Diastolic Dysfunction in Individuals With Human Immunodeficiency Virus Infection: Literature Review, Rationale and Design of the Characterizing Heart Function on Antiretroviral Therapy (CHART) Study

• Published in: Journal of cardiac failure Vol. 24; no. 4; pp. 255 - 265
• Main Authors: Butler, Javed, Kalogeropoulos, Andreas P., Anstrom, Kevin J., Hsue, Priscilla Y., Kim, Raymond J., Scherzer, Rebecca, Shah, Sanjiv J., Shah, Svati H., Velazquez, Eric J., Hernandez, Adrian F., Desvigne-Nickens, Patrice, Braunwald, Eugene
• Format: Journal Article
• Language: English
• Published: United States Elsevier Inc 01.04.2018
• Subjects: Anti-Retroviral Agents - therapeutic use; diastolic dysfunction; Global Health; heart failure; Heart Failure, Diastolic - epidemiology; Heart Failure, Diastolic - etiology; Heart Failure, Diastolic - physiopathology; HIV; HIV Infections - complications; HIV Infections - drug therapy; Human immunodeficiency virus; Humans; Incidence; pathophysiology; Prognosis; Stroke Volume - physiology; Ventricular Function, Left - physiology; diastolic dysfunction; heart failure; Human immunodeficiency virus; pathophysiology
• ISSN: 1071-9164; 1532-8414; 1532-8414
• DOI: 10.1016/j.cardfail.2018.02.001

Antiretroviral therapy (ART) has been associated with a shift in the epidemiology of human immunodeficiency virus (HIV)–associated cardiomyopathy from a phenotype of primarily left ventricular (LV) systolic dysfunction to LV diastolic dysfunction (DD). Patients with HIV receiving ART have higher rates of DD compared with age-matched control subjects and develop DD at a younger age. However, little is known about the natural history and pathogenesis of DD in virally suppressed HIV-infected patients. Current evidence suggests that immune processes modulate the risk for cardiac involvement in HIV-infected persons. Ongoing inflammation appears to have myocardial effects, and accelerated myocardial fibrosis appears to be a key mediator of HIV-induced DD. The Characterizing Heart Function on Antiretroviral Therapy (CHART) study aims to systematically investigate determinants, mechanisms, and consequences of DD in HIV-infected patients. We will compare ART-treated virally suppressed HIV-infected individuals with and without DD and HIV− individuals with DD regarding (1) systemic inflammation, myocardial stress, and subclinical myocardial necrosis as indicated by circulating biomarkers; (2) immune system activation as indicated by cell surface receptors; (3) myocardial fibrosis according to cardiac magnetic resonance examination; (4) markers of fibrosis and remodeling, oxidative stress, and hypercoagulability; (5) left atrial function according to echocardiographic examination; (6) myocardial stress and subclinical necrosis as indicated by circulating biomarkers; (7) proteomic and metabolic profiles; and (8) phenotype signatures derived from clinical, biomarker, and imaging data.