Key result
HIV-infected adults with cardiovascular disease risk factors had significantly greater right and left carotid 18FDG uptake compared to healthy controls (1.77 and 1.33 vs 1.05 and 1.03 TBRmax; P < 0.03), indicating increased vascular inflammation.
Why the study?
Does 18FDG PET-CT imaging detect greater arterial inflammation and early atherosclerosis in HIV-infected adults with CVD risk factors compared to healthy controls?
Cross-Sectional (n=14)
Single-blind
No
Does 18FDG PET-CT imaging detect greater arterial inflammation and early atherosclerosis in HIV-infected adults with CVD risk factors compared to healthy controls?
p-value: p=<0.03
18FDG PET-CT imaging can successfully detect increased arterial inflammation and early atherosclerosis in HIV-infected adults with modest cardiovascular risk factors compared to healthy controls.
May support 18FDG PET-CT for detecting vascular inflammation in HIV; hypothesis-generating, should not yet change practice.
BACKGROUND: Persistent vascular inflammation has been implicated as an important cause for a higher prevalence of cardiovascular disease (CVD) in HIV-infected adults. In several populations at high risk for CVD, vascular 18Fluorodeoxyglucose (18FDG) uptake quantified using 3D-positron emission-computed tomography (PET-CT) has been used as a molecular level biomarker for the presence of metabolically active proinflammatory macrophages in rupture-prone early atherosclerotic plaques. We hypothesized that 18FDG PET-CT imaging would detect arterial inflammation and early atherosclerosis in HIV-infected adults with modest CVD risk. METHODS: We studied 9 HIV-infected participants with fully suppressed HIV viremia on antiretroviral therapy (8 men, median age 52 yrs, median BMI 29 kg/m2, median CD4 count 655 cells/μL, 33% current smokers) and 5 HIV-negative participants (4 men, median age 44 yrs, median BMI 25 kg/m2, no current smokers). Mean Framingham Risk Scores were higher for HIV-infected persons (9% vs. 2%, p < 0.01). 18FDG (370 MBq) was administered intravenously. 3D-PET-CT images were obtained 3.5 hrs later. 18FDG uptake into both carotid arteries and the aorta was compared between the two groups. RESULTS: Right and left carotid 18FDG uptake was greater (P < 0.03) in the HIV group (1.77 ±0.26, 1.33 ±0.09 target to background ratio (TBR)) than the control group (1.05 ± 0.10, 1.03 ± 0.05 TBR). 18FDG uptake in the aorta was greater in HIV (1.50 ±0.16 TBR) vs control group (1.24 ± 0.05 TBR), but did not reach statistical significance (P = 0.18). CONCLUSIONS: Carotid artery 18FDG PET-CT imaging detected differences in vascular inflammation and early atherosclerosis between HIV-infected adults with CVD risk factors and healthy HIV-seronegative controls. These findings confirm the utility of this molecular level imaging approach for detecting and quantifying glucose uptake into inflammatory macrophages present in metabolically active, rupture-prone atherosclerotic plaques in HIV infected adults; a population with increased CVD risk.
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Yarasheski et al. (2012) conducted a cross-sectional in HIV infection with cardiovascular disease risk factors (n=14). HIV infection with CVD risk factors vs. Healthy HIV-seronegative controls was evaluated on Right and left carotid 18FDG uptake (target to background ratio [TBRmax]) (p=<0.03). HIV-infected adults with cardiovascular disease risk factors had significantly greater right and left carotid 18FDG uptake compared to healthy controls (1.77 and 1.33 vs 1.05 and 1.03 TBRmax; P < 0.03), indicating increased vascular inflammation.
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