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Atherosclerosis is associated with multiple pathogenic mechanisms in HIV-infected antiretroviral-naive or treated

Stefania Piconi1, Serena Parisotto, Giuliano Rizzardini

  • 1Infectious Diseases Unit, University of Milano, Milan, Italy.

AIDS (London, England)
|October 20, 2012
PubMed

Insights

Atherosclerosis in HIV infection differs based on antiretroviral therapy (ART) status. Inflammation drives the condition in ART-naive patients, while metabolic factors are more significant in ART-treated individuals.

Area of Science:

  • Cardiovascular Health
  • Infectious Diseases
  • Immunology

Background:

  • HIV-infected patients exhibit increased atherosclerotic disease burden compared to the general population.
  • Antiretroviral therapy (ART) has altered the landscape of HIV comorbidities, including cardiovascular disease.
  • Understanding the distinct drivers of atherosclerosis in treated versus untreated HIV is crucial for effective management.

Purpose of the Study:

  • To compare the roles of inflammation, endothelial function, and metabolic factors in atherosclerosis development in ART-treated and ART-naive HIV patients.
  • To elucidate the differential pathogenesis of atherosclerosis in the context of HIV infection and its treatment.
  • To identify key factors contributing to cardiovascular risk in diverse HIV patient populations.

Main Methods:

  • Cross-sectional study of 79 HIV-infected patients (55 ART-treated, 24 ART-naive).
  • Assessment of intima-media thickness (IMT) via echo-Doppler, alongside inflammatory, endothelial, metabolic, and cholesterol efflux markers.
  • Multivariate analysis adjusted for age, CD4 nadir, BMI, and Framingham risk score.

Main Results:

  • Inflammation appears to be a primary driver of atherogenesis in ART-naive HIV patients.
  • Metabolic factors, including LDL, ApoB, and lipoprotein A, play a more prominent role in ART-treated HIV patients.
  • ATP-binding cassette transporter A1 (ABCA-1), involved in cholesterol efflux, is upregulated in ART-treated individuals.

Conclusions:

  • Atherosclerosis in HIV infection is multifactorial, with distinct dominant pathways in treated versus untreated individuals.
  • Inflammatory and HIV-driven processes may be more critical in the absence of ART.
  • Metabolic, non-inflammatory factors gain importance in patients undergoing ART, necessitating tailored cardiovascular risk management strategies.
Abstract

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