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(Circulation. 2009;119:1192-1194.)
© 2009 American Heart Association, Inc.

Editorial

Cardiac Resynchronization Therapy in Dyssynchronous Heart Failure

Zooming in on Cellular and Molecular Mechanisms

From the Cardiovascular Center, Onze Lieve Vrouwziekenhuis, Aalst, Belgium.

Correspondence to Marc Vanderheyden, MD, Cardiovascular Center, Onze Lieve Vrouwziekenhuis, Moorselbaan 164, 9400 Aalst, Belgium. E-mail marc.vanderheyden@olvz-aalst.be

Key Words: Editorials • pacing • remodeling

An extract of the first 250 words of the full text is provided, because this article has no abstract.

Cardiac resynchronization therapy (CRT) has been implemented as a novel "hemodynamic therapy" for advanced heart failure patients.¹ Resynchronizing the mechanical coordination between left and right ventricles with reduction of the inefficient dyssynchronous contractions improves the mechanical efficiency of the chamber contraction-relaxation cycle, leading to a better hemodynamic profile.² Various randomized trials demonstrated an improvement in symptoms and exercise tolerance in patients with congestive heart failure and cardiac dyssynchrony on top of optimal medical therapy, which translates into better prognosis and improved survival.^3–5 Favorable alterations of clinical outcome were consistent across multiple studies, and CRT has evolved into a Class I indication for such patients with broad QRS complex and severely depressed left ventricular function.¹

Articles pp 1220 and 1231

The dyssynchronous contractions in heart failure patients with left bundle-branch block morphology represent a specific disease entity, named dyssynchronous heart failure. Besides typical ventricular dilatation and asymmetric hypertrophy, the disease is characterized by regional differences in loading and contractile work, as well as in myocardial blood flow and oxygen consumption. In dyssynchronous hearts, the workload is typically lowest in the septum and highest in the left ventricular lateral wall and is accompanied by regional differences in wall stress.⁶ This ultimately results in regional differences in wall thickness and chamber remodeling.⁷ In contrast to other forms of cardiomyopathy where wall thickness is reduced in all regions, cardiomyopathy related to dyssynchronous electrical activation is characterized by regional differences in relative wall thickening with hypertrophy and molecular alterations most pronounced in the late-activated lateral . . . [Full Text of this Article]