Sanyog G Shitole1, Jason M Lazar2, David B Hanna3, Ryung S Kim3, Kathryn Anastos4, Mario J Garcia5, Phyllis C Tien6, João A C Lima7, Robert C Kaplan3,8, Jorge R Kizer1,9. 1. Cardiology Section, San Francisco VA Healthcare System and Department of Medicine, University of California San Francisco, San Francisco, CA. 2. Division of Cardiology, Department of Medicine, State University of New York Health Science Center - Brooklyn, Brooklyn. 3. Department of Epidemiology and Population Health, Albert Einstein College of Medicine. 4. Division of General Internal Medicine, Department of Medicine. 5. Division of Cardiology, Department of Medicine, Albert Einstein College of Medicine and Montefiore Health System, Bronx, NY. 6. Section of Infectious Diseases, San Francisco VA Healthcare System, and Departments of Medicine and Clinical Pharmacy, University of California San Francisco, San Francisco, CA. 7. Division of Cardiology, Department of Medicine, Johns Hopkins University, Baltimore, MD. 8. Division of Public Health Sciences, Fred Hutchinson Cancer Research Center, Seattle, WA. 9. Department of Epidemiology and Biostatistics, University of California San Francisco, San Francisco, CA, USA.
Abstract
BACKGROUND: HIV and HCV have each been linked with cardiac dysfunction. Studies of HIV have often lacked appropriate controls and primarily involved men, whereas data for HCV are sparse. METHODS: We performed repeat echocardiography over a median interval of 12 years in participants from the Women's Interagency HIV Study in order to evaluate the relationships of HIV and HCV with incident left ventricular (LV) dysfunction (systolic or diastolic). RESULTS: Of the 311 women included (age 39 ± 9), 70% were HIV-positive and 20% HCV-positive. Forty three participants (13.8%) developed LV dysfunction, of which 79.1% was diastolic. Compared with participants with neither infection, the group with HIV--HCV coinfection showed a significantly increased risk of incident LV dysfunction after adjustment for risk factors [RR = 2.96 (95% CI = 1.05-8.31)], but associations for the HCV monoinfected and HIV monoinfected groups were not statistically significant [RR = 2.54 (0.83-7.73) and RR = 1.66 (0.65-4.25), respectively]. Comparison of HCV-positive and HCV-negative women showed a significantly increased risk independent of covariates [RR = 1.96 (1.02-3.77)] but this was not the case for HIV-positive vs. HIV-negative women [RR = 1.43 (0.76-2.69)]. There was no evidence of HCV-by-HIV interaction. A more restrictive definition of LV diastolic dysfunction led to fewer incident cases, but a similar, though nonsignificant, risk estimate for HCV. CONCLUSION: Among mostly middle-aged women, HCV but not HIV infection was associated with a pronounced risk of incident LV dysfunction. Although the influence of residual confounding cannot be excluded, these findings bolster the potential benefits that could be realized by adopting recent recommendations for expanding HCV screening and treatment.
BACKGROUND: HIV and HCV have each been linked with cardiac dysfunction. Studies of HIV have often lacked appropriate controls and primarily involved men, whereas data for HCV are sparse. METHODS: We performed repeat echocardiography over a median interval of 12 years in participants from the Women's Interagency HIV Study in order to evaluate the relationships of HIV and HCV with incident left ventricular (LV) dysfunction (systolic or diastolic). RESULTS: Of the 311 women included (age 39 ± 9), 70% were HIV-positive and 20% HCV-positive. Forty three participants (13.8%) developed LV dysfunction, of which 79.1% was diastolic. Compared with participants with neither infection, the group with HIV--HCV coinfection showed a significantly increased risk of incident LV dysfunction after adjustment for risk factors [RR = 2.96 (95% CI = 1.05-8.31)], but associations for the HCV monoinfected and HIV monoinfected groups were not statistically significant [RR = 2.54 (0.83-7.73) and RR = 1.66 (0.65-4.25), respectively]. Comparison of HCV-positive and HCV-negative women showed a significantly increased risk independent of covariates [RR = 1.96 (1.02-3.77)] but this was not the case for HIV-positive vs. HIV-negative women [RR = 1.43 (0.76-2.69)]. There was no evidence of HCV-by-HIV interaction. A more restrictive definition of LV diastolic dysfunction led to fewer incident cases, but a similar, though nonsignificant, risk estimate for HCV. CONCLUSION: Among mostly middle-aged women, HCV but not HIV infection was associated with a pronounced risk of incident LV dysfunction. Although the influence of residual confounding cannot be excluded, these findings bolster the potential benefits that could be realized by adopting recent recommendations for expanding HCV screening and treatment.
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