postmenopausal women with coronary disease who have the ER-alpha IVS1-401 C/C genotype, or several other closely related genotypes, have an augmented response of HDL cholesterol to hormone-replacement therapy.
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            Association of estrogen receptor-alpha gene polymorphisms with coronary artery disease in patients with familial hypercholesterolemia.

            To investigate the association of estrogen receptor (ER)-alpha gene polymorphisms with coronary artery disease (CAD), we studied 197 men and 98 postmenopausal women with heterozygous familial hypercholesterolemia. We examined the known polymorphisms, including PvuII, XbaI, TA repeat, and CA repeat, and identified 6 novel polymorphisms in the ER-alpha gene. The distributions of -1989T/G (a novel polymorphism in promoter B) and XbaI in intron 1 were associated with CAD in postmenopausal women and in men, with a higher frequency of the G/G genotype (P=0.03) or X1/X1 genotype (P=0.02) in the CAD group. The frequency of alleles of TA repeats >17 was found to be significantly higher in postmenopausal women with CAD than in those without CAD (P=0.04), but not in men. Logistic regression analysis with all coronary risk factors as covariates showed that the G/G genotype was a higher risk for CAD (odds ratio 4.5, 95% CI 1.0 to 19.5;P=0.04) but that X1/X1 was not. We conclude that -1989T/G or its linked polymorphisms in the ER-alpha gene may confer risk for CAD and that the G/G genotype may be an independent predictor for CAD in patients with familial hypercholesterolemia.
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              Association of polymorphism of human alpha oestrogen receptor gene with coronary artery disease in men: a necropsy study.


                Author and article information

                S. Karger AG
                June 2003
                27 June 2003
                : 99
                : 3
                : 163-165
                aInstitute of Histology and Embryology, Medical Faculty, University of Ljubljana, and bDivision of Medical Genetics, Department of Obstetrics and Gynecology, University Medical Centre Ljubljana, Ljubljana, Slovenia
                70673 Cardiology 2003;99:163–165
                © 2003 S. Karger AG, Basel

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                Page count
                Tables: 2, References: 9, Pages: 3


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