Markov modeling of phase singularity interaction effects in human atrial and ventricular fibrillation.

dc.contributor.authorJenkins, E.V.
dc.contributor.authorDharmaprani, D.
dc.contributor.authorSchopp, M.
dc.contributor.authorQuah, J.X.
dc.contributor.authorTiver, K.
dc.contributor.authorMitchell, L.
dc.contributor.authorNash, M.P.
dc.contributor.authorClayton, R.H.
dc.contributor.authorPope, K.
dc.contributor.authorGanesan, A.N.
dc.date.issued2023
dc.description.abstractAtrial and ventricular fibrillation (AF/VF) are characterized by the repetitive regeneration of topological defects known as phase singularities (PSs). The effect of PS interactions has not been previously studied in human AF and VF. We hypothesized that PS population size would influence the rate of PS formation and destruction in human AF and VF, due to increased inter-defect interaction. PS population statistics were studied in computational simulations (Aliev-Panfilov), human AF and human VF. The influence of inter-PS interactions was evaluated by comparison between directly modeled discrete-time Markov chain (DTMC) transition matrices of the PS population changes, and M/M/∞ birth-death transition matrices of PS dynamics, which assumes that PS formations and destructions are effectively statistically independent events. Across all systems examined, PS population changes differed from those expected with M/M/∞. In human AF and VF, the formation rates decreased slightly with PS population when modeled with the DTMC, compared with the static formation rate expected through M/M/∞, suggesting new formations were being inhibited. In human AF and VF, the destruction rates increased with PS population for both models, with the DTMC rate increase exceeding the M/M/∞ estimates, indicating that PS were being destroyed faster as the PS population grew. In human AF and VF, the change in PS formation and destruction rates as the population increased differed between the two models. This indicates that the presence of additional PS influenced the likelihood of new PS formation and destruction, consistent with the notion of self-inhibitory inter-PS interactions.
dc.description.statementofresponsibilityEvan V. Jenkins, Dhani Dharmaprani, Madeline Schopp, Jing Xian Quah, Kathryn Tiver, Lewis Mitchell, Martyn P. Nash, Richard H. Clayton, Kenneth Pope, and Anand N. Ganesan
dc.identifier.citationChaos, 2023; 33(6)
dc.identifier.doi10.1063/5.0141890
dc.identifier.issn1054-1500
dc.identifier.issn1089-7682
dc.identifier.orcidDharmaprani, D. [0000-0003-4660-0119]
dc.identifier.orcidMitchell, L. [0000-0001-8191-1997]
dc.identifier.urihttps://hdl.handle.net/2440/138816
dc.language.isoen
dc.publisherAIP Publishing
dc.relation.granthttp://purl.org/au-research/grants/nhmrc/2010522
dc.rightsPublished under a nonexclusive license by AIP Publishing
dc.source.urihttps://doi.org/10.1063/5.0141890
dc.subjectHeart Atria
dc.subjectHumans
dc.subjectAtrial Fibrillation
dc.subjectVentricular Fibrillation
dc.subjectProbability
dc.subjectMarkov Chains
dc.subject.meshHeart Atria
dc.subject.meshHumans
dc.subject.meshAtrial Fibrillation
dc.subject.meshVentricular Fibrillation
dc.subject.meshProbability
dc.subject.meshMarkov Chains
dc.titleMarkov modeling of phase singularity interaction effects in human atrial and ventricular fibrillation.
dc.typeJournal article
pubs.publication-statusPublished

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