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Cardiomyopathy and Heart Failure in Patients With HIV Infection

Panagiotis Savvoulidis1, Javed Butler2, Andreas Kalogeropoulos3

  • 1Royal Brompton & Harefield NHS Foundation Trust, London, United Kingdom.

The Canadian Journal of Cardiology
|January 10, 2019
PubMed

Insights

Antiretroviral therapy (ART) has shifted HIV-associated heart failure from systolic to diastolic dysfunction. Ongoing inflammation, not ART toxicity, drives heart disease in people with HIV, necessitating new research for optimal treatment.

Area of Science:

  • Cardiology
  • Infectious Diseases
  • Public Health

Background:

  • Antiretroviral therapy (ART) has improved life expectancy for HIV-infected individuals, leading to new health challenges.
  • Prolonged exposure to chronic immune activation, systemic inflammation, and cardiometabolic burden impacts cardiovascular health in HIV.
  • The traditional HIV-cardiomyopathy phenotype is evolving due to these factors.

Purpose of the Study:

  • To describe the changing epidemiology of cardiomyopathy and heart failure (HF) in the context of modern HIV treatment.
  • To explore the roles of chronic inflammation, immune activation, and ART in HIV-associated cardiovascular disease.
  • To highlight the need for further research into optimal screening and treatment strategies for cardiac abnormalities in HIV patients.

Main Methods:

  • This study is a review of the current literature on HIV-associated cardiomyopathy and heart failure.
  • Analysis of epidemiological shifts in cardiac dysfunction among HIV-infected populations.
  • Examination of the impact of chronic inflammation, immune activation, and highly active ART (HAART) on cardiovascular outcomes.

Main Results:

  • The prevalence of HIV-associated cardiomyopathy with overt left ventricular systolic dysfunction has decreased.
  • Cardiomyopathy now presents with a more insidious course, increased ischemic background, and highly prevalent left ventricular diastolic dysfunction.
  • HIV-infected patients exhibit increased susceptibility to coronary artery disease and HF post-myocardial infarction.
  • Ongoing inflammation and immune activation remain central drivers of cardiac issues, despite HAART.

Conclusions:

  • The changing landscape of HIV-associated heart disease necessitates a re-evaluation of therapeutic approaches.
  • The prognostic significance of prevalent diastolic abnormalities in HIV-infected patients requires further investigation.
  • Systematic research is a public health priority to address the unique cardiovascular challenges in the HIV-infected population.

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