ArticleFrontiers in physiology2018
Heart Rhythm Insights Into Structural Remodeling in Atrial Tissue: Timed Automata Approach.
Article in Frontiers in physiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed, 13 citations in OpenAlex.
- Unified mechanism of local drivers in a percolation model of atrial fibrillation.Physical review. E · 2019Article
- The Reversal Effect of Sigma-1 Receptor (S1R) Agonist, SA4503, on Atrial Fibrillation After Depression and Its Underlying Mechanism.Frontiers in physiology · 2019Article
- Understanding the transition from paroxysmal to persistent atrial fibrillation.Physical review researchArticle
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Authors and funding
3 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The heart rhythm of a person following heart transplantation (HTX) is assumed to display an intrinsic cardiac rhythm because it is significantly less influenced by the autonomic nervous system-the main source of heart rate variability in healthy people. Therefore, such a rhythm provides evidence for arrhythmogenic processes developing, usually silently, in the cardiac tissue. A model is proposed to simulate alterations in the cardiac tissue and to observe the effects of these changes on the resulting heart rhythm. The hybrid automata framework used makes it possible to represent reliably and simulate efficiently both the electrophysiology of a cardiac cell and the tissue organization. The curve fitting method used in the design of the hybrid automaton cycle follows the well-recognized physiological phases of the atrial myocyte membrane excitation. Moreover, knowledge of the complex architecture of the right atrium, the ability of the almost free design of intercellular connections makes the automata approach the only one possible. Two particular aspects are investigated: impairment of the impulse transmission between cells and structural changes in intercellular connections. The first aspect models the observed fatigue of cells due to specific cardiac tissue diseases. The second aspect simulates the increase in collagen deposition with aging. Finally, heart rhythms arising from the model are validated with the sinus heart rhythms recorded in HTX patients. The modulation in the impairment of the impulse transmission between cells reveals qualitatively the abnormally high heart rate variability observed in patients living long after HTX.
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