Frequency of Subclinical Atherosclerosis in Brazilian HIV-Infected Patients

Péricles Sidnei Salmazo1, Silméia Garcia Zanati Bazan1, Flávio Gobbis Shiraishi1

  • 1Faculdade de Medicina de Botucatu (UNESP), Botucatu, SP - Brazil.

Insights

HIV-infected patients have a significantly higher risk of atherosclerosis, linked to traditional cardiovascular factors. Protease inhibitor treatment did not increase arterial plaque risk, suggesting the Framingham Risk Score may be unsuitable for this population.

Area of Science:

  • Cardiology
  • Infectious Diseases
  • Public Health

Background:

  • Acquired Immunodeficiency Syndrome (AIDS) and atherosclerosis are major public health concerns.
  • Increased cardiovascular events in HIV-infected individuals with longer survival are not fully understood.

Purpose of the Study:

  • To determine the prevalence of subclinical atherosclerosis in HIV-infected patients compared to controls.
  • To analyze associations between atherosclerosis and clinical/laboratory variables, cardiovascular risk factors, and the Framingham coronary heart disease risk score (FCRS).

Main Methods:

  • A prospective, cross-sectional, case-control study involving 264 HIV-infected patients and 279 controls.
  • Assessment included carotid artery ultrasound, arterial stiffness (PWV, AIx), blood tests, and FCRS.
  • Statistical significance was set at p < 0.05.

Main Results:

  • Atherosclerotic plaques were found in 37% of HIV patients versus 4% of controls (p < 0.001).
  • HIV patients exhibited higher carotid intima-media thickness (p < 0.001).
  • HIV presence, adjusted for confounders, increased atherosclerotic plaque risk nearly fivefold (OR: 4.9; p < 0.001).
  • Protease inhibitor use showed no association with plaque frequency or arterial stiffness.

Conclusions:

  • HIV-infected patients face elevated atherosclerosis risk, associated with conventional cardiovascular risk factors.
  • Protease inhibitors do not appear to promote arterial dysfunction or increase plaque burden.
  • The FCRS may be inadequate for assessing cardiovascular risk in HIV-infected populations.
Abstract

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