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Patient-specific Modeling of the Heart: Estimation of Ventricular Fiber Orientations
Published on: January 8, 2013
Models of stretch-activated ventricular arrhythmias
Natalia A Trayanova1, Jason Constantino, Viatcheslav Gurev
1Department of Biomedical Engineering and Institute for Computational Medicine, Johns Hopkins University, Baltimore, MD 21218, USA. ntrayanova@jhu.edu
Journal of Electrocardiology
|July 20, 2010
Summary
Computer models reveal how stretch-activated channels contribute to heart arrhythmias. These simulations explore mechanoelectric coupling
Area of Science:
- Cardiac Electrophysiology
- Computational Biology
- Biophysics
Background:
- Mechanoelectric coupling is crucial in cardiac function.
- Stretch-activated channels are key components, opening upon mechanical stimuli.
- Understanding their role in ventricular arrhythmogenesis is limited by experimental resolution.
Purpose of the Study:
- To illustrate the utility of whole-heart computer simulations in determining the role of mechanoelectric coupling in ventricular arrhythmogenesis.
- To investigate the mechanisms of commotio cordis and precordial thump using computational models.
- To gain insight into electromechanical dysfunction during acute regional ischemia.
Main Methods:
- Review of stretch-activated channel modeling approaches.
- Electrophysiologic modeling of rabbit ventricles.
- Development of a 3D coupled electromechanical model of rabbit ventricles.
Main Results:
- Stretch-activated channels significantly affect cardiac electrophysiologic properties.
- Commotio cordis can initiate ventricular tachycardia via stretch-activated channels.
- Precordial thump can terminate arrhythmias; electromechanical dysfunction contributes to ischemia-induced arrhythmogenesis.
Conclusions:
- Sophisticated computer simulations are essential for understanding mechanoelectric coupling in cardiac arrhythmias.
- Modeling provides mechanistic insights into mechanically induced arrhythmias and their termination.
- Electromechanical dysfunction plays a role in arrhythmogenesis during ischemia.
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