---
title: "Electrophysiological substrate and rotor frequency drive antiarrhythmic drug response in paroxysma"
id: "biorxiv-10-electrophysiological-dependent-antiarrhythmic-drug-response-in-population-based"
canonical_url: "https://medichelpline.com/clinical-feed/biorxiv-10-electrophysiological-dependent-antiarrhythmic-drug-response-in-population-based"
content_type: "clinical_feed_article"
specialty: "Cardiology"
source_name: "bioRxiv (Biomedical Preprints)"
source_url: "https://www.biorxiv.org/content/10.64898/2026.09.18.752633v1?rss=1"
published_at: "2026-09-21T12:00:00.000Z"
evidence_level: "Verified Feed"
license: "CC-BY-NC-4.0 / Informational Use"
---
# Electrophysiological substrate and rotor frequency drive antiarrhythmic drug response in paroxysma
## Provenance & Clinical Metadata
- **Canonical URL:** https://medichelpline.com/clinical-feed/biorxiv-10-electrophysiological-dependent-antiarrhythmic-drug-response-in-population-based
- **Specialty:** [Cardiology](https://medichelpline.com/clinical-feed/cardiology.md)
- **Primary Source:** bioRxiv (Biomedical Preprints)
- **Source URL:** [Original Journal Publication](https://www.biorxiv.org/content/10.64898/2026.09.18.752633v1?rss=1)
- **Published At:** 2026-09-21T12:00:00.000Z
- **Evidence Rating:** Verified Feed
## Executive GIST (TL;DR)
- Study used population-based computational models of human left atrial tissue to test how **electrophysiological substrate** and inter-individual ionic variability affect antiarrhythmic drug efficacy in paroxysmal atrial fibrillation (pAF). - Two calibrated model populations were created from the same experimental pAF datasets: a reference **pAF** population and an inward-rectifier-enhanced **IRE-pAF** population with 2-fold increases in IK1 and IK,ACh. - Sustained reentrant activity was induced in 2D tissue simulations to evaluate cardioversion success for flecainide, vernakalant and tertiapin-Q across the two populations. - The IRE-pAF population displayed a more arrhythmogenic phenotype: shorter refractoriness, higher **dominant frequency (DF)** and more stable rotors compared with pAF, despite identical calibration criteria. - Drug cardioversion efficacy differed by substrate: flecainide decreased from 34% (pAF) to 21% (IRE-pAF); vernakalant was 41% (pAF) versus 44% (IRE-pAF); tertiapin-Q was 11% (pAF) versus 18% (IRE-pAF). - Across drugs and substrates, higher rotor **DF** was strongly associated with lower termination rates; drug-induced DF reduction correlated with successful cardioversion. - Prolongation of effective refractory period (ERP) alone did not reliably predict treatment success; vernakalant achieved higher cardioversion than flecainide in pAF despite a smaller ERP increase but larger DF reduction. - Ionic analyses indicated elevated IK,ACh favored responsiveness to vernakalant and tertiapin-Q, illustrating that interactions between substrate, rotor dynamics and drug-specific mechanisms determine cardioversion efficacy. - The authors conclude that **DF** is a robust marker of pharmacological susceptibility and could guide drug-mediated AF termination, and that substrates differing in inward rectifier activity show distinct drug response patterns.
## Clinical Analysis & Structured Key Points
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Violeta Puche-García 1 UPV: Universitat Politecnica de Valencia; * [Find this author on Google Scholar](https://www.biorxiv.org/lookup/google-scholar?link_type=googlescholar&gs_type=author&author%5B0%5D=Violeta%2BPuche-Garc%C3%ADa%2B "Open in new tab") * [Find this author on PubMed](https://www.biorxiv.org/lookup/external-ref?access_num=Puche-Garc%C3%ADa%20V&link_type=AUTHORSEARCH "Open in new tab") * [Search for this author on this site](https://www.biorxiv.org/search/author1%3AVioleta%2BPuche-Garc%25C3%25ADa%2B) * [ORCID record for Violeta Puche-García](http://orcid.org/0000-0002-3386-1478 "Open in new tab") * For correspondence: viopucga@ci2b.upv.es David Filgueiras-Rama 2 CNIC: Centro Nacional de Investigaciones Cardiovasculares Carlos III; * [Find this author on Google Scholar](https://www.biorxiv.org/lookup/google-scholar?link_type=googlescholar&gs_type=author&author%5B0%5D=David%2BFilgueiras-Rama%2B "Open in new tab") * [Find this author on PubMed](https://www.biorxiv.org/lookup/external-ref?access_num=Filgueiras-Rama%20D&link_type=AUTHORSEARCH "Open in new tab") * [Search for this author on this site](https://www.biorxiv.org/search/author1%3ADavid%2BFilgueiras-Rama%2B) Laura Martinez-Mateu 3 Rey Juan Carlos University: Universidad Rey Juan Carlos * [Find this author on Google Scholar](https://www.biorxiv.org/lookup/google-scholar?link_type=googlescholar&gs_type=author&author%5B0%5D=Laura%2BMartinez-Mateu%2B "Open in new tab") * [Find this author on PubMed](https://www.biorxiv.org/lookup/external-ref?access_num=Martinez-Mateu%20L&link_type=AUTHORSEARCH "Open in new tab") * [Search for this author on this site](https://www.biorxiv.org/search/author1%3ALaura%2BMartinez-Mateu%2B) Lucía Romero 1 UPV: Universitat Politecnica de Valencia; * [Find this author on Google Scholar](https://www.biorxiv.org/lookup/google-scholar?link_type=googlescholar&gs_type=author&author%5B0%5D=Luc%C3%ADa%2BRomero%2B "Open in new tab") * [Find this author on PubMed](https://www.biorxiv.org/lookup/external-ref?access_num=Romero%20L&link_type=AUTHORSEARCH "Open in new tab") * [Search for this author on this site](https://www.biorxiv.org/search/author1%3ALuc%25C3%25ADa%2BRomero%2B) * [ORCID record for Lucía Romero](http://orcid.org/0000-0003-4605-8630 "Open in new tab") Javier Saiz 1 UPV: Universitat Politecnica de Valencia; * [Find this author on Google Scholar](https://www.biorxiv.org/lookup/google-scholar?link_type=googlescholar&gs_type=author&author%5B0%5D=Javier%2BSaiz%2B "Open in new tab") * [Find this author on PubMed](https://www.biorxiv.org/lookup/external-ref?access_num=Saiz%20J&link_type=AUTHORSEARCH "Open in new tab") * [Search for this author on this site](https://www.biorxiv.org/search/author1%3AJavier%2BSaiz%2B) * [Abstract](https://www.biorxiv.org/content/10.64898/2026.09.18.752633v1)[](https://www.biorxiv.org/panels_ajax_tab/biorxiv_tab_art/node:5799385/1) * [Info/History](https://www.biorxiv.org/content/10.64898/2026.09.18.752633v1.article-info)[](https://www.biorxiv.org/panels_ajax_tab/biorxiv_tab_info/node:5799385/1) * [Metrics](https://www.biorxiv.org/content/10.64898/2026.09.18.752633v1.article-metrics)[](https://www.biorxiv.org/panels_ajax_tab/article_tab_metrics/node:5799385/1) * [ Preview PDF](https://www.biorxiv.org/content/10.64898/2026.09.18.752633v1.full.pdf+html)[](https://www.biorxiv.org/panels_ajax_tab/biorxiv_tab_pdf/node:5799385/1) ![Loading](https://www.biorxiv.org/sites/all/modules/contrib/panels_ajax_tab/images/loading.gif) ## Abstract Response to antiarrhythmic drugs varies markedly across patients with atrial fibrillation (AF), suggesting that treatment efficacy depends on the interaction between drug-specific mechanisms and patient-specific electrophysiological substrate. Here, we used population-based computational models to investigate how electrophysiological substrate and inter-individual ionic variability influence pharmacological efficacy and the underlying mechanisms. Two populations of human atrial models were generated from distinct substrates: a reference left atrial model and a second model incorporating inward-rectifier-enhancement (IRE) through a 2-fold increase in IK1 and IK,ACh. Both populations were independently calibrated against the same experimental datasets from patients with paroxysmal AF (pAF), yielding pAF and IRE-pAF populations. Sustained reentrant activity was induced in two-dimensional tissue simulations and subsequently used to assess cardioversion efficacy of flecainide, vernakalant and tertiapin-Q. Despite satisfying the same calibration criteria, IRE-pAF population exhibited a more arrhythmogenic phenotype: shorter refractoriness, higher dominant frequency (DF) and greater rotor stability. Antiarrhythmic efficacy markedly differed between substrates. Flecainide cardioversion decreased in IRE-pAF compared with pAF (34% vs 21%), whereas IK,ACh-targeting therapies preserved or improved efficacy in IRE-pAF (vernakalant: 41% vs 44%, tertiapin-Q: 11% vs 18%). Across drugs and substrates, rotor DF strongly influenced cardioversion outcome, with higher-frequency rotors showing lower termination rates. Drug-induced DF reduction emerged as a key mechanism associated with successful cardioversion, whereas effective refractory period (ERP) prolongation alone did not consistently explain treatment efficacy. In pAF, vernakalant achieved higher cardioversion efficacy than flecainide despite a smaller increase in ERP and greater DF reduction. Ionic analyses further showed that elevated IK,ACh favored responses to vernakalant and tertiapin-Q. These findings demonstrate that cardioversion efficacy emerges from the interaction between electrophysiological substrate, rotor dynamics and drug-specific mechanisms. In particular, substrates differing in inward rectifier activity exhibit distinct response patterns, while DF emerges as a robust marker of pharmacological susceptibility and a potential guide for drug-mediated AF termination. ### Competing Interest Statement The authors have declared no competing interest. Copyright The copyright holder for this preprint is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under a [CC-BY 4.0 International license](http://creativecommons.org/licenses/by/4.0/). bioRxiv and medRxiv thank the following for their generous financial support: > The Chan Zuckerberg Initiative, Cold Spring Harbor Laboratory, the Sergey Brin Family Foundation, California Institute of Technology, Centre National de la Recherche Scientifique, Fred Hutchinson Cancer Center, Imperial College London, Massachusetts Institute of Technology, Stanford University, The University of Edinburgh, University of Washington, and Vrije Universiteit Amsterdam. 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