Related Experiment Video
Updated: Mar 13, 2026

Studying Left Ventricular Reverse Remodeling by Aortic Debanding in Rodents
Published on: July 14, 2021
Reversible transition from a hypertrophic to a dilated cardiomyopathy
Frank Spillmann1, Uwe Kühl1, Sophie Van Linthout2
1Department of Cardiology Charité-University Medicine of Berlin, Campus Virchow Klinikum Berlin Germany.
Abstract:
We report the case of a 17-year-old female patient with known hypertrophic cardiomyopathy and a Wolff-Parkinson-White syndrome. She came to our department for further evaluation of a new diagnosed dilated cardiomyopathy characterized by an enlargement of the left ventricle and a fall in ejection fraction. Clinically, she complained about atypical chest pain, arrhythmic episodes with presyncopal events, and dyspnea (NYHA III) during the last 6 months. Non-invasive and invasive examinations including magnetic resonance imaging, electrophysiological examinations, and angiography did not lead to a conclusive diagnosis. Therefore, endomyocardial biopsies (EMBs) were taken to investigate whether a specific myocardial disease caused the impairment of the left ventricular function. EMB analysis resulted in the diagnosis of a virus-negative, active myocarditis. Based on this diagnosis, an immunosuppressive treatment with prednisolone and azathioprine was started, which led to an improvement of cardiac function and symptoms within 3 months after initiating therapy. In conclusion, we show that external stress triggered by myocarditis can induce a reversible transition from a hypertrophic cardiomyopathy to a dilated cardiomyopathy phenotype. This case strongly underlines the need for a thorough and invasive examination of heart failure of unknown causes, including EMB investigations as recommend by the actual ESC position statement.
Related Concept Videos
Cardiomyopathy III: Hypertrophic Cardiomyopathy
Cardiomyopathy II: Dilated Cardiomyopathy
Cardiomyopathy V: Interprofessional Care
Cardiomyopathy I: Introduction and Classification
Heart Failure II: Pathophysiology
Cardiomyopathy IV: Restrictive Cardiomyopathy

