ArticleAmerican journal of physiology. Heart and circulatory physiology2023
Modeling incomplete penetrance in long QT syndrome type 3 through ion channel heterogeneity: an in silico population study.
Article in American journal of physiology. Heart and circulatory physiology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 12 citations in OpenAlex.
- Patient-Specific Heart Rate Modulates Developmental Electrophysiology in Transcriptomic-Guided In Silico Models of Pediatric Human Atrial Cardiomyocytes.bioRxiv : the preprint server for biology · 2026Article
- Interplay between variability in intrinsic cellular properties and heart failure-associated remodeling in a simulated population with human heart failure.Journal of molecular and cellular cardiology · 2026Article
- Hypernatremia Enhances Transient Outward Potassium and Late Sodium Currents in a Mouse Model of Long QT Syndrome Type 3.bioRxiv : the preprint server for biology · 2025Article
- Calcium Homeostatic Feedback Control Predicts Atrial Fibrillation Initiation, Remodeling, and Progression.JACC. Clinical electrophysiology · 2025Article
- COMPUTATIONAL ANALYSIS OF THE NOVEL LQT3 MUTATIONS G1481V AND Q1491H IN MYOCARDIAL AND PURKINJE CELLS.Annual Modeling and Simulation Conference (ANNSIM). Annual Modeling and Simulation Conference (Online) · 2025Article
- Age-Associated Perinexal Narrowing Masks Consequences of Sodium Channel Gain of Function in Guinea Pig Hearts.JACC. Clinical electrophysiology · 2025Article
- Reconstructing ventricular cardiomyocyte dynamics and parameter estimation using data assimilation.Biophysical journal · 2024Article
- Connecting transcriptomics with computational modeling to reveal developmental adaptations in pediatric human atrial tissue.American journal of physiology. Heart and circulatory physiology · 2024Article
- Computational modeling of cardiac electrophysiology and arrhythmogenesis: toward clinical translation.Physiological reviews · 2024Review
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Many cardiac diseases are characterized by an increased late sodium current, including heart failure, hypertrophic cardiomyopathy, and inherited long QT syndrome type 3 (LQT3). The late sodium current in LQT3 is caused by a gain-of-function mutation in the voltage-gated sodium channel Nav1.5. Despite a well-defined genetic cause of LQT3, treatment remains inconsistent because of incomplete penetrance of the mutation and variability of antiarrhythmic efficacy. Here, we investigate the relationship between LQT3-associated mutation incomplete penetrance and variability in ion channel expression, simulating a population of 1,000 individuals with the O'Hara-Rudy model of the human ventricular myocyte. We first simulate healthy electrical activity (i.e., in the absence of a mutation) and then incorporate heterozygous expression for three LQT3-associated mutations (Y1795C, I1768V, and ΔKPQ), to directly compare the effects of each mutation on individuals across a diverse population. For all mutations, we find that susceptibility, defined by either the presence of an early afterdepolarization (EAD) or prolonged action potential duration (APD), primarily depends on the balance between the conductance of
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