Abstract

Introduction: HIV-infected individuals have increased arterial inflammation and higher risk of cardiovascular disease (CVD), likely related to chronic monocyte/macrophage (MΦ) activation. Arterial inflammation as assessed by 18 fluorodeoxyglucose (FDG) PET/CT correlates with MΦ activity and is predictive of CVD risk. Since MΦ that participate in atherosclerosis originate in the bone marrow and transiently reside in the spleen, we sought to evaluate the relationship between arterial inflammation and bone marrow and spleen activity in HIV using FDG-PET/CT. Methods: 20 HIV-infected men and 20 non-infected controls (matched for age, gender and Framingham Risk Score) were studied. Individuals underwent PET-CT imaging and FDG uptake was quantified as standardized uptake values (SUV) in the bone marrow, spleen, wall of the ascending aorta, and control tissues (muscle and subcutaneous fat). For between-subject comparisons, SUV was corrected for blood background (SUVc). Results: The mean age (±SEM) of the participants was 54±2 years. Arterial inflammation was higher among HIV infected individuals vs. controls (SUVc:3.07±0.17 vs. 2.05±0.06, p <0.001, Figure 1a). Similarly, SUVc in both the bone marrow and spleen were higher among in HIV (2.87±0.28 vs 1.73±0.07 p=0.002 and 2.10±0.20 vs 1.56±0.05 p=0.006, respectively). Aortic SUV was strongly related to splenic SUV (r= 0.69, p <0.001, Figure1B) and bone marrow SUV (r=0.62, p<0.001) but was not associated with SUV of muscle (r=0.26, p=0.11) or fat (r=0.24, p=0.20). Conclusions: We demonstrate that arterial inflammation is increased in HIV-infected individuals and is positively associated with bone marrow and splenic activity. In contrast, FDG-uptake in control tissues does not correlate with arterial inflammation. Thus, up regulation of immune cell activity in the bone marrow and splenic reservoir may contribute to arterial inflammation in the setting of HIV infection.

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