Emerging research suggests links between menopausal hot flashes and cardiovascular risk. The mechanisms underlying these associations are unclear due, in part, to the incomplete understanding of the physiology of hot flashes. We aimed to examine the longitudinal associations between hot flashes/night sweats and both inflammatory and hemostatic markers, controlling for cardiovascular risk factors and estradiol concentrations.
Participants in the Study of Women's Health Across the Nation (n = 3,199), a longitudinal cohort study, were aged 42 to 52 years at cohort entry. Women completed interviews (hot flashes, night sweats: none, 1-5, and ≥6 d in the past 2 weeks), physical measures (blood pressure, height, weight), and a blood draw (high-sensitivity C-reactive protein, plasminogen activator inhibitor-1, factor VIIc, tissue plasminogen activator antigen [tPA-ag], fibrinogen, glucose, serum estradiol) yearly for 8 years. Hot flashes/night sweats were examined in relation to each inflammatory/hemostatic marker in linear mixed models adjusting for demographic factors, cardiovascular risk factors, and medication use, as well as serum estradiol.
Compared with experiencing no flashes, reporting hot flashes was associated with higher tPA-aglog (hot flashes 1-5 d: percent change, or % change [95% CI], 3.88 [2.22-5.58]; P < 0.0001; ≥6 d: % change [95% CI], 4.11 [1.95-6.32]; P < 0.001) and higher factor VIIclog (hot flashes ≥6 d: % change [95% CI], 2.13 [0.80-3.47]; P < 0.01) in multivariable models. Findings persisted after adjusting for estradiol. Findings for night sweats were similar but attenuated with adjustment.
Frequent hot flashes were associated with higher factor VIIc and tPA-ag. Hemostatic pathways may be relevant to understanding hot flash physiology and links between hot flashes and cardiovascular risk.
In the Study of Women's Health Across the Nation, frequent hot flashes were associated with higher levels of hemostatic factors Factor VIIc and tPA-ag during a period of 7 years. Hemostatic pathways may be relevant to the understanding of the physiology of hot flashes and of the possible links between hot flashes and cardiovascular risk.
From the 1Department of Psychiatry, University of Pittsburgh School of Medicine, Pittsburgh, PA; 2Department of Epidemiology, University of Pittsburgh Graduate School of Public Health, Pittsburgh, PA; 3Department of Medicine, David Geffen School of Medicine, University of California-Los Angeles, Los Angeles, CA; 4Department of Public Health Sciences, University of California Davis School of Medicine, Davis, CA; and 5Kaiser Permanente Division of Research, Oakland, CA.
Received March 15, 2011; revised and accepted April 11, 2011.
Funding/support: The Study of Women's Health Across the Nation has grant support from the NIH and Department of Health and Human Services, through the National Institute on Aging, the National Institute of Nursing Research, and the NIH Office of Research on Women's Health (Grants NR004061 and Grants AG012505, AG012535, AG012531, AG012539, AG012546, AG012553, AG012554, and AG012495). R.C.T. was supported by NIH Grant AG029216.
Financial disclosure/conflicts of interest: None reported.
The content of this article is solely the responsibility of the authors and does not necessarily represent the official views of the National Institute on Aging, National Institute of Nursing Research, Office of Research on Women's Health, or the NIH.
Address correspondence to: Rebecca C. Thurston, PhD, 3811 O'Hara St., Pittsburgh, PA 15213. E-mail: firstname.lastname@example.org