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

Abstract

Study Design To compare arterial inflammation (AI) between people living with HIV (PLWH) and uninfected people as assessed by 18F-Fluorodeoxyglucose (18F-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 18F-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 (TBRmax). The independent relationships between HIV status and both TBRmax 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 TBRmax 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-TBRmax 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 TBRmax in AA. PLWH also had an increased independent risk of IFN-γ, IL-10, and VCAM-1 levels.

Association of HIV Infection With Cardiovascular Pathology Based on Advanced Cardiovascular Imaging

“…Another 16 studies involving 1698 participants, 1203 of whom were HIV positive and 495 were HIV negative, evaluated cardiac MR imaging . Ten studies involving 681 participants, 435 of whom were HIV positive and 246 were HIV negative, evaluated vascular PET scans . Three studies involving 146 participants, 134 of whom were HIV positive and 12 were HIV negative, evaluated both computed tomographic coronary angiographic and vascular PET scans (see eTable 1 in the Supplement for full study characteristics).…”

“…Eleven studies used 18 F-fluorodeoxyglucose ( 18 F-FDG), one used 18 F-sodium fluoride (NaF), one used both 18 F-FDG and NaF tracers to evaluate vascular inflammation in people living with HIV ( eTable 8 in the Supplement). Seven studies compared vascular inflammation in people living with HIV with uninfected individuals in the aorta using 18 F-FDG.…”

“…Seven studies compared vascular inflammation in people living with HIV with uninfected individuals in the aorta using 18 F-FDG. Four studies demonstrated a significant increase in aortic inflammation in people living with HIV compared with uninfected individuals, 2 found no significant difference, and 1 observed a significant difference only in participants who were statin naive with an undetectable viral load (Table 2). Differences in vascular target to background ratio, using 18 F-FDG, in those with and without HIV ranged from 0.06 (95% CI, 0.01-0.11) to 0.37 (95% CI, 0.02-0.72) with moderate heterogeneity when pooling was attempted ( I 2 = 64%; P = .07; eFigure 22 in the Supplement).…”

Significance of Vascular Cell Adhesion Molecule-1 and Tumor Necrosis Factor-Alpha in HIV-Infected Patients

“…HIV-infected patients had higher values of VCAM-1 than HIV-uninfected patients [7]. The HIV-linked serum VCAM-1 concentration may be a marker of HIV-dependent endothelial activation and HIV infection progression [8].…”