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Rapid Screening of HIV Reverse Transcriptase and Integrase Inhibitors
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Rapid Screening of HIV Reverse Transcriptase and Integrase Inhibitors

Published on: April 9, 2014

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Highly active antiretroviral therapy-related mechanisms of endothelial and platelet function alterations

Paolo Gresele, Emanuela Falcinelli, Stefania Momi

  • 1Division of Internal and Cardiovascular Medicine and Division of Infectious Disease, Department of Medicine, University of Perugia, Perugia, Italy.

Reviews in Cardiovascular Medicine
|July 3, 2014
PubMed

Insights

Highly active antiretroviral therapy (HAART) has made human immunodeficiency virus (HIV) a chronic condition, increasing risks for coronary artery disease (CAD). This review explores how HIV and HAART impact endothelial function, inflammation, and platelets, contributing to cardiovascular complications.

Area of Science:

  • Cardiovascular disease research
  • Infectious disease epidemiology
  • Pharmacological research

Background:

  • Highly active antiretroviral therapy (HAART) has transitioned human immunodeficiency virus (HIV) infection into a manageable chronic condition.
  • Aging HIV-positive populations face increased risks of chronic degenerative diseases, notably atherosclerotic cardiovascular disease and coronary artery disease (CAD).
  • Traditional cardiovascular risk factors like dyslipidemia, insulin resistance, and altered fat distribution are implicated in HIV-associated CAD, potentially linked to HIV infection or HAART toxicity.

Purpose of the Study:

  • To analyze the emerging mechanisms contributing to cardiovascular complications in HIV-infected individuals on HAART.
  • To investigate the specific roles of endothelial dysfunction, endothelium-leukocyte interactions, and platelet activation in HIV-associated cardiovascular risk.

Main Methods:

  • Review of current scientific literature on HIV, HAART, and cardiovascular disease.
  • Analysis of proposed pathophysiological pathways linking HIV and HAART to endothelial function, inflammation, and platelet behavior.
  • Synthesis of evidence regarding non-traditional mechanisms of cardiovascular risk in the context of HIV infection.

Main Results:

  • HIV and HAART significantly impact endothelial function, a key factor in cardiovascular health.
  • Alterations in endothelium-leukocyte interactions are observed, suggesting a role for chronic inflammation in HIV-associated CAD.
  • Platelet activation and function are affected, potentially contributing to an pro-thrombotic state in HIV-infected patients.

Conclusions:

  • Beyond traditional risk factors, HIV and HAART exert direct effects on vascular biology, increasing cardiovascular risk.
  • Endothelial dysfunction, inflammation, and platelet abnormalities represent critical pathways for HIV-associated CAD.
  • Further research into these mechanisms is essential for developing targeted prevention and treatment strategies for cardiovascular disease in the HIV-positive population.

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