Background: There are many factors associated with human immunodeficiency virus (HIV) patients having a greater risk of cardiovascular diseases (CVD). HIV damages vessel endothelium through chronic inflammation, which, combined with dys­lipidaemia, arterial hypertension, and antiretroviral therapy leads to the progression of atherosclerotic changes.

Aim: Our goal was to determine if a CD4 nadir along with immunological, inflammatory, biochemical, and metabolic mark­ers can be associated with higher vessel stiffness and therefore an increased risk of CVD in patients undergoing antiretroviral therapy for HIV.

Methods: Endothelial damage was evaluated in 20 patients (including four female) during successful antiretroviral therapy. We assessed the endothelial stiffness by recording the reactive hyperaemia of peripheral arteries using an Endo-PAT2000 (ITAMAR^®) device. This device allowed us to measure the arterial tonometry and to determine the augmentation index for a pulse rate of 75/min (AI@75). We set the normal value for vessel stiffness at reactive hyperaemia index (RHI) > 1.67, as recommended by the manufacturer. Additionally, we recorded the length of antiretroviral therapy, number of CD4 lymphocytes, CD4 nadir, HIV viremia, and biochemical and immunologic results. Finally, we compared patients with normal and dysfunctional endothelium.

Results: The only parameter significantly differentiating between the group with and group without endothelium dysfunction was platelet count (p = 0.012).

Conclusions: We were not able to confirm the significance of a CD4 nadir in the progression of endothelial stiffness in HIV patients. However, platelet values could be an important complementary marker for assessing the risk for CVD amongst HIV patients undergoing antiretroviral treatment.