Evidence map›Paper›PMID 39664764›Full record

ArticleFrontiers in cardiovascular medicine2024

ECG analysis of ventricular fibrillation dynamics reflects ischaemic progression subject to variability in patient anatomy and electrode location.

Hector Martinez-Navarro, Ambre Bertrand, Ruben Doste, Hannah Smith, Jakub Tomek, Giuseppe Ristagno, Rafael S Oliveira, Rodrigo Weber Dos Santos, Sandeep V Pandit, Blanca Rodriguez

Abstract read
In one paragraph

Article in Frontiers in cardiovascular medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Article
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4 · The record

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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

10 authors.

Hector Martinez-NavarroDepartment of Computer Science, British Heart Foundation Centre of Research Excellence, University of Oxford, Oxford, United Kingdom.
Ambre BertrandDepartment of Computer Science, British Heart Foundation Centre of Research Excellence, University of Oxford, Oxford, United Kingdom.
Ruben DosteDepartment of Computer Science, British Heart Foundation Centre of Research Excellence, University of Oxford, Oxford, United Kingdom.
Hannah SmithDepartment of Computer Science, British Heart Foundation Centre of Research Excellence, University of Oxford, Oxford, United Kingdom.
Jakub TomekDepartment of Physiology, Anatomy, and Genetics, University of Oxford, Oxford, United Kingdom.
Giuseppe RistagnoDipartimento di Fisiopatologia Medico-Chirurgica e dei Trapianti, Università degli Studi di Milano Statale, Milano, Italy.
Rafael S OliveiraComputer Science Department, Universidade Federal de São João del Rei, São João del Rei, Brazil.
Rodrigo Weber Dos SantosDepartamento de Ciência da Computação, Universidade Federal de Juiz de Fora, Juiz de Fora, Brazil.
Sandeep V PanditScientific Affairs, ZOLL Medical Corporation, Chelmsford, MA, United States.
Blanca RodriguezDepartment of Computer Science, British Heart Foundation Centre of Research Excellence, University of Oxford, Oxford, United Kingdom.

Funding

Wellcome Trust
6 · The paper itself

Abstract

Background: Ventricular fibrillation (VF) is the deadliest arrhythmia, often caused by myocardial ischaemia. VF patients require urgent intervention planned quickly and non-invasively. However, the accuracy with which electrocardiographic (ECG) markers reflect the underlying arrhythmic substrate is unknown. Methods: We analysed how ECG metrics reflect the fibrillatory dynamics of electrical excitation and ischaemic substrate. For this, we developed a human-based computational modelling and simulation framework for the quantification of ECG metrics, namely, frequency, slope, and amplitude spectrum area (AMSA) during VF in acute ischaemia for several electrode configurations. Simulations reproduced experimental and clinical findings in 21 scenarios presenting variability in the location and transmural extent of regional ischaemia, and severity of ischaemia in the remote myocardium secondary to VF. Results: Regional acute myocardial ischaemia facilitated re-entries, potentially breaking up into VF. Ischaemia in the remote myocardium modulated fibrillation dynamics. Cases presenting a mildly ischaemic remote myocardium yielded sustained VF, enabled by the high proliferation of phase singularities (PS, 11-22) causing remarkably disorganised activation patterns. Conversely, global acute ischaemia induced stable rotors (3-12 PS). Changes in frequency and morphology of the ECG during VF reproduced clinical findings but did not show a direct correlation with the underlying wave dynamics. AMSA allowed the precise stratification of VF according to ischaemic severity in the remote myocardium (healthy: 23.62-24.45 mV Hz; mild ischaemia: 10.58-21.47 mV Hz; moderate ischaemia: 4.82-11.12 mV Hz). Within the context of clinical reference values, apex-anterior and apex-posterior electrode configurations were the most discriminatory in stratifying VF based on the underlying ischaemic substrate. Conclusion: This

Indexed as

arrhythmiacardiac electrophysiologyelectrocardiogrammodelling and simulationmyocardial ischaemiaventricular fibrillation

Identifiers

PMID39664764
PMCPMC11631900

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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.