ArticleFrontiers in physiology2017
Mechanisms Underlying the Emergence of Post-acidosis Arrhythmia at the Tissue Level: A Theoretical Study.
Article in Frontiers in physiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed.
- Pseudo-Ischemic ECG Changes in a Patient With Profound Mixed Metabolic Acidosis Due to Metformin Use.JACC. Case reports · 2026Article
- Digital twin for sex-specific identification of class III antiarrhythmic drugs based on in vitro measurements, computer models, and machine learning tools.PLoS computational biology · 2025Article
- A pilot study of the proarrhythmic effects of pimobendan injection in clinically healthy cats.Veterinary research communications · 2024Article
- The Influence of Arrhythmias and Metabolic Profile on Inpatient Mortality in Patients with Left Ventricular Assist Devices.Journal of clinical medicine · 2024Article
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- An Unexpected Cause of Cardiotoxicity: Kombucha Tea.Anatolian journal of cardiology · 2022Article
- How synergy between mechanistic and statistical models is impacting research in atrial fibrillation.Frontiers in physiology · 2022Review
- Understanding PITX2-Dependent Atrial Fibrillation Mechanisms through Computational Models.International journal of molecular sciences · 2021Review
- The therapeutic importance of acid-base balance.Biochemical pharmacology · 2021Review
- PITX2 upregulation increases the risk of chronic atrial fibrillation in a dose-dependent manner by modulatingAnnals of translational medicine · 2020Article
- In silico investigation of the mechanisms underlying atrial fibrillation due to impaired Pitx2.PLoS computational biology · 2020Article
- In silico study of the effects of anti-arrhythmic drug treatment on sinoatrial node function for patients with atrial fibrillation.Scientific reports · 2020Article
- Proarrhythmia in the p.Met207Val PITX2c-Linked Familial Atrial Fibrillation-Insights From Modeling.Frontiers in physiology · 2019Article
- Ectopic beats arise from micro-reentries near infarct regions in simulations of a patient-specific heart model.Scientific reports · 2018Article
- Ionic and cellular mechanisms underlying TBX5/PITX2 insufficiency-induced atrial fibrillation: Insights from mathematical models of human atrial cells.Scientific reports · 2018Article
- Computational Cardiac Modeling Reveals Mechanisms of Ventricular Arrhythmogenesis in Long QT Syndrome Type 8:Frontiers in physiology · 2017Article
- Association of Acidemia With Short-Term Mortality of Acute Myocardial Infarction: A Retrospective Study Base on MIMIC-III Database.Clinical and applied thrombosis/hemostasis : official journal of the International Academy of Clinical and Applied Thrombosis/HemostasisArticle
Corrections and comments
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4 authors.
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No grant is acknowledged in the PubMed record.
Abstract
Acidosis has complex electrophysiological effects, which are associated with a high recurrence of ventricular arrhythmias. Through multi-scale cardiac computer modeling, this study investigated the mechanisms underlying the emergence of post-acidosis arrhythmia at the tissue level. In simulations, ten Tusscher-Panfilov ventricular model was modified to incorporate various data on acidosis-induced alterations of cellular electrophysiology and intercellular electrical coupling. The single cell models were incorporated into multicellular one-dimensional (1D) fiber and 2D sheet tissue models. Electrophysiological effects were quantified as changes of action potential profile, sink-source interactions of fiber tissue, and the vulnerability of tissue to the genesis of unidirectional conduction that led to initiation of re-entry. It was shown that acidosis-induced sarcoplasmic reticulum (SR) calcium load contributed to delayed afterdepolarizations (DADs) in single cells. These DADs may be synchronized to overcome the source-sink mismatch arising from intercellular electrotonic coupling, and produce a premature ventricular complex (PVC) at the tissue level. The PVC conduction can be unidirectionally blocked in the transmural ventricular wall with altered electrical heterogeneity, resulting in the genesis of re-entry. In conclusion, altered source-sink interactions and electrical heterogeneity due to acidosis-induced cellular electrophysiological alterations may increase susceptibility to post-acidosis ventricular arrhythmias.
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