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Ventricular dyssynchrony and mechanisms of resynchronization therapy

D.A Kass*

Division of Cardiology, Department of Medicine, The Johns Hopkins Medical Institutions, Baltimore, Maryland, U.S.A.

* Correspondence: David A. Kass, Division of Cardiology, Department of Medicine, The Johns Hopkins Medical Institutions, Baltimore, MA 21287, U.S.A.

Abstract

Patients with dilated cardiomyopathy (DCM) that is further complicated by intra-ventricular conduction delay with discoordinate wall motion have increased mortality risk as compared with the general DCM population. Dyssynchrony reduces cardiac systolic function while increasing oxygen consumption, and may be a source of arrhythmia. The recent development of endocardial lead systems to activate the left ventricle prematurely has yielded the novel therapeutic option of resynchronization therapy to correct cardiac dyssynchrony. Using either biventricular or left ventricular pre-excitation, systolic function and energetic efficiency can be substantially enhanced in heart failure patients who have underlying discoordinate contraction. The present review addresses the pathophysiology of cardiac dyssynchrony and the mechanisms that underlie resynchronization treatment.

Key Words: Bi-entricular • heart failure • haemodynamic • pacemaker • pacing


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