Amir S Heravi1, Erin D Michos2, Di Zhao3, Bharath Ambale-Venkatesh2, Henrique Doria De Vasconcellos2, Donald Lloyd-Jones4, Pamela J Schreiner5, Jared P Reis6, Colin Wu6, Cora E Lewis7, James M Shikany7, Stephen Sidney8, Eliseo Guallar3, Chiadi E Ndumele2, Pamela Ouyang2, Ron C Hoogeveen9, Joao A C Lima2, Dhananjay Vaidya1, Wendy S Post2,3. 1. Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA. 2. Division of Cardiology, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA. 3. Department of Epidemiology, Johns Hopkins University Bloomberg School of Public Health, Baltimore, Maryland, USA. 4. Department of Preventive Medicine, Northwestern University Feinberg School of Medicine, Chicago, Illinois, USA. 5. Division of Epidemiology and Community Health, University of Minnesota School of Public Health, Minneapolis, Minnesota, USA. 6. National Heart, Lung, and Blood Institute, Bethesda, Maryland, USA. 7. Division of Preventive Medicine, University of Alabama at Birmingham School of Public Health, Birmingham, Alabama, USA. 8. Division of Research, Kaiser-Permanente, Oakland, California, USA. 9. Division of Cardiovascular Research, Department of Medicine, Baylor College of Medicine, Houston, Texas, USA.
Abstract
Background: Low endogenous estrogen concentrations after menopause may contribute to higher oxidative stress and greater cardiovascular disease (CVD) risk. However, differences in oxidative stress between similarly aged premenopausal and postmenopausal women are not well-characterized on a population level. We hypothesized that urinary isoprostane concentrations, a standard measure of systemic oxidative stress, are higher in women who have undergone menopause compared to premenopausal women. Methods and Results: We examined differences in urinary 8-isoprostane (iPF2α-III) and 2,3-dinor-8-isoprostane (iPF2α-III-M) indexed to urinary creatinine between 279 postmenopausal and 196 premenopausal women in the Coronary Artery Risk Development in Young Adults (CARDIA) study, using linear regression with progressive adjustment for sociodemographic factors and traditional CVD risk factors. Unadjusted iPF2α-III-M concentrations were higher among postmenopausal compared to premenopausal women (Median [25th, 75th percentile]: 1762 [1178, 2974] vs. 1535 [1067, 2462] ng/g creatinine; p = 0.01). Menopause was associated with 25.5% higher iPF2α-III-M (95% confidence interval [6.5-47.9]) adjusted for age, race, college education, and field center. Further adjustments for tobacco use (21.2% [2.9-42.6]) and then CVD risk factors (18.8% [0.1-39.6]) led to additional partial attenuation. Menopause was associated with higher iPF2α-III in Black but not White women. Conclusions: We conclude that postmenopausal women had higher oxidative stress, which may contribute to greater CVD risk. ClinicalTrials.gov Identifier: NCT00005130.
Background: Low endogenous estrogen concentrations after menopause may contribute to higher oxidative stress and greater cardiovascular disease (CVD) risk. However, differences in oxidative stress between similarly aged premenopausal and postmenopausal women are not well-characterized on a population level. We hypothesized that urinary isoprostane concentrations, a standard measure of systemic oxidative stress, are higher in women who have undergone menopause compared to premenopausal women. Methods and Results: We examined differences in urinary 8-isoprostane (iPF2α-III) and 2,3-dinor-8-isoprostane (iPF2α-III-M) indexed to urinary creatinine between 279 postmenopausal and 196 premenopausal women in the Coronary Artery Risk Development in Young Adults (CARDIA) study, using linear regression with progressive adjustment for sociodemographic factors and traditional CVD risk factors. Unadjusted iPF2α-III-M concentrations were higher among postmenopausal compared to premenopausal women (Median [25th, 75th percentile]: 1762 [1178, 2974] vs. 1535 [1067, 2462] ng/g creatinine; p = 0.01). Menopause was associated with 25.5% higher iPF2α-III-M (95% confidence interval [6.5-47.9]) adjusted for age, race, college education, and field center. Further adjustments for tobacco use (21.2% [2.9-42.6]) and then CVD risk factors (18.8% [0.1-39.6]) led to additional partial attenuation. Menopause was associated with higher iPF2α-III in Black but not White women. Conclusions: We conclude that postmenopausal women had higher oxidative stress, which may contribute to greater CVD risk. ClinicalTrials.gov Identifier: NCT00005130.
Authors: Pavel Rossner; Marilie D Gammon; Mary Beth Terry; Meenakshi Agrawal; Fang Fang Zhang; Susan L Teitelbaum; Sybil M Eng; Mia M Gaudet; Alfred I Neugut; Regina M Santella Journal: Cancer Epidemiol Biomarkers Prev Date: 2006-04 Impact factor: 4.254
Authors: Julie M Proudfoot; Anne E Barden; Wai Mun Loke; Kevin D Croft; Ian B Puddey; Trevor A Mori Journal: J Lipid Res Date: 2008-12-02 Impact factor: 5.922
Authors: Martin F Bourgonje; Arno R Bourgonje; Amaal E Abdulle; Lyanne M Kieneker; Sacha la Bastide-van Gemert; Ron T Gansevoort; Stephan J L Bakker; Douwe J Mulder; Andreas Pasch; Jumana Saleh; Sanne J Gordijn; Harry van Goor Journal: Front Cardiovasc Med Date: 2021-02-09
Authors: Catherine Kim; James C Slaughter; James G Terry; David R Jacobs; Nisha Parikh; Duke Appiah; Benjamin Leader; Molly B Moravek; Melissa F Wellons Journal: Fertil Steril Date: 2020-07-16 Impact factor: 7.490
Authors: G Kapuku; F Treiber; F Raouane; J Halbert; H Davis; S Young-Mayes; V Robinson; G Harshfield Journal: J Hum Hypertens Date: 2016-06-16 Impact factor: 3.012