title: A levels of endogenous gonadal hormones and their relationship with selected coronary artery disease risk factors among young women post myocardial infarction.
abstract: In recent decades a significant raise in the incidence of myocardial infarction among young women has been recorded. It is presumed that, apart from the classical risk factors, other reasons exist for premature atherosclerosis in young women, related to the homeostasis of gonadal hormones. The aim of the study was to analyze the levels of gonadal hormones (estradiol, progesterone, follicle-stimulating hormone, luteinizing hormone, testosterone and dehydroepiandrosterone) measured in the luteal phase, in 65 normally menstruating women post myocardial infarction (MI) and to investigate a possible relationship between the hormone profile and selected coronary artery disease (CAD) risk factors. The levels of gonadal hormones: estradiol, progesterone, follicle-stimulating hormone, luteinizing hormone, testosterone and dehydroepiandrosterone were measured in the luteal phase. All examined women had normal mean levels of gonadal hormones. In the post MI patients leading a sedentary life style, a significantly lower mean progesterone concentration was observed (16.29 ± 9.11 versus 29.43 ± 21.14 nmol/l, p < 0.05) and significantly higher mean testosterone concentration (2.34 ± 0.98 versus 1.76 ± 1.09 nmol/l, p < 0.05) when compared to patients from the same group, but leading a more active life. In obese post MI women (BMI ≥ 30 kg/m(2)) a lower mean concentration of progesterone was detected (18.02 ± 8.12 versus 26.16 ± 14.72 nmol/l, p < 0.05), than in slimmer patients from the same group. In post MI women with a positive family history for CAD, a significantly higher mean concentration of testosterone was detected (2.31 ± 1.22 versus 1.67 ± 0.74 nmol/l, p < 0.05) than in patients with no family history. The results suggest a correlation between levels of gonadal hormones and classical CAD risk factors.
authors.affiliation: Department of Acquired Heart Valve Diseases, National Institute of Cardiology, Warszawa, Poland.
authors.forename: Urszula
authors.initials: U
authors.lastname: Ablewska
authors.forename: Krzysztof
authors.initials: K
authors.lastname: Jankowski
authors.forename: Ewa
authors.initials: E
authors.lastname: Rzewuska
authors.forename: Danuta
authors.initials: D
authors.lastname: Liszewska-Pfejfer
authors.forename: Tomasz
authors.initials: T
authors.lastname: Hryniewiecki
mesh_terms: D000328:Adult; D003324:Coronary Artery Disease / Q000453:epidemiology / Q000209:etiology / Q000378:metabolism*; D003687:Dehydroepiandrosterone / Q000097:blood; D004958:Estradiol / Q000097:blood; D005260:Female; D005640:Follicle Stimulating Hormone / Q000097:blood; D042341:Gonadal Hormones / Q000097:blood*; D012739:Gonadal Steroid Hormones / Q000378:metabolism*; D006801:Humans; D007986:Luteinizing Hormone / Q000097:blood; D008875:Middle Aged; D009203:Myocardial Infarction / Q000150:complications*; D011237:Predictive Value of Tests; D011374:Progesterone / Q000097:blood; D012016:Reference Values; D012307:Risk Factors; D013739:Testosterone / Q000097:blood
chemical_list: D042341:Gonadal Hormones; D012739:Gonadal Steroid Hormones; D013739:Testosterone; D003687:Dehydroepiandrosterone; D011374:Progesterone; D004958:Estradiol; D007986:Luteinizing Hormone; D005640:Follicle Stimulating Hormone