Vinita Subramanya1, Di Zhao2, Pamela Ouyang3, Joao A Lima4, Dhananjay Vaidya5, Chiadi E Ndumele6, David A Bluemke7, Sanjiv J Shah8, Eliseo Guallar9, Chike C Nwabuo10, Matthew A Allison11, Susan R Heckbert12, Wendy S Post13, Erin D Michos14. 1. Division of Cardiology, Johns Hopkins School of Medicine, Baltimore, MD, USA. Electronic address: vsubram4@jhmi.edu. 2. Department of Epidemiology, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD, USA. Electronic address: dizhao@jhu.edu. 3. Division of Cardiology, Johns Hopkins School of Medicine, Baltimore, MD, USA. Electronic address: pouyang@jhmi.edu. 4. Division of Cardiology, Johns Hopkins School of Medicine, Baltimore, MD, USA. Electronic address: jlima@jhmi.edu. 5. Department of Epidemiology, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD, USA; Division of General Internal Medicine, Johns Hopkins School of Medicine, Baltimore, MD, USA. Electronic address: dvaidya1@jhmi.edu. 6. Division of Cardiology, Johns Hopkins School of Medicine, Baltimore, MD, USA; Department of Epidemiology, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD, USA. Electronic address: cndumel2@jhmi.edu. 7. Department of Radiology, University of Wisconsin School of Medicine and Public Health, Madison WI, USA. Electronic address: DBluemke@uwhealth.org. 8. Division of Cardiology, Northwestern School of Medicine, Chicago, IL, USA. Electronic address: sanjiv.shah@northwestern.edu. 9. Department of Epidemiology, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD, USA. Electronic address: eguallar@jhu.edu. 10. Department of Medicine, Mount Auburn Hospital, Harvard Medical School, Cambridge, MA, USA. Electronic address: chikenwabuo@yahoo.com. 11. Division of Preventive Medicine, University of California San Diego, La Jolla, CA, USA. Electronic address: mallison@ucsd.edu. 12. Cardiovascular Health Research Unit and Department of Epidemiology, University of Washington, Seattle, WA, USA. Electronic address: heckbert@uw.edu. 13. Division of Cardiology, Johns Hopkins School of Medicine, Baltimore, MD, USA; Department of Epidemiology, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD, USA. Electronic address: wpost@jhmi.edu. 14. Division of Cardiology, Johns Hopkins School of Medicine, Baltimore, MD, USA; Department of Epidemiology, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD, USA. Electronic address: edonnell@jhmi.edu.
Abstract
OBJECTIVE: Sex hormone (SH) levels may contribute to sex differences in the risk of heart failure with preserved ejection fraction (HFpEF). We examined the associations of SH levels with left ventricular mass (LVM) and mass (M):volume (V) ratio, which are risk markers for HFpEF. STUDY DESIGN: We studied 1941 post-menopausal women and 2221 men, aged 45-84 years, participating in the Multi-Ethnic Study of Atherosclerosis (MESA). Serum SH levels, cardiac magnetic resonance imaging (MRI) and ejection fraction (EF) ≥50% had been recorded at baseline (2000-2002). Of these participants, 2810 underwent repeat MRI at Exam 5 (2010-2012). Stratified by sex, linear mixed-effect models were used to test associations between SH and sex hormone binding globulin (SHBG) level [per 1 SD greater log-transformed (SH)] with baseline and change in LV structure. Models were adjusted for age, race/ethnicity, center, height, weight, education, physical activity and smoking, and, in women, for hormone therapy and years since menopause. MAIN OUTCOME MEASURES: LVM and M:V ratio. RESULTS: After a median of 9.1 years, higher free testosterone levels were independently associated with a modest increase in LVM (g/yr) in women [0.05 (95% CI 0.01, 0.10)] and men [0.16 (0.03, 0.28)], while higher SHBG levels were associated with less LVM change (g/yr) in women [-0.07 (-0.13, -0.01)] and men [-0.15 (-0.27, -0.02)]. In men, higher dehydroepiandrosterone and estradiol levels were associated with increased LVM. Among women, free testosterone levels were positively and SHBG levels inversely associated with change in M:V ratio. CONCLUSION: A more androgenic profile (higher free testosterone and lower SHBG levels) is associated with a greater increase in LVM in men and women and greater increase in M:V ratio in women over the course of 9 years.
OBJECTIVE: Sex hormone (SH) levels may contribute to sex differences in the risk of heart failure with preserved ejection fraction (HFpEF). We examined the associations of SH levels with left ventricular mass (LVM) and mass (M):volume (V) ratio, which are risk markers for HFpEF. STUDY DESIGN: We studied 1941 post-menopausal women and 2221 men, aged 45-84 years, participating in the Multi-Ethnic Study of Atherosclerosis (MESA). Serum SH levels, cardiac magnetic resonance imaging (MRI) and ejection fraction (EF) ≥50% had been recorded at baseline (2000-2002). Of these participants, 2810 underwent repeat MRI at Exam 5 (2010-2012). Stratified by sex, linear mixed-effect models were used to test associations between SH and sex hormone binding globulin (SHBG) level [per 1 SD greater log-transformed (SH)] with baseline and change in LV structure. Models were adjusted for age, race/ethnicity, center, height, weight, education, physical activity and smoking, and, in women, for hormone therapy and years since menopause. MAIN OUTCOME MEASURES: LVM and M:V ratio. RESULTS: After a median of 9.1 years, higher free testosterone levels were independently associated with a modest increase in LVM (g/yr) in women [0.05 (95% CI 0.01, 0.10)] and men [0.16 (0.03, 0.28)], while higher SHBG levels were associated with less LVM change (g/yr) in women [-0.07 (-0.13, -0.01)] and men [-0.15 (-0.27, -0.02)]. In men, higher dehydroepiandrosterone and estradiol levels were associated with increased LVM. Among women, free testosterone levels were positively and SHBG levels inversely associated with change in M:V ratio. CONCLUSION: A more androgenic profile (higher free testosterone and lower SHBG levels) is associated with a greater increase in LVM in men and women and greater increase in M:V ratio in women over the course of 9 years.
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