Abstract 11650: Association of Macrophage Inflammation Biomarkers With Progression of Subclinical Carotid Atherosclerosis in HIV-infected Women and Men
Introduction: Monocytes and monocyte-derived macrophages promote atherosclerosis through inflammation and vascular remodeling. We suspect that this is especially true in chronic HIV infection due to increased inflammation. We hypothesized that 4 serum macrophage inflammation markers, soluble (s)CD163, sCD14, galectin-3 binding protein (Gal-3BP), and galectin-3 (Gal-3), are associated with progression of subclinical carotid artery atherosclerosis even after adjustment for the systemic inflammation markers C-reactive protein (CRP) and interleukin-6 (IL-6).
Methods: We examined 778 women (74% HIV+) in the Women’s Interagency HIV Study and 503 men (65% HIV+) in the Multicenter AIDS Cohort Study who underwent repeated B-mode carotid artery ultrasound imaging in 2004–2013. Baseline marker levels were determined from previously frozen serum specimens. We assessed the association of each marker with new plaque formation (focal IMT >1.5 mm) over a median 7 years, adjusting for demographic, behavioral, and cardiometabolic risk factors, and levels of high sensitivity CRP and IL-6.
Results: Levels of each marker were significantly higher in HIV+ compared with HIV- individuals. Presence of focal plaque increased from 8 to 15% in women and 25 to 34% in men over 7 years. After adjustment for risk factors plus hsCRP and IL-6, each standard deviation (SD) of sCD14 was associated with a 21% increased risk of new plaque formation (RR 1.21, 95% CI 1.05-1.41), and this pattern was consistent in women and men. sCD163 was marginally associated with increased risk in men (RR 1.24 per SD, 95% CI 0.97-1.59) but not women (RR 0.96, 95% CI 0.75-1.23). Gal-3BP and Gal-3 were not associated with new plaque formation, nor was IL-6. Among men, the association of sCD163 with plaque formation was most pronounced among HIV+ with CD4+ counts <200 cells/uL. Among women, the association between sCD163 and plaque formation was greatest among HIV/HCV co-infected individuals.
Conclusions: Higher sCD14 and sCD163 levels were associated with new carotid artery plaque formation over 7 years in the context of HIV infection. Monocyte activation may play a disproportionately strong role in the development of atherosclerosis among HIV+ compared with HIV- individuals.
Author Disclosures: D.B. Hanna: None. J. Lin: None. W.S. Post: None. X. Xue: None. K. Anastos: None. M.H. Cohen: None. S.J. Gange: None. S.L. Heath: None. J.M. Lazar: None. C. Liu: None. W.J. Mack: None. I. Ofotokun: None. P.C. Tien: None. H.N. Hodis: None. A.L. Landay: None. L.A. Kingsley: None. R.P. Tracy: None. R.C. Kaplan: None.
- © 2016 by American Heart Association, Inc.