Association of Macrophage Inflammation Biomarkers With Progression of Subclinical Carotid Artery Atherosclerosis in HIV-Infected Women and Men

Abstract

Background.

Monocytes and monocyte-derived macrophages promote atherosclerosis through increased inflammation and vascular remodeling. This may be especially true in chronic human immunodeficiency virus (HIV) infection.

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. We assessed baseline associations of the serum macrophage inflammation markers soluble (s)CD163, sCD14, galectin-3 (Gal-3), and Gal-3 binding protein (Gal-3BP) with carotid plaque formation (focal intima-media thickness >1.5 mm) over 7 years.

Results.

Marker levels were higher in HIV⁺ persons versus HIV^– persons. Presence of focal plaque increased over time: from 8% to 15% in women, and 24% to 34% in men. After adjustment for demographic, behavioral, and cardiometabolic factors, and CRP and interleukin-6, each standard deviation increase in sCD14 was associated with increased plaque formation (risk ratio [RR] 1.24, 95% confidence interval [CI] 1.07–1.43). This pattern was consistentby sex. sCD163 was associated with plaque formation in virally suppressed HIV⁺ men (RR 1.52, 95% CI 1.04–2.22); Gal-3BP and Gal-3 were not associated with increased plaque.

Conclusions.

sCD14 and sCD163 may play important roles in atherogenesis among HIV⁺ persons.

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