Cardiovascular risks in Asian HIV-infected patients receiving boosted-protease inhibitor-based antiretroviral treatment.

INTRODUCTION

Increased risk of cardiovascular disease in HIV-infected patients was tought to be the cause of multiple mechanistic factors, which changing the HIV care landscape. Antiretroviral therapy (ART), especially protease inhibitors (PI), is one of common HIV treatments that may have some association with this. The mechanism of PI in comparison to other regimens, however, are not clearly understood.

METHODOLOGY

Age-and gender-match HIV-infected patients treated with either boosted-PI-based regimen (boosted-PI group, N=30) or NNRTI-based ART (non-PI group, N = 30) were recruited for this cross-sectional study. Parameters determined cardiovascular risks, inflammation, endothelial function, and bone metabolic function were evaluated.

RESULTS

Compared with non-PI, patients in the boosted-PI group had more evidence of dyslipidemia. No statistical difference in the prevalence of subclinical atherosclerosis was found between the two groups. Circulating levels of inflammatory markers, C-reactive protein (CRP) (5.4±9.1 vs. 14.9 ± 19.4 mg/L, p = 0.019) and lectin-liked oxidized lipoprotein receptor-1 (LOX-1) (387 ± 299 vs. 554 ± 324 pg/mL, p = 0.042) were lower in boosted-PI group. Contrastingly, Vascular adhesion molecules-1 (VCAM-1) (160.2 ± 80.0 vs. 147.8 ± 66.3 ng/mL, p = 0.010), and osteoprotegerin (OPG) (153.7 ± 57.1 vs. 126.4 ± 35.8, p = 0.031) were higher. After adjustment in the multivariate analysis, PI treatment is the only independent parameter associated with the changes of CRP, LOX-1, VCAM-1, and OPG. Subgroup analysis showed that ARV treatment effects differed among participant having dyslipidemia.

CONCLUSIONS

The major mechanism in which PI-mediated was triggering atherogenesis could be through alteration of lipid metabolism and endothelial function, but no evidence of accelerated pro-inflammatory response was attested.