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Marker of endothelial dysfunction asymmetric dimethylarginine is elevated in HIV infection but not associated with sub-clinical atherosclerosis

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BACKGROUND: Cardiovascular disease (CVD) contributes to excess morbidity and mortality in HIV infection, and endothelial dysfunction may contribute to this pattern. We aimed to determine endothelial function in treated and untreated HIV-infected individuals and investigate potential associations with viral replication, immune activation, coagulation, platelet function, and subclinical atherosclerosis.

METHODS: Asymmetric dimethylarginine (ADMA, marker of endothelial dysfunction) and soluble CD14 (sCD14, marker of monocyte activation) were measured in plasma from two previously established cross-sectional cohorts: Cohort A including 50 untreated and 50 anti-retroviral therapy (ART) treated HIV-infected individuals with previously assessed coagulation and platelet function, and Cohort B including 105 HIV-infected individuals on ART and 105 uninfected controls with previously assessed coronary artery calcium score (CACS), myocardial perfusion defects (MPD), and carotid intima-media thickness (cIMT).

RESULTS: Concentrations of ADMA were higher in HIV-infected individuals compared to uninfected controls, and higher ADMA was found in ART treated compared to untreated HIV-infected individuals. ADMA was associated with viral load, sCD14, D-dimer, and low CD4T-cell count in untreated HIV infection. Only viral load remained significant in multivariate analyses. In ART-treated HIV-infected individuals, ADMA was not associated with CACS, MPD, or cIMT.

CONCLUSIONS: Evidence of endothelial dysfunction was found in HIV infection and in untreated compared to treated HIV infection. In untreated HIV infection, the main driver of endothelial dysfunction was viral replication. Importantly, in treated HIV infection, ADMA was not associated with sub-clinical atherosclerosis. Thus, our data question the potential of ADMA as a useful biomarker of early atherosclerosis in treated HIV infection.

TidsskriftJournal of acquired immune deficiency syndromes (1999)
Udgave nummer5
Sider (fra-til)507-13
StatusUdgivet - dec. 2016

ID: 49162096