Key result
HIV links to ~17% less subcutaneous adipose tissue, which correlates with arterial injury and inflammation.
Why the study?
Persons living with HIV well treated on antiretroviral therapies remain at risk for arterial disease, and the relationship between adipose depots and arterial injury and inflammation markers is unclear.
Are visceral and subcutaneous adipose depots associated with markers of arterial injury and inflammation in individuals with HIV?
Cross-Sectional (n=225)
Are visceral and subcutaneous adipose depots associated with markers of arterial injury and inflammation in individuals with HIV?
Absolute Event Rate: 199% vs 239%
p-value: p=0.04
Fat redistribution phenotypes, characterized by subcutaneous fat loss and visceral fat accumulation, are independently associated with biomarkers of arterial injury and inflammation in individuals with HIV.
Subcutaneous fat loss was associated with arterial injury markers in HIV; leaves open causal role and need for prospective studies.
OBJECTIVE: Persons living with HIV (PLWH) well treated on antiretroviral therapies remain at risk for ensuing arterial disease. We investigated the relationship between adipose depots and biomarkers of arterial injury and inflammation to gain insight into the link between body composition and CVD risk. DESIGNS/METHODS: One hundred and fifty-five HIV-infected and 70 non-HIV infected individuals were well phenotyped for body composition. Adipose depots were assessed via single-slice abdominal computed tomography (CT). Circulating markers of arterial disease and generalized inflammation [lipoprotein-associated phospholipase A2 (LpPLA2), oxidized low-density lipoprotein (oxLDL), high-sensitivity cardiac troponin T (hs-cTnT), high-sensitivity C-reactive protein (hsCRP)] were evaluated. RESULTS: Despite similar BMI and visceral adipose tissue (VAT), HIV-infected individuals had significantly lower subcutaneous adipose tissue [SAT, 199 (126-288) vs. 239 (148-358) cm(2), P = 0.04] than non-HIV infected individuals. Among HIV-infected individuals, reduced SAT inversely correlated with LpPLA2 (ρ = -0.19, P = 0.02) and hs-cTnT (ρ = -0.24, P = 0.004), whereas increased VAT significantly and positively related to LpPLA2 (ρ = 0.25, P = 0.003), oxLDL (ρ = 0.28, P = 0.0005), hs-cTnT (ρ = 0.28, P = 0.0007) and hsCRP (ρ = 0.32, P = < 0.0001). Similar analyses among the non-HIV infected individuals revealed significant relationships between SAT and LpPLA2 (ρ = -0.24, P = 0.05), as well as VAT and LpPLA2 (ρ = 0.37, P = 0.002), oxLDL (ρ = 0.24, P = 0.05) and hsCRP (ρ = 0.29, P = .02). In modelling performed among the HIV group, simultaneously controlling for VAT, SAT, age and relevant HIV-related parameters, reduced SAT was an independent predictor of LpPLA2 (P = 0.04) and hs-cTnT (P = 0.005) and increased VAT was an independent predictor of LpPLA2 (P = 0.001), oxLDL (P = 0.02), hs-cTnT (P = 0.04) and hsCRP (P = 0.04). CONCLUSION: Fat redistribution phenotypes, characterized by SAT loss and/or VAT accumulation, may be linked to arterial injury and inflammation in HIV.
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Srinivasa et al. (2018) conducted a cross-sectional in HIV (n=225). HIV infection vs. Non-HIV infected individuals was evaluated on Subcutaneous adipose tissue (SAT) area in cm2 (p=0.04). HIV-infected individuals had significantly lower subcutaneous adipose tissue than uninfected controls (199 vs 239 cm2; P=0.04), which independently correlated with markers of arterial injury and inflammation.
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