Related Experiment Video
Updated: Nov 16, 2025

Measuring Frailty in HIV-infected Individuals. Identification of Frail Patients is the First Step to Amelioration and Reversal of Frailty
Published on: July 24, 2013
Etiology and pathophysiology of heart failure in people with HIV
Harry Choi1, Amit K Dey1, Gaurav Sharma2
1Section of Inflammation and Cardiometabolic Diseases, National Institute of Health, Bethesda, MD, USA.
Insights
People with HIV (PHIV) on antiretroviral therapy still face high risks of heart failure and cardiomyopathy due to chronic inflammation. This review explores mechanisms and management strategies for HIV-associated heart conditions.
Area of Science:
- Cardiology
- Infectious Diseases
- Immunology
Background:
- HIV-associated cardiomyopathy (HIVACM) remains a significant concern in people living with HIV (PHIV).
- Highly active antiretroviral therapy (HAART) has reduced AIDS-related mortality but not eliminated the risk of cardiomyopathy and heart failure in PHIV.
- Chronic HIV infection, even with HAART, is linked to persistent inflammation and immune dysregulation contributing to cardiac dysfunction.
Purpose of the Study:
- To review the proposed mechanisms underlying HIV-associated cardiomyopathy and heart failure in patients on HAART.
- To discuss the evolving pathophysiology of HIVACM since the introduction of HAART.
- To briefly cover the evaluation, work-up, and management of cardiomyopathy in PHIV.
Main Methods:
- Literature review of proposed mechanisms of HIV-associated cardiomyopathy.
- Analysis of the impact of HAART on HIVACM pathophysiology.
- Summary of current approaches to evaluation and management of cardiomyopathy in PHIV.
Main Results:
- HAART has shifted HIVACM from a rapidly progressive disease to a chronic condition characterized by inflammation and immune dysregulation.
- Despite HAART, PHIV experience elevated risks of cardiomyopathy and heart failure, independent of traditional cardiovascular risk factors.
- The increasing prevalence of cardiomyopathy and heart failure mortality in PHIV highlights the need for further research into immune-related mechanisms.
Conclusions:
- Chronic HIV infection and its treatment with HAART contribute to ongoing cardiac risks through inflammatory and immune pathways.
- Understanding these mechanisms is crucial for improving the evaluation and management of cardiomyopathy in people living with HIV.
- Further research into immune-related mechanisms may offer novel therapeutic targets for HIV-associated heart disease.
Abstract:
HIV-associated cardiomyopathy is a well-established sequela in people infected with HIV (PHIV). Despite significant advances in HIV management through the use of highly active anti-retroviral therapy (HAART), PHIV on HAART continue to have elevated risk of cardiomyopathy and heart failure, even when accounting for known cardiovascular risk factors. This review article will explore the proposed mechanisms by which chronic HIV infection induces cardiomyopathy and heart failure in the setting of HAART. Evaluation, work-up, and management of cardiomyopathy in PHIV will also be briefly discussed. The advent of HAART has altered the pathophysiology HIV-associated cardiomyopathy from a rapidly progressive cardiomyopathy, often with pericardial involvement, into a chronic process involving inflammation and persistent immune dysregulation. With the significant decrease in AIDS-related deaths, the prevalence of cardiomyopathy and the mortality associated with heart failure in PHIV have increased. Multiple immune-related and inflammatory mechanisms have been proposed, which may provide insight into evaluation and management of cardiomyopathy in PHIV.
Related Concept Videos
Pathophysiology of Heart Failure
Heart Failure I: Introduction
Heart Failure II: Pathophysiology
Heart Failure III: Clinical Manifestations
Heart Failure IV: Classification and Diagnostic Evaluation
Imbalances in Cardiac Output
CHF can occur due to the failure of either side of the heart. Left-side failure leads to pulmonary congestion—the right side continues to send...

