HIV and arterial inflammation

Patients with Human Immunodeficiency Virus (HIV) demonstrate a high prevalence of noncalcified coronary atherosclerotic lesions.  However, the specific mechanisms that lead to this remain unknown.  In this study Subramanian et al. used 18fluorine-2-deoxy-D-glucose positron emission tomography (18F-FDG-PET) to assess arterial wall inflammation in patients with HIV, and compared this to traditional and nontraditional risk makers.

A group of 27 HIV patients without known cardiac disease underwent 18F-FDG-PET and coronary computed tomography for coronary artery calcium scanning also.  Two separate non-HIV control groups were used; one was matched to the HIV group for age, sex, and Framingham risk score (FRS) and also had no known atherosclerotic disease, the other was matched on sex and selected based on the presence of known atherosclerotic disease.   The main outcome measure the ratio of FDG uptake in the arterial wall of the ascending aorta to venous background (target-to-background ratio, TBR).

All HIV patients were receiving antiretroviral therapy and had good CD4 counts.  Arterial inflammation in the aorta (aortic TBR) was higher in the HIV patients when compared to the non-HIV patients matched for FRS (P<.001), even after adjustment for traditional risk factors (P=.002).  However, aortic inflammation was similar in the HIV group compared to the non-HIV atherosclerotic control group.  Among patients with HIV, aortic TBR was associated with sCD163 levels (a circulating marker of monocyte and macrophage activation), but not with C-reactive protein or D-dimer.


Using FDG-PET, this study found that patients with HIV had increased arterial inflammation when compared to noninfected control participants with similar cardiovascular risk factors.

  • Subramanian S, Tawakol A, Burdo TH et al.  Arterial Inflammation in Patients with HIV.  JAMA 2012;308:379-386.

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