Evidence map›Paper›PMID 25969391›Full record

ArticleCardiovascular research2015

Stochastic spontaneous calcium release events trigger premature ventricular complexes by overcoming electrotonic load.

Fernando O Campos, Yohannes Shiferaw, Anton J Prassl, Patrick M Boyle, Edward J Vigmond, Gernot Plank

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cardiovascular research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
3.0field-weighted citation impact, top 8% 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

23 citing papers in PubMed, 43 citations in OpenAlex.

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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

6 authors at 4 institutions in 4 countries.

Fernando O CamposInstitute of Biophysics, Medical University of Graz, Graz, Austria.
Yohannes ShiferawDepartment of Physics, California State University, Northridge, CA, USA.
Anton J PrasslInstitute of Biophysics, Medical University of Graz, Graz, Austria.
Patrick M BoyleInstitute for Computational Medicine, Johns Hopkins University, Baltimore, MD, USA.
Edward J VigmondLIRYC Institute, University of Bordeaux, Bordeaux, France Department of Electrical and Computer Engineering, University of Calgary, Calgary, Canada.
Gernot PlankInstitute of Biophysics, Medical University of Graz, Graz, Austria gernot.plank@medunigraz.at.
Medical University of Graz · ATCalifornia State University, Northridge · USJohns Hopkins University · USUniversity of Calgary · CA

Funding

NHLBI NIH HHS 1R01 HL 10119601
6 · The paper itself

Abstract

aimsPremature ventricular complexes (PVCs) due to spontaneous calcium (Ca) release (SCR) events at the cell level can precipitate ventricular arrhythmias. However, the mechanistic link between SCRs and PVC formation remains incompletely understood. The aim of this study was to investigate the conditions under which delayed afterdepolarizations resulting from stochastic subcellular SCR events can overcome electrotonic source-sink mismatch, leading to PVC initiation. METHODS AND

resultsA stochastic subcellular-scale mathematical model of SCR was incorporated in a realistic model of the rabbit ventricles and Purkinje system (PS). Elevated levels of diastolic sarcoplasmic reticulum Ca(2+) (CaSR) were imposed until triggered activity was observed, allowing us to compile statistics on probability, timing, and location of PVCs. At CaSR≥ 1500 µmol/L PVCs originated in the PS. When SCR was incapacitated in the PS, PVCs also emerged in the ventricles, but at a higher CaSR (≥1550 µmol/L) and with longer waiting times. For each model configuration tested, the probability of PVC occurrence increased from 0 to 100% within a well-defined critical CaSR range; this transition was much more abrupt in organ-scale models (∼50 µmol/L CaSR range) than in the tissue strand (∼100 µmol/L) or single-cell (∼450 µmol/L) models. Among PVCs originating in the PS, ∼68% were located near Purkinje-ventricular junctions (<1 mm).

conclusionSCR events overcome source-sink mismatch to trigger PVCs at a critical CaSR threshold. Above this threshold, PVCs emerge due to increased probability and reduced variability in timing of SCR events, leading to significant diastolic depolarization. Sites of lower electronic load, such as the PS, are preferential locations for triggering.

Indexed as

Action PotentialsAnimalsArrhythmias, CardiacBundle of HisCalciumComputer SimulationHeart FailureHeart VentriclesRabbitsCalciumArrhythmiaComputer-based modelDelayed afterdepolarizationPurkinje systemTriggered activity

Identifiers

PMID25969391
PMCPMC4560047
OpenAlexW2178210849

What OpenQuestion holds

Textmetadata
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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.