Pattern of arterial inflammation and inflammatory markers in people living with HIV compared with uninfected people.

STUDY DESIGN

To compare arterial inflammation (AI) between people living with HIV (PLWH) and uninfected people as assessed by F-Fluorodeoxyglucose (F-FDG)-positron emission tomography (PET).

METHODS

We prospectively enrolled 20 PLWH and 20 uninfected people with no known cardiovascular disease and at least 3 traditional cardiovascular risk factors. All patients underwent F-FDG-PET/computed tomography (CT) of the thorax and neck. Biomarkers linked to inflammation and atherosclerosis were also determined. The primary outcome was AI in ascending aorta (AA) measured as mean maximum target-to-background ratio (TBR). The independent relationships between HIV status and both TBR and biomarkers were evaluated by multivariable linear regression adjusted for body mass index, creatinine, statin therapy, and atherosclerotic cardiovascular 10-year estimated risk (ASCVD).

RESULTS

Unadjusted mean TBR in AA was slightly higher but not statistically different (P = .18) in PLWH (2.07; IQR 1.97, 2.32]) than uninfected people (2.01; IQR 1.85, 2.16]). On multivariable analysis, PLWH had an independent risk of increased mean log-TBR in AA (coef = 0.12; 95%CI 0.01,0.22; P = .032). HIV infection was independently associated with higher values of interleukin-10 (coef = 0.83; 95%CI 0.34, 1.32; P = .001), interferon-γ (coef. = 0.90; 95%CI 0.32, 1.47; P = .003), and vascular cell adhesion molecule-1 (VCAM-1) (coef. = 0.75; 95%CI: 0.42, 1.08, P < .001).

CONCLUSIONS

In patients with high cardiovascular risk, HIV status was an independent predictor of increased TBR in AA. PLWH also had an increased independent risk of IFN-γ, IL-10, and VCAM-1 levels.