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Human immunodeficiency virus per se exerts atherogenic effects

Ugo Oliviero1, Giovanni Bonadies, Valentina Apuzzi

  • 1Department of Internal Medicine, University Federico II, Naples, Italy.

Atherosclerosis
|December 17, 2008
PubMed

Insights

Human Immunodeficiency Virus (HIV) infection causes early vascular damage, including thickened carotid arteries and impaired blood vessel function, independent of treatment or metabolic issues. This suggests HIV itself contributes to atherosclerosis development.

Area of Science:

  • Cardiovascular Medicine
  • Infectious Diseases
  • Vascular Biology

Background:

  • Premature atherosclerosis in HIV patients is often linked to highly active antiretroviral therapy (HAART) and metabolic complications.
  • The independent role of Human Immunodeficiency Virus (HIV) infection in promoting atherosclerosis remains unclear.
  • This study investigates whether HIV infection itself contributes to atherogenic effects.

Purpose of the Study:

  • To determine if HIV infection per se induces atherogenic vascular changes.
  • To evaluate the impact of HIV on vascular structure and function in treatment-naïve patients.

Main Methods:

  • Carotid intima-media thickness (IMT) and brachial artery vasodilation (flow-mediated dilation [FMD] and non-dependent vasodilation [NMD]) were measured.
  • 38 treatment-naïve, untreated HIV-infected patients and 41 healthy controls were studied.
  • Controls were matched for metabolic risk factors.

Main Results:

  • HIV patients exhibited significantly higher mean carotid IMT compared to controls (0.85±0.2mm vs. 0.63±0.1mm).
  • Carotid IMT was associated with duration of HIV infection and CD4 T-cell count.
  • Brachial FMD was significantly impaired in HIV patients (8.8±3% vs. 12.2±3% in controls), correlating inversely with HIV viral load (HIV-RNA copies).
  • NMD did not differ significantly between groups.

Conclusions:

  • HIV infection causes early functional and structural vascular alterations, independent of HAART and metabolic factors.
  • Findings support the theory that viral infection contributes to atherosclerosis.
  • Early vascular assessment in HIV-infected patients is recommended.
Abstract

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