Myocardial substrate after cardiac resynchronization therapy and the risk of ventricular arrhythmias

Myocardial substrate after cardiac resynchronization therapy and the risk of ventricular arrhythmias EDITORIAL Myocardial substrate after cardiac resynchronization therapy and the risk of ventricular arrhythmias Saurabh Malhotra, MD, MPH, FASNC Division of Cardiovascular Medicine, Clinical and Translation Research Center, Jacob School of Medicine and Biomedical Sciences at the University at Buffalo, Buffalo, NY Received Mar 9, 2016; accepted Mar 10, 2016 doi:10.1007/s12350-016-0474-7 prevention and CRT-pacemaker seemed to offer a sim- See related article, pp. 1282–1288 ilar level of survival, suggesting an anti-arrhythmic effect of CRT alone. Since then other studies have reported a potential Myocardial remodeling is a central feature of failing anti-arrhythmic benefit from CRT. Ermis et al prospec- hearts. It can take several forms, and the most easily tively followed 18 patients undergoing an upgrade of a recognizable ones are electrical remodeling (wide QRS defibrillator to a CRT-defibrillator, for arrhythmic complex with or without left bundle branch block) and events. Prior to an upgrade to CRT-defibrillator, 72% of mechanical remodeling (dilated and hypofunctioning the patients experienced an arrhythmic outcome as left ventricle). This remodeling results in disorganized opposed to only 11% following the upgrade, suggesting left ventricular (LV) contraction, which further pro- a role of CRT in ameliorating ventricular arrhythmias in motes heart failure (HF) progression and has been http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Journal of Nuclear Cardiology Springer Journals

Myocardial substrate after cardiac resynchronization therapy and the risk of ventricular arrhythmias

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Publisher
Springer US
Copyright
Copyright © 2016 by American Society of Nuclear Cardiology
Subject
Medicine & Public Health; Cardiology; Nuclear Medicine; Imaging / Radiology
ISSN
1071-3581
eISSN
1532-6551
D.O.I.
10.1007/s12350-016-0474-7
Publisher site
See Article on Publisher Site

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