ArticlePLoS computational biology2021
A computational model of pig ventricular cardiomyocyte electrophysiology and calcium handling: Translation from pig to human electrophysiology.
Article in PLoS computational biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 14 citations in OpenAlex.
- In silico modeling of methadone-related ion current effects to predict QT interval prolongation.Journal of pharmacokinetics and pharmacodynamics · 2026Article
- Multiscale Electrophysiological Remodeling in Ischemic Heart Failure: Simulation Analysis of Ventricular Ectopic Activation.Biomedicines · 2026Article
- In silico predictions of action potential propagation in doxorubicin cardiotoxicity: A parametric study using preclinical 3D magnetic resonance imaging-based fibrotic left ventricle models.The Journal of physiology · 2026Article
- In silico assessment of arrhythmic risk following the implantation of engineered heart tissues in porcine hearts with varying infarct locations.PLoS computational biology · 2026Article
- Integrated multi-modal data analysis for computational modeling of healthy and location-dependent myocardial infarction conditions in porcine hearts.PLoS computational biology · 2026Article
- Mechanistic interpretations of sustained ventricular fibrillation: The role of mapping methodology, model and time.Heart international · 2026Review
- Computational Medicine: What Electrophysiologists Should Know to Stay Ahead of the Curve.Current cardiology reports · 2024Review
- A novel computational model of swine ventricular myocyte reveals new insights into disease mechanisms and therapeutic approaches in Timothy Syndrome.Scientific reports · 2024Article
- Measurement of magnetostimulation thresholds in the porcine heart.Magnetic resonance in medicine · 2022Article
- Antioxidant Activity of Vitamin C against LPS-Induced Septic Cardiomyopathy by Down-Regulation of Oxidative Stress and Inflammation.Current issues in molecular biology · 2022Article
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Authors and funding
7 authors at 3 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The pig is commonly used as an experimental model of human heart disease, including for the study of mechanisms of arrhythmia. However, there exist differences between human and porcine cellular electrophysiology: The pig action potential (AP) has a deeper phase-1 notch, a longer duration at 50% repolarization, and higher plateau potentials than human. Ionic differences underlying the AP include larger rapid delayed-rectifier and smaller inward-rectifier K+-currents (IKr and IK1 respectively) in humans. AP steady-state rate-dependence and restitution is steeper in pigs. Porcine Ca2+ transients can have two components, unlike human. Although a reliable computational model for human ventricular myocytes exists, one for pigs is lacking. This hampers translation from results obtained in pigs to human myocardium. Here, we developed a computational model of the pig ventricular cardiomyocyte AP using experimental datasets of the relevant ionic currents, Ca2+-handling, AP shape, AP duration restitution, and inducibility of triggered activity and alternans. To properly capture porcine Ca2+ transients, we introduced a two-step process with a faster release in the t-tubular region, followed by a slower diffusion-induced release from a non t-tubular subcellular region. The pig model behavior was compared with that of a human ventricular cardiomyocyte (O'Hara-Rudy) model. The pig, but not the human model, developed early afterdepolarizations (EADs) under block of IK1, while IKr block led to EADs in the human but not in the pig model. At fast rates (pacing cycle length = 400 ms), the human cell model was more susceptible to spontaneous Ca2+ release-mediated delayed afterdepolarizations (DADs) and triggered activity than pig. Fast pacing led to alternans in human but not pig. Developing species-specific models incorporating electrophysiology and Ca2+-handling provides a tool to aid translating antiarrhythmic and arrhythmogenic assessment from the bench to the clinic.
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