Wilco Kroon1, Joost Lumens2, Mark Potse1, Daniel Suerder3, Catherine Klersy4, Francois Regoli3, Romina Murzilli3, Tiziano Moccetti3, Tammo Delhaas2, Rolf Krause1, Frits W Prinzen5, Angelo Auricchio6. 1. Center for Computational Medicine in Cardiology, Institute of Computational Science, University of Lugano, Lugano, Switzerland. 2. Department of Biomedical Engineering, Cardiovascular Research Institute Maastricht, Maastricht University, Maastricht, The Netherlands. 3. Division of Cardiology, Fondazione Cardiocentro Ticino, Lugano, Switzerland. 4. Service of Biometry & Statistics, IRCCS Fondazione Policlinico San Matteo, Pavia, Italy. 5. Department of Physiology, Cardiovascular Research Institute Maastricht, Maastricht University, Maastricht, The Netherlands. 6. 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: angelo.auricchio@cardiocentro.org.
Abstract
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.
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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