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The effects of CD4 nadirs on vessel stiffness in HIV patients undergoing antiretroviral therapy
Tomasz Mikuła, Paweł Balsam1, Michał Peller
11st Chair and Department of Cardiology, Medical University of Warsaw, Warsaw, Poland, Poland. pawel.balsam@me.com.
Insights
Platelet count, not CD4 nadir, significantly differentiates endothelial dysfunction in HIV patients on antiretroviral therapy. Higher platelet values may indicate increased cardiovascular disease risk in this population.
Area of Science:
- Cardiology
- Infectious Diseases
- Immunology
Background:
- Human immunodeficiency virus (HIV) infection increases cardiovascular disease (CVD) risk due to chronic inflammation, dyslipidemia, hypertension, and antiretroviral therapy.
- HIV-related endothelial damage contributes to atherosclerotic changes and heightened CVD risk.
Purpose of the Study:
- To investigate the association between CD4 nadir, immunological, inflammatory, biochemical, and metabolic markers with vessel stiffness and CVD risk in HIV patients.
- To evaluate endothelial stiffness and its relationship with various clinical markers in patients on antiretroviral therapy.
Main Methods:
- Assessed endothelial stiffness using peripheral artery reactive hyperemia and arterial tonometry (Endo-PAT2000) in 20 HIV patients on antiretroviral therapy.
- Measured reactive hyperemia index (RHI) and augmentation index (AI@75), comparing patients with normal (RHI > 1.67) and dysfunctional endothelium.
- Collected data on CD4 count, CD4 nadir, HIV viremia, therapy duration, and biochemical/immunologic markers.
Main Results:
- Platelet count was the sole significant differentiator between patients with and without endothelial dysfunction (p = 0.012).
- CD4 nadir did not show a significant association with endothelial stiffness in this cohort.
Conclusions:
- The study did not confirm CD4 nadir's significance in the progression of endothelial stiffness among HIV patients.
- Platelet values may serve as a valuable complementary marker for assessing cardiovascular disease risk in HIV patients undergoing antiretroviral treatment.
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 dys-lipidaemia, 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 mark-ers 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.
