Abstract P262: HIV/HCV Co-infection and the Risk of Cardiovascular Disease: A Systematic Review and Meta-analysis

Introduction: With improved antiretroviral therapy, the life expectancy of people living with human immunodeficiency virus (HIV) has increased. However, these individuals are now more susceptible to developing cardiovascular diseases (CVD). Prior studies examining the association between HIV and hepatitis C virus (HCV) co-infection and the risk of CVD, compared to HIV mono-infection, have differed in their conclusions. We conducted a systematic review and meta-analysis to clarify and quantify the association between HIV/HCV co-infection and CVD risk. We hypothesized that CVD risk will be synergistically increased by the persistent inflammatory responses of both viruses. Methods: We searched EMBASE, CINAHL, Google Scholar, PubMed, and Web of science from inception to October 2016 to identify studies on HIV/HCV co-infection and CVD, defined as coronary artery disease, congestive heart failure and stroke. The search was supplemented with a review of the reference list of articles. We used a random-effects model to abstract and pool data on the hazard ratios (HRs) for CVD. Hazard ratios were adjusted for traditional CVD risk factors. Results: Among the 280 articles reviewed, 4 cohort studies met the inclusion criteria with a total of 33,723 participants. Of these, 8,109 (24%) were HIV/HCV coinfected, 18,958 (56%) were HIV monoinfected while 6,656 (20%) comprised HCV monoinfected, HIV uninfected, and HIV/HBV coinfected participants. Pooled adjusted HRs for the association between HIV/HCV co-infection and CVD was 1.24 (95% CI 1.07-1.40) compared to HIV mono-infection. Test for homogeneity was not statistically significant [I 2 = 0.0%, P=0.397] (Figure). Conclusion: We found a consistent positive association showing that individuals with HIV/HCV coinfection had an increased CVD risk compared to those with HIV monoinfection. However, more research is needed to further examine this association, determine potential underlying mechanisms and evaluate whether treatment for HIV and HCV infections can reduce CVD outcomes.