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Europace 2009 11(Supplement 5):v10-v14; doi:10.1093/europace/eup272
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Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2009. For permissions please email: journals.permissions@oxfordjournals.org.

This article appears in the following Europace issue: Spotlight Issue: Cardiac Resynchronization Therapy [View the issue table of contents]

Pathophysiological mechanisms underlying ventricular dyssynchrony

Alan Cheng1, Robert H. Helm2,* and Theodore P. Abraham1

1 Division of Cardiology, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD, USA; 2 Division of Cardiology, Department of Medicine, Boston University School of Medicine, Baltimore, MD, USA

Left ventricular dyssynchrony due to conduction system disease creates cardiac inefficiency even in normal hearts. Dyssynchrony in the failing heart results in the development of a discrete heart failure phenotype as it induces chamber heterogeneity at the cellular and molecular levels that leads to impaired excitation-contraction coupling, increased arrhythmia susceptibility, and decreased myocyte survival among other pathologic changes. Recent research has demonstrated that these biomolecular changes are amazingly reversed with cardiac resynchronization therapy, providing insight into how to target the therapy.

Key Words: Cardiac resynchronization therapy, Heart failure, Dyssynchrony, Pathophysiology


* Corresponding author: Section of Cardiology, Boston University School of Medicine, 88 East Newton Street, Collamore Building Room 817D, Boston, MA 02118, USA. Tel: +1 617-638-8985, Fax: +1 617-638-8814. Email: robert.helm{at}bmc.org


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