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In vivo electromechanical assessment of heart failure patients with prolonged QRS duration.

Authors:
Wilco Kroon Joost Lumens Mark Potse Daniel Suerder Catherine Klersy Francois Regoli Romina Murzilli Tiziano Moccetti Tammo Delhaas Rolf Krause Frits W Prinzen Angelo Auricchio

Heart Rhythm 2015 Jun 5;12(6):1259-67. Epub 2015 Mar 5.

Center for Computational Medicine in Cardiology, Institute of Computational Science, University of Lugano, Lugano, Switzerland; Division of Cardiology, Fondazione Cardiocentro Ticino, Lugano, Switzerland. Electronic address:

Background: Combined measurement of electrical activation and mechanical dyssynchrony in heart failure (HF) patients is scarce but may contain important mechanistic and diagnostic clues.

Objective: The purpose of this study was to characterize the electromechanical (EM) coupling in HF patients with prolonged QRS duration.

Methods: Ten patients with QRS width >120 ms underwent left ventricular (LV) electroanatomic contact mapping using the Noga® XP system (Biosense Webster). Recorded voltages during the cardiac cycle were converted to maps of depolarization time (TD). Electrode positions were tracked and converted into maps of time-to-peak shortening (TPS) using custom-made deformation analysis software. Correlation analysis was performed between the 2 maps to quantify EM coupling. Simulations with the CircAdapt cardiovascular system model were performed to mechanistically unravel the observed relation between TD and TPS.

Results: The delay between earliest LV electrical activation and peak shortening differed considerably between patients (TPSmin-TDmin = 360 ± 73 ms). On average, total mechanical dyssynchrony exceeded total electrical activation (ΔTPS = 177 ± 47 ms vs ΔTD = 93 ± 24 ms, P <.001), but a large interpatient variability was observed. The TD and TPS maps correlated strongly in all patients (median R = 0.87, P <.001). These correlations were similar for regions with unipolar voltages above and below 6mV (Mann-Whitney U test, P = .93). Computer simulations revealed that increased passive myocardial stiffness decreases ΔTPS relative to ΔTD and that lower contractility predominantly increases TPSmin-TDmin.

Conclusion: EM coupling in HF patients is maintained, but the relationship between TD and TPS differs strongly between patients. Intra-individual and inter-individual differences may be explained by local and global differences in passive and contractile myocardial properties.

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http://dx.doi.org/10.1016/j.hrthm.2015.03.006DOI Listing
June 2015

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