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T-world Virtual Human Cardiomyocyte. Ii. Organ-scale Simulations And Applications.

Home
T-world Virtual Human Cardiomyocyte. Ii. Organ-scale Simulations And Applications.

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T-World Virtual Human Cardiomyocyte. II. Organ-Scale Simulations and Applications.

Jakub Tomek^1,2, Maxx Holmes³, Hector Martinez-Navarro³

¹Department of Anatomy, Physiology and Genetics (J.T.), University of Oxford, United Kingdom.

Circulation Research

|April 8, 2026

View abstract on PubMed

Summary

This summary is machine-generated.

The T-World model accurately simulates human heart function, predicting arrhythmias and drug effects across scales. This open-source platform advances cardiac research, drug development, and personalized medicine through predictive modeling.

Keywords:

adrenergic agents arrhythmias, cardiac calibration myocytes, cardiac stroke volume

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Area of Science:

Cardiovascular Physiology
Computational Biology
Pharmacology

Background:

Current human cardiomyocyte models lack the generality for predictive translation across scales.
The T-World model reproduces major cellular arrhythmia mechanisms and aligns with experimental data.
Demonstrating T-World's utility for organ-level and translational research is crucial.

Purpose of the Study:

To demonstrate the utility of the T-World model for organ-level and translational cardiac research.
To validate T-World's predictive capabilities in simulating arrhythmogenesis and whole-heart physiology.
To assess T-World's application in drug safety, efficacy, and disease modeling.

Main Methods:

Embedding T-World into anatomically realistic biventricular models for organ-scale simulations.

Assessing drug safety using populations of single-cell models exposed to 60 compounds.

Conducting mechanistic drug-efficacy studies and disease modeling for type 2 diabetes and Na_V1.8 expression.

Main Results:

T-World accurately reproduced human ECG morphology and ventricular mechanics, simulating ventricular fibrillation under ischemia.
The model achieved 87% accuracy and 100% specificity in torsadogenic risk assessment, identifying drug inaccuracies.
Simulations elucidated mexiletine's antiarrhythmic benefits, linked type 2 diabetes to early afterdepolarizations, and identified Na_V1.8 as a trigger for arrhythmias.

Conclusions:

T-World offers a unified, human-specific, open-source platform for multiscale cardiac research.
Its predictive performance bridges cellular mechanisms to organ-level dynamics and translational outcomes.
T-World is a powerful tool for cardiac digital twins, therapeutic discovery, and advancing regulatory science.