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1 Biomedical Engineering, Eindhoven University of Technology, Eindhoven, The Netherlands
2 Laboratory of Cardiac Energetics, NHLBI, National Institutes of Health,, Bethesda, MD, USA
3 Physiology, Maastricht University, Maastricht, The Netherlands
4 Biomedical Engineering, Eindhoven University of Technology, Eindhoven, The Netherlands; Biophysics, Maastricht University, Maastricht, The Netherlands
* To whom correspondence should be addressed. E-mail: p.h.m.bovendeerd{at}tue.nl.
Intraventricular synchrony of cardiac activation is important for efficient pump function. Ventricular pacing restores the beating frequency, but induces more asynchronous depolarization and more inhomogeneous contraction than in the normal heart. We investigated whether the increased inhomogeneity in the left ventricle can be described by a relatively simple mathematical model of cardiac electromechanics, containing normal mechanical and impulse conduction properties. Simulations of a normal heartbeat and of pacing at the right ventricular apex (RVA) were performed. All properties in the two simulations were equal, except for the depolarization sequence. Simulation results of RVA pacing on local depolarization time and systolic midwall circumferential strain were compared with those measured in dogs, using an epicardial sock electrode and MRI tagging, respectively. We used the same methods for data processing for simulation and experiment. Model and experiment agreed in the following aspects: 1) ventricular pacing decreased systolic pressure and ejection fraction relative to natural sinus rhythm. 2) Shortening during ejection and stroke work declined in early depolarized regions and increased in late depolarized regions. 3) The relation between epicardial depolarization time and systolic midwall circumferential strain was linear and similar for the simulation (slope = -3.80 ± 0.14 s-1, R2 = 0.87) and the experiments (slopes per animal -2.62 ± 0.21 s-1 (R2 = 0.59), -2.97 ±0.19 s-1 (R2 = 0.69) and -4.44 ± 0.26 s-1 (R2 = 0.76). We conclude that our model of electromechanics is suitable to simulate ventricular pacing and that the apparently complex events observed during pacing are caused by well known basic physiological processes.
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