Arrhythmia-Induced Cardiomyopathies: Mechanisms, Recognition, and Management

Rakesh Gopinathannair, MD, MA^∗^∗ (rakesh.gopinathannair{at}louisville.edu) (drrakeshg{at}yahoo.com),
Susan P. Etheridge, MD^†,
Francis E. Marchlinski, MD^‡,
Francis G. Spinale, MD, PhD^§,
Dhanunjaya Lakkireddy, MD^‖ and
Brian Olshansky, MD^¶

^∗Division of Cardiovascular Medicine, University of Louisville, Louisville, Kentucky
^†Division of Pediatric Cardiology, University of Utah, Salt Lake City, Utah
^‡Division of Cardiology, University of Pennsylvania, Philadelphia, Pennsylvania
^§Department of Internal Medicine, University of South Carolina, Charleston, South Carolina
^‖Division of Cardiology, University of Kansas, Kansas City, Kansas
^¶Mercy Heart and Vascular Institute, Mercy Medical Center North Iowa, Mason City, Iowa

↵∗Reprint requests and correspondence:
Dr. Rakesh Gopinathannair, Division of Cardiovascular Medicine, University of Louisville, 550 South Jackson Street, ACB/A3L41, Louisville, Kentucky 40202.

Abstract

Arrhythmia-induced cardiomyopathy (AIC) is a potentially reversible condition in which left ventricular dysfunction is induced or mediated by atrial or ventricular arrhythmias. Cellular and extracellular changes in response to the culprit arrhythmia have been identified, but specific pathophysiological mechanisms remain unclear. Early recognition of AIC and prompt treatment of the culprit arrhythmia using pharmacological or ablative techniques result in symptom resolution and recovery of ventricular function. Although cardiomyopathy in response to an arrhythmia may take months to years to develop, recurrent arrhythmia can result in rapid decline in ventricular function with development of heart failure, suggesting residual ultrastructural abnormalities. Reports of sudden death in patients with normalized left ventricular ejection fraction cast doubt on the complete reversibility of this condition. Several aspects of AIC, including specific pathophysiological mechanisms, predisposing factors, optimal therapeutic strategies to prevent ultrastructural changes, and long-term risk of sudden death remain unresolved and need further research.

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Footnotes

The views expressed in this paper by the American College of Cardiology's (ACC's) Electrophysiology Section Leadership Council do not necessarily reflect the views of the Journal of the American College of Cardiology or the ACC.
Dr. Spinale’s research is supported by National Institutes of Health (NIH) grants HL057952, HL059165, and HL095608 and a merit award from the Veterans Affairs Health Administration. Dr. Gopinathannair has served as a consultant to St. Jude Medical and Abiomed; and has served on speakers bureaus for Pfizer/Bristol-Myers Squibb. Dr. Marchlinski’s research is sponsored by Biosense Webster, Boston Scientific, St. Jude Medical, and Medtronic. Dr. Marchlinski has served on advisory boards for Biosense Webster, Boston Scientific, and Medtronic; and has received lecture honoraria from Biosense Webster, Biotronik, Boston Scientific, St. Jude Medical, and Medtronic. Dr. Spinale’s research is supported by NIH grants HL057952, HL059165, and HL095608; and a merit award from the Veterans Affairs Health Administration. Dr. Lakkireddy has served as a speaker and consultant to Janssen, Pfizer, St. Jude Medical, Biosense Webster, and Bristol-Myers Squibb; and has served on advisory boards for Atritech and SentreHeart. Dr. Olshansky has served as a consultant to Boston Scientific, Medtronic, Daiichi-Sankyo, Biotronik, Cardionomics, BioControl, Amarin, Boehringer Ingelheim, On-X, Abbott Vascular, and Sanofi. Dr. Etheridge has reported that she has no relationships relevant to the contents of this paper to disclose.
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