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Published on: October 17, 2017
Short Communication: Carotid Artery Plaque Burden in HIV Is Associated with Soluble Mediators and Monocytes
Dominic C Chow1, Makoa Mau1, Howard N Hodis2
1Hawai'i Center for AIDS, Department of Medicine, University of Hawai'i, John A. Burns School of Medicine, Honolulu, Hawai'i, USA.
Insights
Maximum carotid plaque thickness (MCPT) in people with HIV correlates with inflammatory markers like monocyte chemoattractant protein-1 (MCP-1) and tumor necrosis factor-alpha (TNF-α). These findings suggest increased carotid plaque burden is linked to heightened inflammation and monocyte activity.
Area of Science:
- Cardiovascular Medicine
- Immunology
- Infectious Diseases
Background:
- Maximum carotid plaque thickness (MCPT) is a potential indicator of cardiovascular disease risk, possibly surpassing carotid artery intima-media thickness (cIMT).
- Understanding the relationship between immune cell populations, inflammatory mediators, and MCPT is crucial for assessing cardiovascular risk in people living with HIV (PLWH).
Purpose of the Study:
- To investigate the associations between monocyte and T cell subsets, plasma soluble mediators, and MCPT in PLWH on stable antiretroviral therapy (ART).
- To determine if inflammatory markers and immune cell activation correlate with carotid plaque burden in this population.
Main Methods:
- A cross-sectional study involving 125 PLWH (age >40, on ART >6 months) was conducted.
- MCPT was measured using high-resolution B-mode ultrasound.
- Monocyte and T cell subsets were analyzed via flow cytometry, and plasma mediators (including MCP-1, TNF-α, sVCAM-1, ApoB6, IL-6) were quantified using Luminex assays.
Main Results:
- Twenty-five PLWH had detectable carotid plaque.
- MCPT showed significant correlations with monocyte chemoattractant protein-1 (MCP-1), tumor necrosis factor-alpha (TNF-α), soluble vascular cell adhesion molecule-1 (sVCAM-1), apolipoprotein B6 (ApoB6), and interleukin-6 (IL-6).
- In multivariable analysis, MCP-1, TNF-α, and sVCAM-1 remained significant predictors of MCPT after adjusting for age.
Conclusions:
- Carotid plaque burden in PLWH on ART is associated with elevated levels of inflammatory markers (MCP-1, TNF-α) and endothelial activation (sVCAM-1).
- These findings highlight the role of inflammation and monocyte activity in atherosclerosis progression within this cohort.
- Further research is warranted to explore the evolution and severity of plaque burden in PLWH.
Abstract:
Maximum carotid plaque thickness (MCPT) measures the largest plaque thickness in the carotid artery and reflects atherosclerosis plaque burden. MCPT may be a better predictor of cardiovascular disease than carotid artery intima-media thickness (cIMT) because it identifies potential unstable arterial atherosclerosis plaques. We assessed the relationships of monocyte and T cell populations and plasma soluble mediators with MCPT measures. We performed a cross-sectional and small follow-up analysis in people living with HIV (PLWH) aged >40 years on stable antiretroviral therapy (ART) >6 months. MCPT was acquired by high-resolution B-mode ultrasound. Existing monocyte subsets and T cell activation frequencies were determined by flow cytometry and plasma mediators of inflammation and apolipoproteins were measured by Luminex assay. One hundred twenty-five ART-treated PLWH, 88% male, 55% Caucasian, with a median age of 51 years, median CD4 count of 477 cells/μL (Q1: 325, Q3: 612), 84% undetectable plasma HIV RNA (<50 copies/mL). Twenty-five PLWH had detectable carotid plaque. MCPT correlated with monocyte chemoattractant protein-1 (MCP-1; r = 0.487, p = .016), tumor necrosis factor-α (TNF-α; r = 0.474 p = .019), soluble vascular cell adhesion molecule-1 (sVCAM-1; r = 0.472, p = .020), apolipoprotein B6 (ApoB6; r = -0.473, p = .019), and interleukin-6 (IL-6; r = 0.455, p = .025). In a multivariable regression model, MCP-1, TNF-α, and sVCAM-1 remained significant after adjustment for age. Carotid plaque burden was associated with increased inflammatory, monocyte, and endothelial measures, including MCP-1, TNF-α, and sVCAM-1 levels. Further investigation on the evolution or severity of plaque burden in this population is warranted.
