Ronit Calderon-Margalit1, David Siscovick2, Sharon S Merkin2, Erica Wang2, Martha L Daviglus2, Pamela J Schreiner2, Barbara Sternfeld2, O Dale Williams2, Cora E Lewis2, Ricardo Azziz2, Stephen M Schwartz2, Melissa F Wellons2. 1. From the Department of Epidemiology and Biostatistics, Hadassah-Hebrew University Braun School of Public Health, Jerusalem, Israel (R.C.-M); New York Academy of Medicine, New York (D.S.); Division of Geriatrics, The David Geffen School of Medicine at UCLA, University of California-Los Angeles (S.S.M.); Department of Obstetrics and Gynecology, Cedars Sinai Medical Center, Los Angeles, CA (E.W.); Institute for Minority Health Research, University of Illinois at Chicago (M.L.D.); School of Public Health, Division of Epidemiology & Community Health, University of Minnesota, Minneapolis (P.J.S.); Division of Research, Kaiser Permanente North California, Oakland (B.S.); Department of Biostatistics, Robert Stempel College of Public Health and Social Work, Florida International University, Miami (O.D.W.); Department of Medicine, University of Alabama at Birmingham (C.E.L.); Georgia Regents University, Augusta (R.A.); Department of Epidemiology, University of Washington, Seattle (S.M.S.); and Department of Medicine, Vanderbilt University, Franklin, TN (M.F.W.). ronitcm@gmail.com ronitc@ekmd.huji.ac.il. 2. From the Department of Epidemiology and Biostatistics, Hadassah-Hebrew University Braun School of Public Health, Jerusalem, Israel (R.C.-M); New York Academy of Medicine, New York (D.S.); Division of Geriatrics, The David Geffen School of Medicine at UCLA, University of California-Los Angeles (S.S.M.); Department of Obstetrics and Gynecology, Cedars Sinai Medical Center, Los Angeles, CA (E.W.); Institute for Minority Health Research, University of Illinois at Chicago (M.L.D.); School of Public Health, Division of Epidemiology & Community Health, University of Minnesota, Minneapolis (P.J.S.); Division of Research, Kaiser Permanente North California, Oakland (B.S.); Department of Biostatistics, Robert Stempel College of Public Health and Social Work, Florida International University, Miami (O.D.W.); Department of Medicine, University of Alabama at Birmingham (C.E.L.); Georgia Regents University, Augusta (R.A.); Department of Epidemiology, University of Washington, Seattle (S.M.S.); and Department of Medicine, Vanderbilt University, Franklin, TN (M.F.W.).
Abstract
OBJECTIVE: To study the independent associations of polycystic ovary syndrome (PCOS), and its 2 components, hyperandrogenism and anovulation, with coronary artery calcification (CAC) and carotid artery intima-media thickness (IMT). APPROACH AND RESULTS: At the year 20 of the Coronary Artery Risk Development in Young Adults (CARDIA) study, a population-based multicenter cohort of young adults, women (mean age, 45 years) with information on menses and hirsutism in their twenties were assessed for CAC (n=982) and IMT (n=988). We defined PCOS as women who had both irregular menses and hyperandrogenism (n=55); isolated oligomenorrhea (n=103) as women who only had irregular menses; and isolated hyperandrogenism (n=156) as women who had either hirsutism or increased testosterone levels. Logistic regressions and general linear models were used to estimate the associations between components of PCOS and subclinical CVD. The prevalence of CAC was 10.3% overall. Women with PCOS had a multivariable adjusted odds ratio of 2.70 (95% confidence interval, 1.31-5.60) for CAC. Women with either isolated oligomenorrhea or isolated hyperandrogenism had no increased risk of CAC when compared with unexposed women. Women with PCOS had significantly increased bulb and internal carotid-IMT measurements; however, no significant differences were noted in bulb or internal carotid artery IMT among women with either isolated oligomenorrhea or isolated hyperandrogenism when compared with unexposed women. There were no differences in common carotid-IMT among the 4 study groups. CONCLUSIONS: In this study, women with PCOS, manifested as both anovulation and hyperandrogenism, but not women with one of these manifestations alone, were at increased risk for the development of subclinical CVD.
OBJECTIVE: To study the independent associations of polycystic ovary syndrome (PCOS), and its 2 components, hyperandrogenism and anovulation, with coronary artery calcification (CAC) and carotid artery intima-media thickness (IMT). APPROACH AND RESULTS: At the year 20 of the Coronary Artery Risk Development in Young Adults (CARDIA) study, a population-based multicenter cohort of young adults, women (mean age, 45 years) with information on menses and hirsutism in their twenties were assessed for CAC (n=982) and IMT (n=988). We defined PCOS as women who had both irregular menses and hyperandrogenism (n=55); isolated oligomenorrhea (n=103) as women who only had irregular menses; and isolated hyperandrogenism (n=156) as women who had either hirsutism or increased testosterone levels. Logistic regressions and general linear models were used to estimate the associations between components of PCOS and subclinical CVD. The prevalence of CAC was 10.3% overall. Women with PCOS had a multivariable adjusted odds ratio of 2.70 (95% confidence interval, 1.31-5.60) for CAC. Women with either isolated oligomenorrhea or isolated hyperandrogenism had no increased risk of CAC when compared with unexposed women. Women with PCOS had significantly increased bulb and internal carotid-IMT measurements; however, no significant differences were noted in bulb or internal carotid artery IMT among women with either isolated oligomenorrhea or isolated hyperandrogenism when compared with unexposed women. There were no differences in common carotid-IMT among the 4 study groups. CONCLUSIONS: In this study, women with PCOS, manifested as both anovulation and hyperandrogenism, but not women with one of these manifestations alone, were at increased risk for the development of subclinical CVD.
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