Key result
Initiation of c-ART in treatment-naive HIV-infected patients was associated with improved LDL particle phenotype and inflammatory biomarkers, but did not prevent progression of carotid intima-media thickness.
Why the study?
The study was conducted to assess the effect of HIV infection and combined antiretroviral therapy on proatherogenic biomarkers and lipids, and investigate their relationship with subclinical atherosclerosis in treatment-naive HIV-infected patients.
Does initiation of combined antiretroviral therapy improve proatherogenic biomarkers, lipid profiles, and subclinical atherosclerosis in treatment-naive HIV-infected patients?
Observational (n=84)
Yes
Does initiation of combined antiretroviral therapy improve proatherogenic biomarkers, lipid profiles, and subclinical atherosclerosis in treatment-naive HIV-infected patients?
p-value: p=0.048
Initiation of antiretroviral therapy in treatment-naive HIV patients improves LDL particle phenotype and inflammatory biomarkers, though HIV infection itself remains associated with progression of carotid intima-media thickness.
OBJECTIVE: To assess the effect of HIV infection and combined antiretroviral therapy (c-ART) on various proatherogenic biomarkers and lipids and to investigate their relationship with subclinical atherosclerosis in a cohort of treatment-naive HIV-infected patients. METHODS: We performed a prospective, comparative, multicenter study of 2 groups of treatment-naive HIV-infected patients (group A, CD4>500 cells/μL, not starting c-ART; and group B, CD4<500 cells/μL, starting c-ART at baseline) and a healthy control group. Laboratory analyses and carotid ultrasound were performed at baseline and at months 12 and 24. The parameters measured were low-density lipoprotein (LDL) particle phenotype, lipoprotein-associated phospholipase A2 (Lp-PLA2), interleukin-6 (IL-6), high-sensitivity C-reactive protein (hs-CRP), sCD14, sCD163, monocyte chemoattractant protein-1(MCP-1), and asymmetric dimethylarginine (ADMA). A linear mixed model based on patient clusters was used to assess differences in biomarkers between the study groups and over time. RESULTS: The study population comprised 62 HIV-infected patients (group A, n = 31; group B, n = 31) and 22 controls. Age was 37 (30-43) years, and 81% were men. At baseline, the HIV-infected patients had a worse LDL particle phenotype and higher plasma concentration of sCD14, sCD163, hs-CRP, and LDL-Lp-PLA2 than the controls. At month 12, there was an increase in total cholesterol (p = 0.002), HDL-c (p = 0.003), and Apo A-I (p = 0.049) and a decrease in sCD14 (p = <0.001) and sCD163 (p<0.001), although only in group B. LDL particle size increased in group B at month 24 (p = 0.038). No changes were observed in group A or in the healthy controls. Common carotid intima-media thickness increased in HIV-infected patients at month 24 (Group A p = 0.053; group B p = 0.048). Plasma levels of sCD14, sCD163, and hs-CRP correlated with lipid values. CONCLUSIONS: In treatment-naive HIV-infected patients, initiation of c-ART was associated with an improvement in LDL particle phenotype and inflammatory/immune biomarkers, reaching values similar to those of the controls. HIV infection was associated with progression of carotid intima-media thickness.
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Yacovo et al. (2020) conducted an observational in HIV infection (n=84). Combined antiretroviral therapy (c-ART) vs. No c-ART (Group A) and healthy controls was evaluated on Change in common carotid intima-media thickness (c-IMT) at 24 months (p=0.048). Initiation of c-ART in treatment-naive HIV-infected patients was associated with improved LDL particle phenotype and inflammatory biomarkers, but did not prevent progression of carotid intima-media thickness.
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