Cardiovascular Toxicology

, Volume 4, Issue 3, pp 261–269

Clinical aspects of endothelial dysfunction associated with human immunodeficiency virus infection and antiretroviral agents


DOI: 10.1385/CT:4:3:261

Cite this article as:
Shankar, S.S. & Dubé, M.P. Cardiovasc Toxicol (2004) 4: 261. doi:10.1385/CT:4:3:261


Endothelial dysfunction is a critical initial step of atherogenesis that subsequently contributes to the progression and clinical manifestations of atherosclerosis. The use of human immunodeficiency virus type 1 (HIV-1) protease inhibitor (PI) agents has been associated with increased cardiovascular events and worsening of multiple coronary heart disease risk factors including dyslipidemia, insulin resistance, and endothelial dysfunction. Endothelial dysfunction may be caused by HIV infection itself as well as treatment-related effects of the antiretroviral agents used to treat HIV. The available evidence suggests that Pls may induce endothelial dysfunction via their effects on both lipid and glucose metabolism. Studies in healthy subjects confirm a role for reduced endothelial nitric oxide production in the endothelial dysfunction associated with the PI indinavir. Further work is needed to determine the relative tendencies of other antiretroviral agents to induce endothelial dysfunction, the physiologic mechanisms involved, and the contribution of the metabolic and body shape changes associated with HIV treatment-related lipodystrophy, and to establish effective interventions for endothelial dysfunction in HIV-infected patients.

Key words

Human immunodeficiency virus endothelial dysfunction anti-retroviral therpay protease inhibitors insulin resistance nitric oxide 

Copyright information

© Humana Press Inc. 2004

Authors and Affiliations

  1. 1.Department of Medicine and Division of EndocrinologyIndiana University School of MedicineIndianapolis
  2. 2.Department of Medicine and Division of Infectious DiseasesIndiana University School of MedicineIndianapolis
  3. 3.Wishard Memorial HospitalIndianapolis

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