Why the study?
Do markers of inflammation and endothelial dysfunction correlate with subclinical atherosclerosis in HIV-infected men under 55?
Do markers of inflammation and endothelial dysfunction correlate with subclinical atherosclerosis in HIV-infected men under 55?
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While HIV infection increases markers of inflammation and endothelial dysfunction, these biomarkers do not improve the assessment of subclinical atherosclerosis beyond traditional risk scores (SCORE).
INTRODUCTION: Antiretroviral therapy in HIV-infected patients appears to be associated with increased incidence of cardiovascular disease (CVD).The aim of our study was to investigate the differences in markers of inflammation, endothelial dysfunction and prothrombotic state between treated and untreated HIV-infected patients with or without subclinical atherosclerosis. METHODS: Eighty-six Slovenian HIV-infected male patients below the age of 55 participated in our study. Levels of high-sensitivity C-reactive protein (hsCRP), vascular cell adhesion molecule 1 (VCAM-1) and plasminogen activator inhibitor 1 (PAI-1) were measured. The presence of subclinical atherosclerosis was determined by measuring carotid intima-media thickness. RESULTS: The level of hsCRP was significantly increased in HIV-infected patients; it was higher in treated than untreated patients. VCAM-1 was significantly increased; it was higher in untreated than treated patients. PAI 1 was significantly increased; there were no differences between untreated and treated patients. Patients with subclinical atherosclerosis had elevated hsCRP; levels of VCAM-1 and PAI-1 were not significantly different. CONCLUSION: Signs of systemic and vascular inflammation persist in both untreated and treated HIV infected patients. None of the studied markers contributed to improved assessment of subclinical atherosclerosis. The usefulness of such markers in routine clinical evaluation of CVD risk in HIV infected patients remains unclear.
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Pirš et al. (2014) studied this question.
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