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Electromechanics of paced left ventricle simulated by straightforward mathematical model: comparison with experiments

¹Department of Biomedical Engineering, Eindhoven University of Technology, Eindhoven, The Netherlands; ²Laboratory of Cardiac Energetics, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland; and ³Department of Physiology, Maastricht University, ⁴Department of Lead Modeling, Medtronic Bakken Research Center, and ⁵Department of Biophysics, Maastricht University, Maastricht, The Netherlands

Submitted 5 April 2005 ; accepted in final form 12 June 2005

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 ± 0.28 s^–1, R² = 0.87) and the experiments [slopes for 3 animals –2.62 ± 0.43 s^–1 (R² = 0.59), –2.97 ± 0.38 s^–1 (R² = 0.69), and –4.44 ± 0.51 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.

eikonal-diffusion equation; electromechanics; ventricular pacing; finite elements

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