ArticleScientific reports2016
Mechanisms of arrhythmogenesis related to calcium-driven alternans in a model of human atrial fibrillation.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 25 citations in OpenAlex.
- The Hodgkin-Huxley-Katz Prize Lecture: Heart digital twins: A new paradigm in arrhythmia medicine.The Journal of physiology · 2026Article
- Computational modeling of cardiac electrophysiology and arrhythmogenesis: toward clinical translation.Physiological reviews · 2024Review
- Up digital and personal: How heart digital twins can transform heart patient care.Heart rhythm · 2024Review
- Cardiac Alternans: From Bedside to Bench and Back.Circulation research · 2023Review
- Sensitivity Analysis of Cardiac Alternans and Tachyarrhythmia to Ion Channel Conductance Using Population Modeling.Bioengineering (Basel, Switzerland) · 2022Article
- Effect of angiotensin receptor-neprilysin inhibitor on atrial electrical instability in atrial fibrillation.Frontiers in cardiovascular medicine · 2022Article
- Computational models of atrial fibrillation: achievements, challenges, and perspectives for improving clinical care.Cardiovascular research · 2021Review
- Altered calcium handling produces reentry-promoting action potential alternans in atrial fibrillation-remodeled hearts.JCI insight · 2020Article
- Prediction of Cardiac Mechanical Performance From Electrical Features During Ventricular Tachyarrhythmia Simulation Using Machine Learning Algorithms.Frontiers in physiology · 2020Article
- The role of personalized atrial modeling in understanding atrial fibrillation mechanisms and improving treatment.International journal of cardiology · 2019Review
- Understanding AF Mechanisms Through Computational Modelling and Simulations.Arrhythmia & electrophysiology review · 2019Review
- Computational models in cardiology.Nature reviews. Cardiology · 2019Review
- Understanding the Beat-to-Beat Variations of P-Waves Morphologies in AF Patients During Sinus Rhythm: A Scoping Review of the Atrial Simulation Studies.Frontiers in physiology · 2019Article
- Increased Vulnerability to Atrial Fibrillation Is Associated With Increased Susceptibility to Alternans in Old Sheep.Journal of the American Heart Association · 2018Article
- Increased thin filament activation enhances alternans in human chronic atrial fibrillation.American journal of physiology. Heart and circulatory physiology · 2018Article
- Mechanisms and Drug Development in Atrial Fibrillation.Pharmacological reviews · 2018Review
- CaAmerican journal of physiology. Heart and circulatory physiology · 2017Article
- Calcium Signaling and Cardiac Arrhythmias.Circulation research · 2017Review
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
The occurrence of atrial fibrillation (AF) is associated with progressive changes in the calcium handling system of atrial myocytes. Calcium cycling instability has been implicated as an underlying mechanism of electrical alternans observed in patients who experience AF. However, the extent to which calcium-induced alternation of electrical activity in the atria contributes to arrhythmogenesis is unknown. In this study, we investigated the effects of calcium-driven alternans (CDA) on arrhythmia susceptibility in a biophysically detailed, 3D computer model of the human atria representing electrical and structural remodeling secondary to chronic AF. We found that elevated propensity to CDA rendered the atria vulnerable to ectopy-induced arrhythmia. It also increased the complexity and persistence of arrhythmias induced by fast pacing, with unstable scroll waves meandering and frequently breaking up to produce multiple wavelets. Our results suggest that calcium-induced electrical instability may increase arrhythmia vulnerability and promote increasing disorganization of arrhythmias in the chronic AF-remodeled atria, thus playing an important role in the progression of the disease.
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