A set of plasma lipid species was found to be associated with carotid artery atherosclerosis, which, when altered, may be associated with HIV and antiretroviral therapies (ARTs), according to study results published in JAMA Cardiology.

HIV is associated with greater progression of carotid artery atherosclerosis and cardiovascular disease. ARTs are known to  affect lipid metabolism, placing individuals with HIV on this treatment at higher risk for cardiovascular disease. However, the associations between HIV, plasma lipidome, and the risk for cardiovascular disease are not well understood.

Researchers examined the associations between the progression of carotid artery atherosclerosis and 211 plasma lipid species over the course of approximately 7 years in patients from 2 prospective cohorts: the Women’s Interagency HIV Study and the Multicenter AIDS Cohort Study (n=737; ages, 35-55; n=520 with HIV; n=217 without HIV). None of the patients had cardiovascular disease or carotid artery plaque at baseline.

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Researchers used high-resolution B-mode carotid artery ultrasonography to measure the risk for plaque, which was defined as an area with localized intima-media thickness >1.5 mm in any of the 6 imaged carotid artery locations (the near and far walls of the common carotid artery, carotid bifurcation, and internal carotid artery). Poisson regression models were used to examine the association between the 211 lipid species and the risk for plaque in all patients.

A total of 120 lipid species from 10 lipid classes were found to be associated with a risk for plaque, with the following lipid species : ceramide (16:0; risk ratio [RR], 1.29; 95% CI, 1.02-1.63), cholesteryl ester (16:1; RR 1.28; 95% CI, 1.08-1.52), diacylglycerol (38:5; RR 1.26; 95% CI, 0.98-1.61), lysophosphatidylcholine (20:4; RR 1.28; 95% CI, 1.05-1.58), lysophosphatidylethanolamine (16:0; RR 1.28; 95% CI, 1.05-1.57), phosphatidylethanolamine (38:6; RR 1.33; 95% CI, 1.08-1.64), triacylglycerol (54:6; RR 1.26; 95% CI, 1.04-1.54), phosphatidylethanolamine-plasmalogen (36:2; RR 1.25; 95% CI, 1.04-1.52), and phosphatidylserine-plasmalogen (36:3; RR 1.19; 95% CI, 1.00-1.43). Phosphatidylcholine (36:4; RR 0.65; 95% CI, 0.54-0.77) was associated with a reduced risk for plaque. 

Patients with vs without HIV had higher levels of plaque-increased lipid species, particularly patients receiving ART. Lipid network analysis identified 9 lipid subnetwork modules. Two modules composed of triacylglycerols and phosphatidylcholines with higher carbon numbers and more double bonds, respectively, had the strongest associations with an increased risk for plaque (RR, 1.36; 95% CI, 1.16-1.58; P =.001 and RR, 1.35; 95% CI, 1.13-1.62 per standard deviation of the lipid module score; P =.006, respectively).

Study limitations include the fact that the levels of lipid species were semi-quantified without absolute values. In addition, the study did not examine incident cardiovascular events, and investigators had difficulty adequately imaging all carotid artery segments.

“[M]ultiple lipid species associated with progression of carotid artery atherosclerosis, independent of traditional CVD risk factors,” concluded the study authors. “These intriguing data implicate structure features of the acyl chains of lipid species in the formation of carotid artery plaques.”

Reference

Chai JC, Deik AA, Hua S, et al. Association of lipidomic profiles with progression of carotid artery atherosclerosis in HIV infection [published online October 23, 2019]. JAMA Cardiol. doi: 10.1001/jamacardio.2019.4025