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Increased arterial inflammation relates to high-risk coronary plaque morphology in HIV-infected patients
Ahmed Tawakol1, Janet Lo, Markella V Zanni
1*Cardiology Division, Massachusetts General Hospital and Harvard Medical School, Boston, MA; †Program in Nutritional Metabolism, Massachusetts General Hospital and Harvard Medical School, Boston, MA; and ‡Cardiovascular Radiology, Massachusetts General Hospital and Harvard Medical School, Boston, MA.
Insights
Arterial inflammation, measured by F-FDG-PET, is linked to high-risk coronary plaque features in HIV patients with early atherosclerosis. This suggests a potential mechanism for increased cardiovascular disease risk in this population.
Area of Science:
- Cardiovascular Imaging and Nuclear Medicine
- Infectious Diseases and Virology
- Cardiology and Cardiovascular Diseases
Background:
- HIV infection is associated with an elevated risk of cardiovascular disease (CVD).
- The underlying mechanisms contributing to this increased CVD risk in HIV-infected individuals are not fully understood.
- Subclinical coronary atherosclerosis is common in HIV patients on antiretroviral therapy.
Purpose of the Study:
- To investigate the relationship between arterial inflammation and high-risk coronary plaque characteristics.
- To assess arterial inflammation using F-FDG-PET and its association with coronary plaque morphology in HIV patients.
- To explore potential mechanisms linking HIV infection to increased CVD risk.
Main Methods:
- Forty-one HIV-infected patients with subclinical coronary atherosclerosis were evaluated using F-FDG-PET.
- Patients were categorized into groups based on aortic target-to-background ratio (TBR), indicating arterial inflammation levels.
- Coronary CT angiography was used to assess high-risk plaque morphology features.
Main Results:
- Higher arterial inflammation (higher TBR) in HIV patients correlated with increased prevalence of low-attenuation coronary plaques.
- Patients with higher TBR showed a greater number of low-attenuation plaques and more vulnerability features in their most diseased plaque.
- Arterial inflammation remained a significant predictor of low-attenuation plaques, independent of traditional CVD risk factors.
Conclusions:
- Arterial inflammation, detectable by F-FDG-PET, is associated with high-risk coronary atherosclerotic plaque features in HIV-infected individuals.
- These findings suggest a potential pathway through which arterial inflammation contributes to CVD risk in the HIV population.
- Further research is warranted to confirm if arterial inflammation and associated plaque morphology predict clinical CVD events in HIV patients.
Background:
Mechanisms predisposing HIV-infected patients to increased cardiovascular disease (CVD) risk remain unclear.
Objective:
To determine the interrelationship between arterial inflammation and high-risk coronary plaque morphology in HIV-infected patients with subclinical coronary atherosclerosis.
Methods:
Forty-one HIV-infected patients on stable antiretroviral therapy without known CVD but with atherosclerotic plaque on coronary CT angiography were evaluated with F-FDG-PET. Patients were stratified into 2 groups based on relative degree of arterial inflammation [aortic target-to-background ratio (TBR)]. High-risk coronary atherosclerotic plaque morphology features were compared between groups.
Results:
HIV-infected patients with higher and lower TBRs were similar with respect to traditional CVD risk parameters. Among HIV-infected patients with higher TBR, an increased percentage of patients demonstrated at least 1 low-attenuation coronary atherosclerotic plaque (40% vs. 10%, P = 0.02) and at least 1 coronary atherosclerotic plaque with both low attenuation and positive remodeling (35% vs. 10%, P = 0.04). Moreover, in the higher TBR group, both the number of low-attenuation plaques per patient (P = 0.02) and the number of vulnerability features in the most vulnerable plaque (P = 0.02) were increased. TBR grouping remained significantly related to the number of low-attenuation plaques/subject (β = 0.35, P = 0.004), controlling for age, gender, low-density lipoprotein, duration of HIV, and CD4.
Conclusions:
These data demonstrate a relationship between arterial inflammation on F-FDG-PET and high-risk coronary atherosclerotic plaque features among HIV-infected patients with subclinical coronary atherosclerosis. Further studies are needed to determine whether arterial inflammation and related high-risk coronary morphology increase the risk of clinical CVD events in the HIV population.
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