To evaluate plasma acylcarnitine profiles and their relationships with progression of carotid artery atherosclerosis among individuals with and without HIV infection.
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.
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.
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)].
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.
aDepartment of Epidemiology and Population Health, Albert Einstein College of Medicine, Bronx, New York
bMetabolomics Platform, Broad Institute of MIT and Harvard, Cambridge, Massachusetts
cDepartment of Epidemiology, Johns Hopkins University Bloomberg School of Public Health, Baltimore, Maryland
dDivision of Cardiology, Department of Medicine, Northwestern University Feinberg School of Medicine, Chicago, Illinois
eDepartment of Medicine, University of Southern California, Los Angeles, California
fDepartment of Immunology and Microbiology, Rush University Medical Center, Chicago, Illinois
gDepartment of Medicine, SUNY Downstate Medical Center, Brooklyn
hDepartment of Medicine (Cardiology), Albert Einstein College of Medicine, Bronx, New York
iDepartment of Epidemiology, Human Genetics, and Environmental Sciences, School of Public Health, The University of Texas Health Science Center at Houston, Houston, Texas
jDivision of Cardiology, Department of Medicine, Johns Hopkins University, Baltimore, Maryland
kPublic Health Sciences Division, Fred Hutchinson Cancer Research Center, Seattle, Washington, USA.
Correspondence to Dr Qibin Qi, Department of Epidemiology and Population Health, Albert Einstein College of Medicine, 1300 Morris Park Avenue, Bronx, NY 10461, USA. Tel: +1 718 430 4203; fax: +1 718 430 8780; e-mail: email@example.com
Received 16 July, 2018
Revised 17 December, 2018
Accepted 21 December, 2018
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