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Non-Classical Monocytes Predict Progression of Carotid Artery Bifurcation Intima-Media Thickness in HIV-infected Individuals on Stable Antiretroviral Therapy
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Abstract
BACKGROUND
Inflammation may contribute to cardiovascular disease (CVD) among antiretrovirally suppressed HIV-infected individuals. We assessed relationships of monocyte, CD8 T-cell activation and plasma biomarkers to changes in carotid artery intima-media thickness (CIMT).
METHODS
Longitudinal study of HIV-infected subjects ≥ 40 years and on stable antiretroviral therapy (ART) ≥ 3 months. Peripheral blood mononuclear cells were immunophenotyped by multiparameteric flow cytometry to quantify classical (CD14 ++CD16 −), intermediate (CD14 ++CD16 +), non-classical (CD14 low/+CD16 ++) and transitional (CD14+CD16−) monocyte subsets and activated (CD38 +HLA-DR +) CD8 + T-cells at baseline. Plasma biomarkers were assessed by multiplex Luminex assay. High resolution B-mode ultrasounds of right carotid arteries were obtained. Changes in CIMT over 2 years at the right common carotid artery (CIMT CCA) and right bifurcation (CIMT BIF) were outcome variables.
RESULTS
We studied 50 subjects: 84% male, median age 49 (Q1, Q3; 46, 56) years, median CD4 count 461 (317, 578) cells/mm 3, and with HIV RNA≤50 copies/mL in 84%. Change in CIMT BIF correlated with log values of baseline absolute count of non-classical monocytes (r=0.37, p=0.020), and with MCP-1 (r=0.42, p=0.0024) and TNF-α (r=0.30, p=0.036) levels. In multivariable linear regression, only non-classical monocytes and MCP-1 predicted the change in CIMT BIF, independent of Framingham Risk Score and baseline CIMT BIF. No correlation was noted between CD8 T-cell activation and CIMT BIF change. Monocyte subsets, CD8 T-cell activation and biomarker concentrations were not correlated with changes in CIMT CCA.