Abstract 11505: Arterial Inflammation in HIV-Infected Patients Assessed by 18F-Fluorodeoxyglucose Positron Emission Tomography
Introduction: HIV-infected patients are at increased risk of myocardial infarction and arterial inflammation has been suggested as an explanation. Vascular inflammation can be assessed in vivo by 18F-fluorodeoxyglucose (FDG) PET.
Hypothesis: Well-treated HIV-infected patients without known cardiovascular disease will have increased uptake of FDG in different arterial regions as compared to healthy controls.
Methods: We prospectively included 26 HIV-infected patients on stable antiretroviral therapy and 25 healthy volunteers. All underwent whole-body PET/CT 3 hours after injection of FDG. FDG uptake was assessed (SUV) in the carotid arteries, the ascending, descending, and abdominal aorta. Carotid intima-media thickness was determined by ultrasound. Soluble biomarkers of endothelial dysfunction and inflammation were measured by ELISA. Known cardiovascular risk factors were recorded for all included.
Results: The HIV-infected patients were on stable antiretroviral therapy with full viral suppression. The HIV-infected group was older (50 vs 41 yrs; p = 0.01), had higher blood pressure and total cholesterol, and accordingly a higher Framingham risk score. FDG uptake was similar in the two groups quantified as SUVmax (figure) in the carotid region (1.67 ± 0.04 vs. 1.67 ± 0.04, p = 0.98), the ascending aorta (1.84 ± 0.06 vs. 1.97 ± 0.06, p = 0.15), the descending aorta (1.89 ± 0.08 vs. 1.93 ± 0.08, p = 0.70), and the abdominal aorta (1.70 ± 0.06 vs. 1.65 ± 0.06, p = 0.56) even when adjusting for differences in risk profile. No significant correlations between SUV, carotid intima-media thickness, known cardiovascular risk factors and soluble biomarkers were found.
Conclusions: We found no evidence of increased arterial inflammation among HIV-infected patients with full viral suppression compared to controls. This may challenge the idea of chronic inflammation as the cause of cardiovascular disease among optimally treated HIV-infected patients.
Author Disclosures: R.S. Ripa: None. A. Knudsen: None. A.F. Hag: None. A. Loft: None. E. von Benzon: None. S.H. Keller: None. H.J. Møller: None. A. Lebech: None. A. Kjær: None.
- © 2014 by American Heart Association, Inc.