• Joost Lumens, Sylvain Ploux, Marc Strik, John Gorcsan, Hubert Cochet, Nicolas Derval, Maria Strom, Charu Ramanathan, Philippe Ritter, Michel Haïssaguerre, Pierre Jaïs, Theo Arts, Tammo Delhaas, Frits W Prinzen, and Pierre Bordachar.
• Hôpital Cardiologique du Haut-Lévêque, CHU Bordeaux, L'Institut de rythmologie et modélisation cardiaque (LIRYC), Université Bordeaux, Bordeaux, France; Maastricht University Medical Center, Cardiovascular Research Institute Maastricht (CARIM), Maastricht, the Netherlands. Electronic address: joost.lumens@maastrichtuniversity.nl.
• J. Am. Coll. Cardiol. 2013 Dec 24;62(25):2395-403.

ObjectivesThe purpose of this study was to enhance understanding of the working mechanism of cardiac resynchronization therapy by comparing animal experimental, clinical, and computational data on the hemodynamic and electromechanical consequences of left ventricular pacing (LVP) and biventricular pacing (BiVP).BackgroundIt is unclear why LVP and BiVP have comparative positive effects on hemodynamic function of patients with dyssynchronous heart failure.MethodsHemodynamic response to LVP and BiVP (% change in maximal rate of left ventricular pressure rise [LVdP/dtmax]) was measured in 6 dogs and 24 patients with heart failure and left bundle branch block followed by computer simulations of local myofiber mechanics during LVP and BiVP in the failing heart with left bundle branch block. Pacing-induced changes of electrical activation were measured in dogs using contact mapping and in patients using a noninvasive multielectrode electrocardiographic mapping technique.ResultsLVP and BiVP similarly increased LVdP/dtmax in dogs and in patients, but only BiVP significantly decreased electrical dyssynchrony. In the simulations, LVP and BiVP increased total ventricular myofiber work to the same extent. While the LVP-induced increase was entirely due to enhanced right ventricular (RV) myofiber work, the BiVP-induced increase was due to enhanced myofiber work of both the left ventricle (LV) and RV. Overall, LVdP/dtmax correlated better with total ventricular myofiber work than with LV or RV myofiber work alone.ConclusionsAnimal experimental, clinical, and computational data support the similarity of hemodynamic response to LVP and BiVP, despite differences in electrical dyssynchrony. The simulations provide the novel insight that, through ventricular interaction, the RV myocardium importantly contributes to the improvement in LV pump function induced by cardiac resynchronization therapy.Copyright © 2013 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.

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