CD4/CD8 ratio is not predictive of multi‐morbidity prevalence in HIV‐infected patients but identify patients with higher CVD risk

BACKGROUND: CD4/CD8<0.8 is a surrogate marker of immune-activation/immunosenescence and independently predicts mortality in the HIV-infected patients due to non-AIDS related events. Most studies showed that patients on antiretroviral therapy (ART) often fail to normalize the CD4/CD8 ratio despite CD4 count normalization. Primary objective of the study was to explore the impact of CD4/CD8<0.8 as independent predictor of HIV-associated non-AIDS (HANA) conditions and multimorbidity (MM) in HIV patients. In patients with no previous history of cardiovascular disease (CVD) a particular insight is provided in the association between impact of CD4/CD8<0.8 and risk prediction of CVD or radiological markers of subclinical CVD. MATERIALS AND METHODS: 914 consecutive patients attending Modena Metabolic HIV Clinic were evaluated in a cross-sectional retrospective study. INCLUSION CRITERIA: stable ART from ≥2 years; HIV-RNA plasma levels<40 copies/mL; stable CD4 count≥350/mmc. CD4/CD8 strata (0.8) was chosen as a cut off representing the median value of the cohort. MM was defined as the presence of≥2 HANA conditions including standard defined: chronic kidney disease, hypertension, previous CVD events, osteoporosis and diabetes mellitus. Calendar year of ART initiation was defined: "PreART" (<2000); "EarlyART" (2000-2005) and "LateART" (>=2006). High CVD risk was defined for Framingham Risk Score (FRS)≥6. Subclinical CVD was defined using cardiac CT scan for calcium score (CAC)≥100. Logistic univariate and multivariable adjusted analysis were performed to assess relationships between variables. RESULTS: Demographic and HIV-specific variables distribution in patients with and without MM are shown in Table 1. CONCLUSIONS: Low CD4/CD8 ratio was not associated with MM prevalence. Patients with CD4/CD8<0.8 ratio displayed higher prevalence of CVD. At multivariable logistic regression CD4/CD8<0.8 is an independent prepredictor of enhanced CVD risk. This may support role of immune-activation/senescence in the pathogenesis of CVD.