Objective: Menopausal hot flashes are considered largely a quality-of-life issue. However, emerging research also links hot flashes to cardiovascular risk. In some investigations, this risk is particularly apparent among women using hormone therapy. The aim of this study was to determine whether a longer history of reported hot flashes over the study period was associated with greater aortic and coronary artery calcification. Interactions with hormone therapy use were examined in an exploratory fashion.
Methods: Participants included 302 women participating in the Healthy Women Study, a longitudinal study of cardiovascular risk during perimenopause and postmenopause, which was initiated in 1983. Hot flashes (any/none) were assessed when women were 1, 2, 5, and 8 years postmenopausal. Electron beam tomography measures of coronary artery calcification and aortic calcification were completed in 1997-2004. Associations between the number of visits with report of hot flashes, divided by the number of visits attended, and aortic or coronary artery calcification (transformed) were examined in linear regression models. Interactions by hormone therapy use were evaluated.
Results: Among women using hormone therapy, a longer history of reported hot flashes was associated with increased aortic calcification, controlling for traditional cardiovascular risk factors (b = 2.87, SE = 1.21, P < 0.05). There were no significant associations between history of hot flashes and coronary artery calcification.
Conclusions: Among postmenopausal women using hormone therapy, a longer history of reported hot flashes measured prospectively was associated with increased aortic calcification, controlling for traditional cardiovascular risk factors. Hot flashes may signal adverse cardiovascular changes among certain postmenopausal women.
Among postmenopausal women using hormone therapy, a longer prospectively measured history of reported hot flashes was associated with increased aortic calcification, controlling for traditional cardiovascular risk factors.
From the 1Department of Psychiatry, School of Medicine, 2Department of Epidemiology, Graduate School of Public Health, and 3Cardiovascular Institute, School of Medicine, University of Pittsburgh, Pittsburgh, PA.
Received July 1, 2009; revised and accepted September 17, 2009.
Funding/support: This research was supported by research grants HL28266, HL076852, HL076858, and AG029216 from the National Institutes of Health.
Financial disclosure/conflicts of interest: None reported.
Address correspondence to: Rebecca C. Thurston, PhD, 3811 O'Hara St., Pittsburgh, PA 15213. E-mail: firstname.lastname@example.org