The effect of HIV infection on atherosclerosis and lipoprotein metabolism: a one year prospective study

Abstract

Objectives: HIV infection is associated with dyslipidaemia and increased risk of cardiovascular disease. The effects of HIV infection and antiretroviral treatment on surrogate markers of atherosclerosis, and lipoprotein metabolism were evaluated in a 12 month prospective study.

Methods and results: Treatment-naive HIV patients were recruited into one of three groups: untreated HIV infection not likely to require initiation of antiretroviral therapy (ART) for at least 12 months; initiating treatment with non nucleoside reverse transcriptase inhibitor-containing ART regimen and initiating treatment with protease inhibitor-containing ART regimen. The patients underwent assessment of carotid intima-media thickness (cIMT), pulse wave velocity (PWV), brachial flow-mediated dilation (FMD) and variables of plasma lipoprotein metabolism at baseline and 12 months. The findings were compared with published values for age and sex matched HIV-negative healthy subjects in a cross-sectional fashion. cIMT and FMD were lower while PWV was higher in HIV-patients compared with HIV-negative individuals; none of the markers changed significantly during 12 months follow up. HIV patients had hypoalphalipoproteinemia and elevated plasma levels of lecithin:cholesterol acyltransferase (LCAT) and cholesteryl ester transfer protein. The only significant changes in lipid-related variables were elevation of total cholesterol and triglycerides in patients treated with PI-containing regimen and elevation of plasma LCAT levels in patients treated with NNRTI-containing regimen. The ability of whole and apoB-depleted plasma to effect cholesterol efflux was not impaired in all three groups.

Conclusions: This study did not find evidence for rapid progression of subclinical atherosclerosis and deterioration of dyslipidaemia in HIV patients within 1 year.

Figure 1. Cholesterol efflux to whole plasma or apoB-depleted plasma of HIV patients

THP-1 cells were differentiated, labeled with [³H] cholesterol and activated with TO-901317 (4 µ mol/L) as described in Methods. Cells were then incubated for 2 h with whole plasma (1%) (A) or apoB-depleted plasma (1%) (B). Cholesterol efflux is expressed as proportion of labeled cholesterol moved from cells to medium. *p<0.01 versus baseline of the same group; this difference disappeared when cholesterol efflux was normalized to plasma apoA-I content.