Computational framework for simulating the mechanisms and ECG of re-entrant ventricular fibrillation.
Ventricular arrhythmias remain an important cause of morbidity and mortality in the Western world. Although the underlying mechanisms of these arrhythmias can be studied experimentally, these investigations are in general limited to mapping electrical activity on the heart surface. Computational models of action potential propagation offer a potentially powerful way to study electrical activation and arrhythmias, but current models are not easy to link to the clinical environment. In this paper, we describe a framework for computing action potential propagation in which the geometry, electrophysiology and regional properties of ventricular myocardium can be specified so that, for example, different models for cardiac cellular electrophysiology can be used. We have computed action potential propagation during both normal beats and re-entry in an anatomically accurate model of ventricular geometry. By computing the resultant electric current flow in the torso we have also generated simulated ECG signals that result from specific activation patterns in the ventricular model. Models can be powerful tools for explaining observations, and this approach is able to provide a direct link between the different configurations of re-entry observed in computational and experimental studies, and the ECG signals observed in patients.
Clayton
Richard H
RH
School of Biomedical Sciences, Worsley Building, University of Leeds, Woodhouse Lane, Leeds LS2 9JT, UK. richard@cbiol.leeds.ac.uk
Holden
Arun V
AV
D000200:Action Potentials / Q000502:physiology; D003198:Computer Simulation; D004562:Electrocardiography; D006801:Humans; D008955:Models, Cardiovascular; D014693:Ventricular Fibrillation / Q000503:physiopathology*; D016276:Ventricular Function / Q000502:physiology