Estimating the time scale and anatomical location of atrial fibrillation spontaneous termination in a biophysical model
Due to their transient nature, spontaneous terminations of atrial fibrillation (AF) are difficult to investigate. Apparently, confounding experimental findings about the time scale of this phenomenon have been reported, with values ranging from 1 s to 1 min. We propose a biophysical modeling approac...
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Published in | Medical & biological engineering & computing Vol. 50; no. 2; pp. 155 - 163 |
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Main Authors | , , , , |
Format | Journal Article |
Language | English |
Published |
Berlin/Heidelberg
Springer-Verlag
01.02.2012
Springer Nature B.V |
Subjects | |
Online Access | Get full text |
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Summary: | Due to their transient nature, spontaneous terminations of atrial fibrillation (AF) are difficult to investigate. Apparently, confounding experimental findings about the time scale of this phenomenon have been reported, with values ranging from 1 s to 1 min. We propose a biophysical modeling approach to study the mechanisms of spontaneous termination in two models of AF with different levels of dynamical complexity. 8 s preceding spontaneous terminations were studied and the evolution of cycle length and wavefront propagation were documented to assess the time scale and anatomical location of the phenomenon. Results suggest that termination mechanisms are dependent on the underlying complexity of AF. During simulated AF of low complexity, the total process of spontaneous termination lasted 3,200 ms and was triggered in the left atrium 800 ms earlier than in the right atrium. The last fibrillatory activity was observed more often in the right atrium. These asymmetric termination mechanisms in both time and space were not observed during spontaneous terminations of complex AF simulations, which showed less predictable termination patterns lasting only 1,600 ms. This study contributes to the interpretation of previous clinical observations, and illustrates how computer modeling provides a complementary approach to study the mechanisms of cardiac arrhythmias. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 0140-0118 1741-0444 |
DOI: | 10.1007/s11517-011-0859-3 |