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Elevated ischemic stroke risk among women living with HIV infection

Chow, Felicia, C.a; Regan, Susanb; Zanni, Markella, V.c; Looby, Sara, E.c,d; Bushnell, Cheryl, D.e; Meigs, James, B.b; Grinspoon, Steven, K.c; Feske, Steve, K.f; Triant, Virginia, A.b,g

doi: 10.1097/QAD.0000000000001650
CLINICAL SCIENCE

Objective: To determine if the greater risk of ischemic stroke observed in women living with HIV infection (WLWH) compared with HIV-uninfected women persists after accounting for both traditional and sex-specific stroke risk factors.

Methods: We performed an observational cohort study of WLWH (n = 1214) and demographics-matched HIV-uninfected women (n = 12 041) seen between 1996 and 2011 at two tertiary care hospitals in Boston. We used Cox proportional hazards regression analyses to model time to ischemic stroke, adjusting first for demographics and traditional stroke risk factors and then for sex-specific stroke risk factors, including menopause and estrogen use. We also constructed demographics-adjusted Cox models to identify HIV-related risk factors associated with ischemic stroke among WLWH.

Results: The incidence of ischemic stroke was higher among WLWH compared with HIV-uninfected women [incidence rate ratio 2.39, 95% confidence interval (CI) 1.62–3.43]. After adjusting for demographics and traditional stroke risk factors, HIV infection was associated with almost twice the risk of ischemic stroke (hazard ratio 1.93, 95% CI 1.31–2.85). The association of HIV with ischemic stroke persisted after inclusion of sex-specific stroke risk factors in the model (hazard ratio 1.89, 95% CI 1.28–2.81). Among WLWH, longer duration of antiretroviral therapy was associated with lower ischemic stroke risk (hazard ratio 0.86 per year, 95% CI 0.76–0.96).

Conclusion: The increased risk of ischemic stroke among WLWH compared with HIV-uninfected women persisted after adjusting for both traditional and sex-specific stroke risk factors. Further investigation into the mechanisms of elevated stroke risk among WLWH, including immunologic factors, will be key for developing targeted preventive strategies for this at-risk population.

aWeill Institute for Neurosciences, Department of Neurology and Division of Infectious Diseases, University of California, San Francisco, California

bDivision of General Internal Medicine

cProgram in Nutritional Metabolism

dYvonne L. Munn Center for Nursing Research, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts

eDepartment of Neurology, Wake Forest School of Medicine, Winston-Salem, North Carolina

fDepartment of Neurology, Brigham and Women's Hospital

gDivision of Infectious Diseases, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts, USA.

Correspondence to Felicia C. Chow, MD, MAS, University of California, San Francisco at Zuckerberg San Francisco General Hospital, 1001 Potrero Avenue, Building 1, Room 101, San Francisco, CA 94110, USA. E-mail: felicia.chow@ucsf.edu

Received 16 May, 2017

Revised 22 August, 2017

Accepted 3 September, 2017

Supplemental digital content is available for this article. Direct URL citations appear in the printed text and are provided in the HTML and PDF versions of this article on the journal's Website (http://www.AIDSonline.com).

Copyright © 2018 Wolters Kluwer Health, Inc.