icon-    folder.gif   Conference Reports for NATAP  
 
  21st Conference on Retroviruses and
Opportunistic Infections
Boston, MA March 3 - 6, 2014
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HIV Infection and the Risk of Cardiovascular Disease in Women
 
 
  Reported by Jules Levin
CROI 2014 March 3-6 Boston, MA
 
Julie A. Womack1, Chung-Chou H. Chang2,3, Kaku A. Armah3, Kathleen McGinnis4, Matthew B. Goetz5,6, Cynthia L. Gibert7,8, Sheldon T. Brown9,10, Alberta L. Warner5, Amy C. Justice11,4, Matthew S. Freiberg12,13, for the VACS Project Team 1Yale University, School of Nursing, West Haven, CT, 2University of Pittsburgh School of Medicine, Pittsburgh, RI, 3University of Pittsburgh, Graduate School of Public Health, Pittsburgh, PA, 4Veterans Affairs Connecticut Health Care System, West Haven, CT, 5VA Greater Los Angeles Health Care System, Los Angeles, CA, 6David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA, 7VA Medical Center, Washington, DC, 8George Washington University School of Medicine, Washington, DC, 9James J. Peters VA Medical Center, Bronx, NY, 10Mount Sinai School of Medicine, New York, NY, 11Yale University School of Medicine, New Haven, CT, 12University of Pittsburgh School of Medicine, Pittsburgh, PA, 13University of Pittsburgh Graduate School of Public Health, Pittsburgh, PA.
 
"...... HIV is an independent predictor of CVD in women. These results have important policy and clinical implications given the growing number of HIV+ women and the fact that heart disease is the leading cause of death among women in the US. Research must explore the etiology and predictors of CVD in this high risk population of women.......
 
.......Incident (new cases of CVD) CVD/1000 person years was significantly higher among HIV+ (13.5) than HIV- women (5.3), p<0.001, despite the fact that the baseline Framingham risk score was 3 for both groups (p=0.28). After adjusting for all covariates, HIV+ women had an increased risk of CVD compared to HIV- (HR 3.12, 95% CI=1.89, 5.11). Median age at and time to CVD event for HIV+ vs. HIV- women was 49.3 vs. 52.0 years (P=0.05), respectively, and 5.85 vs 6.05 years (p<0.001).
 
......In time updated analyses, HIV+ women with HIV-1 RNA level ≥500 copies/mL (HR=3.23, 95% CI=1.61, 6.47) and <500 copies/mL (HR=3.27, 95% CI=1.82, 5.88) were both at greater risk of CVD compared to HIV- women. There was no difference in risk between the two HIV groups (p=0.97)"

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Program Abstract-
 
Background: HIV infection is associated with increased risk of cardiovascular disease (CVD) in women. However, whether HIV is an independent predictor of CVD is unclear. We investigated this question in a cohort of HIV infected (HIV+) and uninfected (HIV-) women.
 
Methodology: We analyzed data on 2190 women participants (32% HIV+) free of CVD at baseline from the Veterans Aging Cohort Study who were followed from their first clinical encounter (on/after 04/01/2003) until a CVD event, death, or the last follow-up date (12/31/2009). The primary outcome was CVD [acute myocardial infarction (AMI), ischemic stroke, heart failure]. AMI events were defined using clinical data, ICD-9-CM codes and or death certificate data; ischemic stroke and heart failure were determined using ICD-9-CM codes. We used Cox proportional hazards models to assess the association of HIV and incident CVD, adjusting for age, race/ethnicity, lipids, smoking, blood pressure, diabetes, renal disease, obesity, hepatitis C, and substance use/abuse. Using the counting process technique for a time updated Cox proportional hazards model, we explored the risk for CVD among HIV+ women with HIV-RNA levels <500 copies/mL and those with CD4 cell count >200 cells/mm3.
 
Results: During a median follow-up time of 5.9 years, there were 86 CVD events (53%, HIV+): AMI: 24%; ischemic stroke: 20%; heart failure: 56%. Incident CVD/1000 person years was significantly higher among HIV+ (13.5, 95% CI 10.1, 18.1) than HIV- women (5.3, 95% CI 3.9, 7.2), p<0.001, despite the fact that the baseline Framingham risk score was 3 for both groups (p=0.28). After adjusting for all covariates, HIV+ women had an increased risk of CVD compared to HIV- (HR 3.12, 95% CI=1.89, 5.11). Median age at and time to CVD event for HIV+ vs. HIV- women was 49.3 vs. 52.0 years (P=0.05), respectively, and 5.85 vs 6.05 years (p<0.001). In time updated analyses, HIV+ women with HIV-1 RNA level ≥500 copies/mL (HR=3.23, 95% CI=1.61, 6.47) and <500 copies/mL (HR=3.27, 95% CI=1.82, 5.88) were both at greater risk of CVD compared to HIV- women. There was no difference in risk between the two HIV groups (p=0.97). Similar associations were found for HIV+ women with CD4 cell count <200 cells/mm3 (HR=2.75, 95% CI=1.54, 4.92) and those with CD4 count ≥200 cells/mm3 (HR= 5.63, 95% CI=2.71, 11.7) compared to HIV- women. However the risk of CVD was greater among those with CD4 cell counts ≥200 cells/mm3 compared to those with CD4 cell counts <200 cells/mm3 (p=0.047).
 
Conclusions: HIV is an independent predictor of CVD in women. These results have important policy and clinical implications given the growing number of HIV+ women and the fact that heart disease is the leading cause of death among women in the US. Research must explore the etiology and predictors of CVD in this high risk population of women.

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