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AIDS. 2019 May 1;33(6):1043-1052. doi: 10.1097/QAD.0000000000002142.

Plasma acylcarnitines and progression of carotid artery atherosclerosis in HIV infection.

Author information

1
Department of Epidemiology and Population Health, Albert Einstein College of Medicine, Bronx, New York.
2
Metabolomics Platform, Broad Institute of MIT and Harvard, Cambridge, Massachusetts.
3
Department of Epidemiology, Johns Hopkins University Bloomberg School of Public Health, Baltimore, Maryland.
4
Division of Cardiology, Department of Medicine, Northwestern University Feinberg School of Medicine, Chicago, Illinois.
5
Department of Medicine, University of Southern California, Los Angeles, California.
6
Department of Immunology and Microbiology, Rush University Medical Center, Chicago, Illinois.
7
Department of Medicine, SUNY Downstate Medical Center, Brooklyn.
8
Department of Medicine (Cardiology), Albert Einstein College of Medicine, Bronx, New York.
9
Department of Epidemiology, Human Genetics, and Environmental Sciences, School of Public Health, The University of Texas Health Science Center at Houston, Houston, Texas.
10
Division of Cardiology, Department of Medicine, Johns Hopkins University, Baltimore, Maryland.
11
Public Health Sciences Division, Fred Hutchinson Cancer Research Center, Seattle, Washington, USA.

Abstract

OBJECTIVE:

To evaluate plasma acylcarnitine profiles and their relationships with progression of carotid artery atherosclerosis among individuals with and without HIV infection.

DESIGN:

Prospective cohort studies of 499 HIV-positive and 206 HIV-negative individuals from the Women's Interagency HIV Study and the Multicenter AIDS Cohort Study.

METHODS:

Twenty-four acylcarnitine species were measured in plasma samples of participants at baseline. Carotid artery plaque was assessed using repeated B-mode carotid artery ultrasound imaging in 2004-2013. We examined the associations of individual and aggregate short-chain (C2-C7), medium-chain (C8-C14) and long-chain acylcarnitines (C16-C26) with incident carotid artery plaque over 7 years.

RESULTS:

Among 24 acylcarnitine species, C8-carnitines and C20 : 4-carnitines showed significantly lower levels comparing HIV-positive to HIV-negative individuals (false discovery rate adjusted P < 0.05); and C20-carnitines and C26-carnitines showed significantly higher levels in HIV positive using antiretroviral therapy than those without antiretroviral therapy (false discovery rate adjusted P < 0.05). In the univariate analyses, higher aggregated short-chain and long-chain acylcarnitine scores were associated with increased risk of carotid artery plaque [risk ratios (RRs) = 1.22 (95% confidence interval 1.02-1.45) and 1.20 (1.02-1.41) per SD increment, respectively]. The association for the short-chain acylcarnitine score remained significant [RR = 1.23 (1.05-1.44)] after multivariate adjustment (including traditional cardiovascular disease risk factors). This association was more evident in HIV-positive individuals without persistent viral suppression [RR = 1.37 (1.11-1.69)] compared with those with persistent viral suppression during follow-up [RR = 1.03 (0.76-1.40)] or HIV-negative individuals [RR = 1.02 (0.69-1.52)].

CONCLUSION:

In two HIV cohorts, plasma levels of most acylcarnitines were not significantly different between HIV-positive and HIV-negative individuals. However, higher levels of aggregated short-chain acylcarnitines were associated with progression of carotid artery atherosclerosis.

PMID:
30946158
PMCID:
PMC6457128
[Available on 2020-05-01]
DOI:
10.1097/QAD.0000000000002142

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