Evidence map›Paper›PMID 41931553›Full record

ArticlePLoS computational biology2026

In silico assessment of arrhythmic risk following the implantation of engineered heart tissues in porcine hearts with varying infarct locations.

Ricardo M Rosales, Gonzalo R Ríos-Muñoz, Ana María Sánchez de la Nava, María Eugenia Fernández-Santos, Javier Bermejo, Manuel Doblaré, Ana Mincholé, Esther Pueyo

Abstract read
In one paragraph

Article in PLoS computational biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors.

Ricardo M RosalesAragón Institute for Health Research (IISA), Zaragoza, Aragón, Spain.ORCID https://orcid.org/0000-0002-8867-3802
Gonzalo R Ríos-MuñozBioengineering Department, Universidad Carlos III de Madrid, Leganés, Spain.ORCID https://orcid.org/0000-0003-2446-3045
Ana María Sánchez de la NavaDepartment of Cardiology, Instituto de Investigación Sanitaria Gregorio Marañón (IiSGM), Hospital General Universitario Gregorio Marañón, Madrid, Spain.
María Eugenia Fernández-SantosDepartment of Cardiology, Instituto de Investigación Sanitaria Gregorio Marañón (IiSGM), Hospital General Universitario Gregorio Marañón, Madrid, Spain.ORCID https://orcid.org/0000-0001-9229-0022
Javier BermejoDepartment of Cardiology, Instituto de Investigación Sanitaria Gregorio Marañón (IiSGM), Hospital General Universitario Gregorio Marañón, Madrid, Spain.
Manuel DoblaréAragón Institute for Health Research (IISA), Zaragoza, Aragón, Spain.ORCID https://orcid.org/0000-0001-8741-6452
Ana MincholéAragón Institute for Health Research (IISA), Zaragoza, Aragón, Spain.
Esther PueyoAragón Institute for Health Research (IISA), Zaragoza, Aragón, Spain.ORCID https://orcid.org/0000-0002-1960-407X

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Engineered heart tissues (EHTs) have shown promise in partially restoring ejection fraction after myocardial infarction (MI); however, their potential to introduce electrophysiological heterogeneities and promote arrhythmias remains underexplored. This study assessed the arrhythmogenic risk following immature EHT engraftment in infarcted ventricles using computational simulations that replicate preclinical protocols. EHT computational models were developed and integrated into nine validated porcine-specific biventricular models from pigs with left circumflex (LCx, n = 4) or left anterior descending (LAD, n = 5) MIs. Ventricular tachycardia (VT) susceptibility was evaluated using an S1-S2 stimulation protocol across varying pacing sites and coupling intervals, accounting for infarct characteristics, implantation site, conductivity, and the ventricular conduction system (CS). VT burden was quantified with a 0-1 inducibility score (IS). In silico reentrant activity qualitatively reproduced the arrhythmic patterns observed experimentally in porcine MI models. VT vulnerability was greater in LAD than in LCx infarcts, consistent with a larger infarct size. Inclusion of the CS modified VT burden by providing conduction shortcuts that either facilitated or suppressed reentry. Remuscularization directly on the MI region (IS = 0.49) heightened VT inducibility in dense, transmural scars (IS = 0.16), whereas lateral EHT implantation (IS = 0.35) reduced this risk with respect to direct implantation. In non-transmural scars, VT inducibility varied with the implantation site. Matching EHT conductivity to host myocardium lowered or contained arrhythmogenicity (LCx-IS: from 0.5 to 0.25; LAD-IS: stable at 0.57). These results highlight the latent arrhythmic risk of EHT-mediated remuscularization after MI, identifying infarct substrate, EHT conductivity, and implantation site as critical determinants, and emphasize the importance of incorporating the CS for accurate risk assessment.

Indexed as

Arrhythmias, CardiacMyocardial InfarctionTissue EngineeringAnimalsComputational BiologyComputer SimulationHeartModels, CardiovascularSwineTachycardia, Ventricular

Identifiers

PMID41931553
PMCPMC13108890

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.