Evidence map›Paper›PMID 26592850›Full record

ArticleHeart rhythm2016

Unmasking atrial repolarization to assess alternans, spatiotemporal heterogeneity, and susceptibility to atrial fibrillation.

Richard L Verrier, Henrique Fuller, Fernanda Justo, Bruce D Nearing, Sridharan Rajamani, Luiz Belardinelli

Abstract read
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In one paragraph

Article in Heart rhythm, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing 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

16 citing papers in PubMed.

  1. Trial
  2. Activation of Small Conductance CaInternational journal of molecular sciences · 2025
    Article
  3. Review
  4. Review
  5. Excitation-contraction coupling and calcium release in atrial muscle.Pflugers Archiv : European journal of physiology · 2021
    Review
  6. Article
  7. Article
  8. Review
  9. Review
  10. Review
  11. Transient outward KAmerican journal of physiology. Heart and circulatory physiology · 2019
    Article
  12. Article
  13. Article
  14. Review
  15. Alternans in atria: Mechanisms and clinical relevance.Medicina (Kaunas, Lithuania) · 2017
    Review
  16. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors.

Richard L VerrierBeth Israel Deaconess Medical Center, Boston, Massachusetts; Harvard Medical School, Boston, Massachusetts. Electronic address: rverrier@bidmc.harvard.edu.
Henrique FullerBeth Israel Deaconess Medical Center, Boston, Massachusetts; Faculdade de Medicina da Universidade de São Paulo, São Paulo, Brazil.
Fernanda JustoBeth Israel Deaconess Medical Center, Boston, Massachusetts; Faculdade de Medicina da Universidade de São Paulo, São Paulo, Brazil.
Bruce D NearingBeth Israel Deaconess Medical Center, Boston, Massachusetts; Harvard Medical School, Boston, Massachusetts.
Sridharan RajamaniGilead Sciences, Inc., Foster City and Fremont, California.
Luiz BelardinelliGilead Sciences, Inc., Foster City and Fremont, California.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundDetection of atrial repolarization waves free of far-field signal contamination by ventricular activation would allow investigation of atrial electrophysiology and factors that influence susceptibility to atrial tachycardia and atrial fibrillation (AF).

objectiveThe purpose of this study was to identify means for high-resolution intracardiac recording of atrial repolarization (Ta) waves using standard clinical electrocatheters and to assess fundamental electrophysiologic properties relevant to AF risk.

methodsIn alpha-chloralose anesthetized Yorkshire pigs, we studied effects of vagus nerve stimulation (VNS) on PTa and QT intervals and effects of acute atrial ischemia or administration of intrapericardial acetylcholine followed by intravenous epinephrine on susceptibility to AF.

resultsElectrocatheters with closely spaced (1-mm) electrode pairs yielded high-resolution tracings of atrial repolarization waves. These recordings permitted detection of differential effects of right or left VNS, which shortened atrial PTa interval by 30% vs. 21% (P <.01) and lengthened QT interval by 1.5% vs. 9%, respectively (P < .05). During atrial ischemia, STa segments were elevated 3.4-fold (P < .01), and the threshold for inducing AF was reduced 3.1-fold (P = .004). Ischemia amplified atrial T-wave alternans (TWAa) and spatiotemporal heterogeneity (TWHa) by 23- and 13-fold, respectively, in inverse correlation to AF threshold (r = 0.74, P <.01; r = 0.61, P = .03). TWAa and TWHa increased by 4.5- and 2-fold shortly before autonomically triggered atrial premature beats and AF.

conclusionThis study used standard electrocatheters to demonstrate that TWAa and TWHa analysis provides means to assess vulnerability to AF without provocative electrical stimuli. These parameters could be evaluated in the clinical electrophysiology laboratory to determine risk for this prevalent arrhythmia and efficacy of contemporary and new agents.

Indexed as

Action PotentialsAnimalsAtrial FibrillationDisease Models, AnimalElectrophysiologic Techniques, CardiacHeart AtriaHeart Conduction SystemMaleSwineVagus Nerve StimulationAtrial fibrillationCardiac electrophysiologic testingCatecholaminesElectrode catheterElectrophysiologic mappingMonophasic action potentialMyocardial ischemiaRepolarization alternansRepolarization heterogeneityVagus nerve stimulation

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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.