Evidence map›Paper›PMID 22157522›Full record

ArticleCirculation. Arrhythmia and electrophysiology2012

Investigating the role of the coronary vasculature in the mechanisms of defibrillation.

Martin J Bishop, Gernot Plank, Edward Vigmond

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in Circulation. Arrhythmia and electrophysiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.4field-weighted citation impact, top 17% of its field
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

14 citing papers in PubMed, 26 citations in OpenAlex.

  1. Review
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  10. Images as drivers of progress in cardiac computational modelling.Progress in biophysics and molecular biology · 2014
    Review
  11. Article
  12. Article
  13. Computational approaches to understand cardiac electrophysiology and arrhythmias.American journal of physiology. Heart and circulatory physiology · 2012
    Review
  14. Advances in modeling ventricular arrhythmias: from mechanisms to the clinic.Wiley interdisciplinary reviews. Systems biology and medicine
    Review
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

3 authors at 2 institutions in 2 countries.

Martin J BishopComputing Laboratory, University of Oxford, Oxford, UK. martin.bishop@comlab.ox.ac.uk
Gernot Plank
Edward Vigmond
University of Oxford · GBMedical University of Graz · AT

Funding

Multi-scale Modeling of Calcium Mediated Triggered Activity in the HeartR01HL101196 · NHLBI · CALIFORNIA STATE UNIVERSITY NORTHRIDGE · PI SHIFERAW, YOHANNES · 2010 to 2013
$1.2M
Austrian Science Fund FWF F 3210NHLBI NIH HHS R01 HL101196Wellcome Trust 085605
6 · The paper itself

Abstract

backgroundThe direct role of coronary vessels in defibrillation, although hypothesized to be important, remains to be elucidated. We investigated how vessel-induced virtual electrode polarizations assist reentry termination. METHODS AND

resultsA highly anatomically detailed rabbit ventricular slice bidomain computer model was constructed from 25-μm magnetic resonance data, faithfully representing both structural and electric properties of blood vessels. For comparison, an equivalent simplified model with intramural cavities filled in was also built. Following fibrillation induction, 6 initial states were selected, and biphasic shocks (5-70 V) were applied using a realistic implanted cardioverter-defibrillator electrode configuration. A fundamental mechanism of biphasic defibrillation was uncovered in both models, involving successive break excitations (after each shock phase) emanating from opposing myocardial surfaces (in septum and left ventricle), which rapidly closed down excitable gaps. The presence of vessels accelerated this process, achieving more-rapid and successful defibrillation. Defibrillation failed in 5 cases (all because of initiation of new activity) compared with 8 with the simplified model (5/8 failures because of surviving activity). At stronger shocks, virtual electrodes formed around vessels, rapidly activating intramural tissue because of break excitations, assisting the main defibrillation mechanism, and eliminating all activity <15 ms of shock end in 60% of successful shocks (36% in simplified model). Subsequent analysis identified that only vessels >200 μm in diameter participated through this mechanism. Consequently, wavefronts could survive intramurally in the simplified model, leading to reentry and shock failure.

conclusionsWe provide new insight into defibrillation mechanisms by showing how intramural blood vessels facilitate more-effective elimination of existing wavefronts, rapid closing down of excitable gaps, and successful defibrillation and give guidance toward the required resolution of cardiac imaging and model generation endeavors for mechanistic defibrillation analysis.

Indexed as

Computer SimulationAnimalsCoronary VesselsElectric CountershockHumansMagnetic Resonance Imaging, CineRabbitsVentricular Fibrillation

Identifiers

PMID22157522
PMCPMC3378488
OpenAlexW2118975313

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

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.