Felicia C Chow1,2, Yifei Ma3, Maura Manion4, Adam Rupert5, Geralyn Lambert-Messerlian6, Cheryl D Bushnell7, Marcelle I Cedars8, Irini Sereti4, Farzaneh A Sorond9, Priscilla Y Hsue10, Phyllis C Tien2,11. 1. Weill Institute for Neurosciences, Department of Neurology, University of California, San Francisco. 2. Department of Medicine, Division of Infectious Diseases, University of California, San Francisco. 3. Department of Medicine, University of California, San Francisco, San Francisco, California. 4. Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland. 5. AIDS Monitoring Laboratory, Frederick National Laboratory for Cancer Research, Frederick, Maryland. 6. Departments of Pathology and Laboratory Medicine and Obstetrics and Gynecology, Women and Infants Hospital of Rhode Island, Providence, Rhode Island. 7. Department of Neurology, Wake Forest School of Medicine, Winston Salem, North Carolina. 8. Department of Obstetrics, Gynecology and Reproductive Sciences, University of California, San Francisco, San Francisco, California. 9. Department of Neurology, Northwestern University, Chicago, Illinois. 10. Department of Medicine, Division of Cardiology, San Francisco General Hospital, University of California, San Francisco. 11. Medical Service, Department of Veteran Affairs Medical Center, San Francisco, California, USA.
Abstract
OBJECTIVE: Women may be disproportionately impacted by the negative effect of HIV on cerebrovascular risk. We examined the association of HIV, sex, menopause, and immune activation with cerebrovascular function among women with HIV (WWH) and at risk for HIV from the Women's Interagency HIV Study and men with HIV. DESIGN: Cross-sectional. METHODS: Participants were aged at least 40 years with coronary heart disease or at least one cardiometabolic risk factor. All persons with HIV were on antiretroviral therapy with undetectable viral load. Cerebral vasoreactivity was assessed by the transcranial Doppler breath-holding test, with lower vasoreactivity corresponding to worse cerebrovascular function. Menopausal status was determined by anti-Müllerian hormone level. We used mixed effects linear regression to identify factors associated with cerebral vasoreactivity. RESULTS: Mean cerebral vasoreactivity was similar in WWH (n = 33) and women at risk for HIV (n = 16). A trend toward higher cerebral vasoreactivity in WWH compared with men with HIV (n = 37) was no longer present after excluding women on estrogen replacement therapy (n = 3). In women, menopausal status was not significantly associated with cerebral vasoreactivity. WWH with higher cardiovascular risk (-0.14 for each additional cardiometabolic risk factor, P = 0.038), sCD163 (-0.20 per doubling, P = 0.033), and proportion of CD4+CX3CR1+ T cells (-0.14 per doubling, P = 0.028) had lower cerebral vasoreactivity. CONCLUSION: Among older women at high cardiovascular risk, women with virologically suppressed HIV and women at risk for HIV had similar cerebrovascular function. Our findings, which must be interpreted in the context of the small sample, highlight the contribution of traditional cardiometabolic risk factors and immune activation to cerebrovascular risk in WWH.
OBJECTIVE: Women may be disproportionately impacted by the negative effect of HIV on cerebrovascular risk. We examined the association of HIV, sex, menopause, and immune activation with cerebrovascular function among women with HIV (WWH) and at risk for HIV from the Women's Interagency HIV Study and men with HIV. DESIGN: Cross-sectional. METHODS: Participants were aged at least 40 years with coronary heart disease or at least one cardiometabolic risk factor. All persons with HIV were on antiretroviral therapy with undetectable viral load. Cerebral vasoreactivity was assessed by the transcranial Doppler breath-holding test, with lower vasoreactivity corresponding to worse cerebrovascular function. Menopausal status was determined by anti-Müllerian hormone level. We used mixed effects linear regression to identify factors associated with cerebral vasoreactivity. RESULTS: Mean cerebral vasoreactivity was similar in WWH (n = 33) and women at risk for HIV (n = 16). A trend toward higher cerebral vasoreactivity in WWH compared with men with HIV (n = 37) was no longer present after excluding women on estrogen replacement therapy (n = 3). In women, menopausal status was not significantly associated with cerebral vasoreactivity. WWH with higher cardiovascular risk (-0.14 for each additional cardiometabolic risk factor, P = 0.038), sCD163 (-0.20 per doubling, P = 0.033), and proportion of CD4+CX3CR1+ T cells (-0.14 per doubling, P = 0.028) had lower cerebral vasoreactivity. CONCLUSION: Among older women at high cardiovascular risk, women with virologically suppressed HIV and women at risk for HIV had similar cerebrovascular function. Our findings, which must be interpreted in the context of the small sample, highlight the contribution of traditional cardiometabolic risk factors and immune activation to cerebrovascular risk in WWH.
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