Depressed right ventricular systolic function in heart failure due to constrictive pericarditis

• Type of Material: Article
• Authors: Veena Raizada, University of New Mexico; Kimi Sato, University of Tsukuba; Alaa Alashi, Texas Tech University; Arnav Kumar, Emory University; Deborah Kwon, Cleveland Clinic; Jay Ramchand, Cleveland Clinic; Amy Dillenbeck, Cleveland Clinic; Ross E Zumwalt, University of New Mexico; Adarsh S Vangala, Arizona Health Sciences Center; Tyler D Earley, Samaritan Health Services; A Klein, Cleveland Clinic
• Language: English
• Date: 2021-06-16
• Publisher: WILEY PERIODICALS, INC
• Publication Version: Final Published Version
• Copyright Statement: © 2021 The Authors. ESC Heart Failure published by John Wiley & Sons Ltd on behalf of European Society of Cardiology.
• License: Creative Commons Attribution-NonCommercial 4.0 International
• Final Published Version (URL): http://dx.doi.org/10.1002/ehf2.13418
• Title of Journal or Parent Work: ESC HEART FAILURE
• Volume: 8
• Issue: 4
• Start Page: 3119
• End Page: 3129
• Grant/Funding Information: There was no financial support including research grants and contracts involved in this research.
• Keywords: PATHOLOGY; CARDIOLOGY; Constrictive pericarditis; Life Sciences & Biomedicine; DISEASE; Cardiac & Cardiovascular Systems; EUROPEAN ASSOCIATION; Cardiovascular System & Cardiology; ECHOCARDIOGRAPHY; Longitudinal strain; Heart failure; AMERICAN SOCIETY; MECHANISMS; Science & Technology; Right ventricle; RECOMMENDATIONS; MYOCARDIAL ISCHEMIA; FIBROSIS
• Research Categories: Health Sciences, Medicine and Surgery

Abstract

Aims: Heart failure in constrictive pericarditis (CP) is attributed to impaired biventricular diastolic filling. However, diseases that cause CP due to myocardial infiltration and fibrosis can also impair biventricular systolic function (sf) and contribute to heart failure. This study of patients with CP examined biventricular sf and the effect of myocardial infiltration by pericardial diseases and the resulting fibrosis on ventricular sf. Methods and results: Histopathologic examinations of right ventricular (RV) and left ventricular (LV) myocardia and pericardia were performed on three autopsied hearts of patients with pericardial diseases. Additionally, in 40 adults with clinical heart failure and 40 healthy adults (controls), sf of both ventricles was examined by echocardiography, including strain measurements, and biventricular diastolic filling and pulmonary artery pressures were assessed by cardiac catheterization. Cardiac histopathology indicated thickening of the pericardium with fibrosis, disease infiltrating the myocardium, greater infiltration of the RV than the LV, and an association of pericardial thickness with myocardial infiltrations. Functional analysis indicated that RVsf was impaired on all echo indices, including strain measurement, but LVsf was preserved. Conclusions: Diseases causing CP are not restricted to the pericardium but also infiltrate the biventricular myocardium and affect the thin-walled RV more than the thick-walled LV, resulting in depressed RVsf. The present results help explain clinical heart failure in the presence of restricted diastolic filling in CP. Depression of RVsf due to progression of fibrosis in the RV myocardium may increase the risk of delayed pericardiectomy.