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Am J Physiol Heart Circ Physiol 290: H968-H977, 2006. First published September 19, 2005; doi:10.1152/ajpheart.00641.2005
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Tailoring cardiac resynchronization therapy using interventricular asynchrony. Validation of a simple model

Xander A. A. M. Verbeek,1 Angelo Auricchio,2 Yinghong Yu,3 Jiang Ding,3 Thierry Pochet,3 Kevin Vernooy,1 Andrew Kramer,3 Julio Spinelli,3 and Frits W. Prinzen1

1Department of Physiology, Cardiovascular Research Institute Maastricht, Maastricht University, Maastricht, The Netherlands; 2Pacing Therapies for Congestive Heart Failure Investigator Group, Division of Cardiology, University Hospital, Magdeburg, Germany; and 3Guidant/CRM, St. Paul, Minnesota

Submitted 14 June 2005 ; accepted in final form 15 September 2005

This study explores the use of interventricular asynchrony (interVA) for optimizing cardiac resynchronization therapy (CRT), an idea emerging from a simple pathway model of conduction in the ventricles. Measurements were performed in six dogs with chronic left bundle branch block (LBBB) and in 29 patients of the Pacing Therapies for Congestive Heart Failure (PATH-CHF)-I study. In the dogs, intraventricular asynchrony (intraVA) was determined using left ventricular (LV) endocardial activation maps. In dogs and patients, the maximum rate of rise of LV pressure (LV dP/dtmax) and the pulse pressure (PP) and interVA [time delay between upslope of LV and right ventricular (RV) pressure curves] were measured during LV, RV, and biventricular (BiV) pacing with various atrioventricular (AV) delays. Measurements in the canine hearts supported the pathway model in that optimal resynchronization occurred at ~50% reduction of intraVA and at an interVA value halfway that during LBBB and LV pacing. In patients with significant hemodynamic response during pacing (n = 22), intrinsic interVA and interVA at peak improvement (interVAp) varied widely between patients (from –83 to –15 ms and from –42 to +31 ms, respectively). However, the model predicted individual interVAp accurately (SD of ±6 ms and ±12 ms for LV dP/dtmax and PP, respectively). At equal interVA, LV and BiV pacing produced equal hemodynamic response, but in 11 of 22 responders, BiV pacing reduced interVA insufficiently to reach the maximum hemodynamic response. LV pacing at short AV delay proved to result in better hemodynamics than predicted by the model, indicating that additional factors determine hemodynamics during LV preexcitation. Guided by a simple pathway model, interVA measurements accurately predict optimal hemodynamic performance in individual CRT patients.

bundle-branch block; conduction; heart failure; pacing; ventricles



Address for reprint requests and other correspondence: F. W. Prinzen, Dept. of Physiology, Maastricht Univ., P.O. Box 616, 6200 MD Maastricht, The Netherlands (e-mail: frits.prinzen{at}fys.unimaas.nl)




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