2253. Comparison of Cardiovascular Risk in Patients Infected with HIV and Hepatitis C
Session: Poster Abstract Session: HIV: Metabolic, Cardiovascular, and Renal Complications
Saturday, October 6, 2018
Room: S Poster Hall
Posters
  • Jimmy Ma - MiM Poster 2018 v3.pdf (251.7 kB)
  • Background: HIV & hepatitis C virus (HCV) are independently associated with poorer cardiovascular & metabolic outcomes compared to the general population. Evidence remains mixed on how these contribute to cardiovascular disease (CVD) risk in co-infection. Prior studies mainly studied established risk models in mono-infected groups or lacked recent scores like Pooled Cohort Equations. This study assesses CVD risk using established risk models & statin usage for primary prevention in matched co-infected & mono-infected cohorts. Methods: Retrospective chart review of HIV &/or HCV infected subjects =18y seen from Jan 1, 2014 to Dec 31, 2016 at Washington University Infectious Disease or Hepatology clinics. Pts included if lipid panel available before statin usage & excluded for prior CVD. Pts matched by gender, age, & race/ethnicity. CVD risk assessed with Framingham general CV Risk Score (FRS), ACC/AHA Pooled Cohort equations (PCEs), & Data Collection on Adverse Effects of Anti-HIV Drugs (D:A:D) HIV model. Multivariate linear models evaluated CVD risk after log transforming skewed data. Results: Each infection group (HIV, HCV, HIV/HCV) had 192 matched subjects. Most were male (76.7%) & African American (73.7%) with overall mean age of 51.2y ±8.6. CVD risk did not differ among infection groups with PCE, FRS, & D:A:D models. PCE predicted the most pts in its highest risk group followed by FRS & then D:A:D. Primary prevention statin use was lower in HIV cohorts but higher in pts with diabetes & dyslipidemia. Conclusion: CVD risk scores did not differ among HIV/HCV co-infected & respective mono-infected cohorts. CVD risk may be underestimated as specific HIV & HCV-related factors may not be fully captured in these scores. Statin uptake remains low in HIV pts despite recent primary prevention guidelines.

    Table 1. Coefficients (95% CI) by log10-transformed risk score model

    Co-infected

    HCV

    HIV

    P value 

    PCE

    Ref

    -0.02 (-0.14, 0.10)

    -0.07 (-0.17, 0.04)

    0.52

    FRS

    Ref

    0.10 (0.01, 0.20)

    0.03 (-0.07, 0.13)

    0.11

    D:A:D

    Ref

    N/A

    0.05 (-0.06, 0.16)

    0.36

    Figure 1a-c. Ten year CVD risk models across infection group based on model specific definitions of risk cutoff. D:A:D distribution extrapolated from 5 year risk score assuming constant risk over 10 years for ease of comparison.

    Jimmy Ma, MD, Department of Medicine, Washington University School of Medicine, Saint Louis, MO, Amber Salter, MPH, PhD, Division of Biostatistics, Washington University School of Medicine, Saint Louis, MO, Rachel Presti, MD, PhD, Department of Medicine, Division of Infectious Diseases, Washington University School of Medicine, Saint Louis, MO and Kevin Korenblat, MD, Department of Medicine, Division of Gastroenterology, Washington University in St. Louis, Saint Louis, MO

    Disclosures:

    J. Ma, None

    A. Salter, None

    R. Presti, None

    K. Korenblat, None

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