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This Article Full Text Full Text (PDF) All Versions of this Article: 296/2/H370    most recent 00952.2008v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Keldermann, R. H. Articles by Panfilov, A. V. Search for Related Content PubMed PubMed Citation Articles by Keldermann, R. H. Articles by Panfilov, A. V.

A computational study of mother rotor VF in the human ventricles

¹Department of Theoretical Biology, Utrecht University, Utrecht, The Netherlands; ²Department of Scientific Computing, Simula Research Laboratory, Lysaker, Norway; ³Auckland Bioengineering Institute and Department of Engineering Science, The University of Auckland, Auckland, New Zealand; ⁴Department of Physiology, Anatomy and Genetics, University of Oxford, Oxford, United Kingdom; ⁵Institute of Mathematics, Physics, and Mechanics, University of Ljubljana, Ljubljana, Slovenia; and ⁶Department of Cardiology and Cardiothoracic Surgery, University College Hospital, London, United Kingdom

Submitted 29 August 2008 ; accepted in final form 24 November 2008

Sudden cardiac death is one of the major causes of death in the industrialized world. It is most often caused by a cardiac arrhythmia called ventricular fibrillation (VF). Despite its large social and economical impact, the mechanisms for VF in the human heart yet remain to be identified. Two of the most frequently discussed mechanisms observed in experiments with animal hearts are the multiple wavelet and mother rotor hypotheses. Most recordings of VF in animal hearts are consistent with the multiple wavelet mechanism. However, in animal hearts, mother rotor fibrillation has also been observed. For both multiple wavelet and mother rotor VF, cardiac heterogeneity plays an important role. Clinical data of action potential restitution measured from the surface of human hearts have been recently published. These in vivo data show a substantial degree of spatial heterogeneity. Using these clinical restitution data, we studied the dynamics of VF in the human heart using a heterogeneous computational model of human ventricles. We hypothesized that this observed heterogeneity can serve as a substrate for mother rotor fibrillation. We found that, based on these data, mother rotor VF can occur in the human heart and that ablation of the mother rotor terminates VF. Furthermore, we found that both mother rotor and multiple wavelet VF can occur in the same heart depending on the initial conditions at the onset of VF. We studied the organization of these two types of VF in terms of filament numbers, excitation periods, and frequency domains. We conclude that mother rotor fibrillation is a possible mechanism in the human heart.

action potential duration-restitution heterogeneity; reentrant arrhythmias; ventricular fibrillation; computer simulation