Evidence map›Paper›PMID 19324301›Full record

ArticleHeart rhythm2009

Atrial cellular electrophysiological changes in patients with ventricular dysfunction may predispose to AF.

Antony J Workman, Davide Pau, Calum J Redpath, Gillian E Marshall, Julie A Russell, John Norrie, Kathleen A Kane, Andrew C Rankin

Open access · bronzeAbstract read
In one paragraph

Article in Heart rhythm, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
3.5field-weighted citation impact, top 7% 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

25 citing papers in PubMed, 45 citations in OpenAlex.

  1. Failure of intravenous nifekalant cardioversion as an independent predictor for persistent atrial fibrillation recurrence after catheter ablation.Journal of interventional cardiac electrophysiology : an international journal of arrhythmias and pacing · 2024
    Article
  2. Review
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  4. Triggered CaCirculation. Arrhythmia and electrophysiology · 2020
    Article
  5. Review
  6. Article
  7. Review
  8. The Stress-Response MAP Kinase Signaling in Cardiac Arrhythmias.Reviews of physiology, biochemistry and pharmacology · 2016
    Review
  9. Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
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  17. Review
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 4 institutions in 1 country.

Antony J WorkmanBritish Heart Foundation Glasgow Cardiovascular Research Centre, Division of Cardiovascular & Medical Sciences, Faculty of Medicine, University of Glasgow, UK. A.J.Workman@clinmed.gla.ac.uk
Davide Pau
Calum J Redpath
Gillian E Marshall
Julie A Russell
John Norrie
Kathleen A Kane
Andrew C Rankin
British Heart Foundation · GBUniversity of Glasgow · GBUniversity of Aberdeen · GBUniversity of Strathclyde · GB

Funding

British Heart Foundation BS/06/003British Heart Foundation BS/06/003/20338British Heart Foundation FS/02/036/13459British Heart Foundation FS/04/087British Heart Foundation FS/04/087/17994British Heart Foundation PG/04/084/17400
6 · The paper itself

Abstract

backgroundLeft ventricular systolic dysfunction (LVSD) is a risk factor for atrial fibrillation (AF), but the atrial cellular electrophysiological mechanisms in humans are unclear.

objectiveThis study sought to investigate whether LVSD in patients who are in sinus rhythm (SR) is associated with atrial cellular electrophysiological changes that could predispose to AF.

methodsRight atrial myocytes were obtained from 214 consenting patients in SR who were undergoing cardiac surgery. Action potentials or ion currents were measured using the whole-cell-patch clamp technique.

resultsThe presence of moderate or severe LVSD was associated with a shortened atrial cellular effective refractory period (ERP) (209 +/- 8 ms; 52 cells, 18 patients vs 233 +/- 7 ms; 134 cells, 49 patients; P <0.05); confirmed by multiple linear regression analysis. The left ventricular ejection fraction (LVEF) was markedly lower in patients with moderate or severe LVSD (36% +/- 4%, n = 15) than in those without LVSD (62% +/- 2%, n = 31; P <0.05). In cells from patients with LVEF <or= 45%, the ERP and action potential duration at 90% repolarization were shorter than in those from patients with LVEF > 45%, by 24% and 18%, respectively. The LVEF and ERP were positively correlated (r = 0.65, P <0.05). The L-type calcium ion current, inward rectifier potassium ion current, and sustained outward ion current were unaffected by LVSD. The transient outward potassium ion current was decreased by 34%, with a positive shift in its activation voltage, and no change in its decay kinetics.

conclusionLVSD in patients in SR is independently associated with a shortening of the atrial cellular ERP, which may be expected to contribute to a predisposition to AF.

Indexed as

Action PotentialsAngiotensin-Converting Enzyme InhibitorsAngiotensin II Type 1 Receptor BlockersAtrial FibrillationCalcium Channel BlockersChi-Square DistributionFemaleHeart AtriaHumansLinear ModelsMaleMiddle AgedMyocytes, CardiacPatch-Clamp TechniquesPotassium ChannelsRisk FactorsAngiotensin-Converting Enzyme InhibitorsAngiotensin II Type 1 Receptor BlockersCalcium Channel BlockersPotassium Channels

Identifiers

PMID19324301
PMCPMC2666890
OpenAlexW2079656921

What OpenQuestion holds

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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.