Evidence map›Paper›PMID 34339897›Full record

ArticleJournal of electrocardiology

Pharmacological and simulated exercise cardiac stress tests produce different ischemic signatures in high-resolution experimental mapping studies.

Brian Zenger, Wilson W Good, Jake A Bergquist, Lindsay C Rupp, Maura Perez, Gregory J Stoddard, Vikas Sharma, Rob S MacLeod

Open access · greenAbstract read
In one paragraph

Article in Journal of electrocardiology. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.3field-weighted citation impact, top 39% 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

3 citing papers in PubMed, 2 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
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

8 authors at 1 institution in 1 country.

Brian ZengerScientific Computing and Imaging Institute, University of Utah, SLC, UT, USA; Nora Eccles Harrison Cardiovascular Research and Training Institute, University of Utah, SLC, UT, USA; Department of Biomedical Engineering, University of Utah, SLC, UT, USA; School of Medicine, University of Utah, SLC, UT, USA. Electronic address: brian.zenger@hsc.utah.edu.
Wilson W GoodScientific Computing and Imaging Institute, University of Utah, SLC, UT, USA; Nora Eccles Harrison Cardiovascular Research and Training Institute, University of Utah, SLC, UT, USA; Department of Biomedical Engineering, University of Utah, SLC, UT, USA.
Jake A BergquistScientific Computing and Imaging Institute, University of Utah, SLC, UT, USA; Nora Eccles Harrison Cardiovascular Research and Training Institute, University of Utah, SLC, UT, USA; Department of Biomedical Engineering, University of Utah, SLC, UT, USA.
Lindsay C RuppScientific Computing and Imaging Institute, University of Utah, SLC, UT, USA; Nora Eccles Harrison Cardiovascular Research and Training Institute, University of Utah, SLC, UT, USA; Department of Biomedical Engineering, University of Utah, SLC, UT, USA.
Maura PerezScientific Computing and Imaging Institute, University of Utah, SLC, UT, USA.
Gregory J StoddardDepartment of Internal Medicine, University of Utah, SLC, UT, USA.
Vikas SharmaSchool of Medicine, University of Utah, SLC, UT, USA.
Rob S MacLeodScientific Computing and Imaging Institute, University of Utah, SLC, UT, USA; Nora Eccles Harrison Cardiovascular Research and Training Institute, University of Utah, SLC, UT, USA; Department of Biomedical Engineering, University of Utah, SLC, UT, USA.
University of Utah · US

Funding

Utah Center for Clinical and Translational ScienceUL1TR002538 · NCATS · UNIVERSITY OF UTAH · PI HESS, RACHEL, MAJERSIK, JENNIFER JUHL · 2018 to 2022
$26.0M
University of Utah Center for Clinical and Translational ScienceUL1TR001067 · NCATS · UNIVERSITY OF UTAH · PI DERE, WILLARD H., HESS, RACHEL · 2013 to 2017
$19.8M
UNIVERSITY OF UTAH CENTER FOR CLINICAL AND TRANSLATIONAL SCIENCE-UL1: BPCAUL1RR025764 · NCRR · UNIVERSITY OF UTAH · PI MCCLAIN, DONALD A. · 2008 to 2011
$19.4M
TRD - VisualizationP41GM103545 · NIGMS · UNIVERSITY OF UTAH · PI MACLEOD, ROB S. · 2012 to 2019
$9.7M
University of Utah Center for Clinical and Translational Science-UL1UL1TR000105 · NCATS · UNIVERSITY OF UTAH · PI MCCLAIN, DONALD A. · 2012 to 2013
$5.1M
Center for Integrative Biomedical Computing Legacy TransitionR24GM136986 · NIGMS · UNIVERSITY OF UTAH · PI JOHNSON, CHRISTOPHER R., MACLEOD, ROB S. · 2020 to 2022
$1.6M
Novel Characterization and Detection Techniques for Acute Myocardial IschemiaF30HL149327 · NHLBI · UNIVERSITY OF UTAH · PI ZENGER, BRIAN · 2020 to 2022
$117k
NCATS NIH HHS UL1 TR000105NCATS NIH HHS UL1 TR001067NCATS NIH HHS UL1 TR002538NCRR NIH HHS UL1 RR025764NHLBI NIH HHS F30 HL149327NIGMS NIH HHS P41 GM103545NIGMS NIH HHS R24 GM136986
6 · The paper itself

Abstract

objectiveTest the hypothesis that exercise and pharmacological cardiac stressors create different electrical ischemic signatures.

introductionCurrent clinical stress tests for detecting ischemia lack sensitivity and specificity. One unexplored source of the poor detection is whether pharmacological stimulation and regulated exercise produce identical cardiac stress.

methodsWe used a porcine model of acute myocardial ischemia in which animals were instrumented with transmural plunge-needle electrodes, an epicardial sock array, and torso arrays to simultaneously measure cardiac electrical signals within the heart wall, the epicardial surface, and the torso surface, respectively. Ischemic stress via simulated exercise and pharmacological stimulation were created with rapid electrical pacing and dobutamine infusion, respectively, and mimicked clinical stress tests of five 3-minute stages. Perfusion to the myocardium was regulated by a hydraulic occluder around the left anterior descending coronary artery. Ischemia was measured as deflections to the ST-segment on ECGs and electrograms.

resultsAcross eight experiments with 30 (14 simulated exercise and 16 dobutamine) ischemic interventions, the spatial correlations between exercise and pharmacological stress diverged at stage three or four during interventions (p<0.05). We found more detectable ST-segment changes on the epicardial surface during simulated exercise than with dobutamine (p<0.05). The intramyocardial ischemia formed during simulated exercise had larger ST40 potential gradient magnitudes (p<0.05).

conclusionWe found significant differences on the epicardium between cardiac stress types using our experimental model, which became more pronounced at the end stages of each test. A possible mechanism for these differences was the larger ST40 potential gradient magnitudes within the myocardium during exercise. The presence of microvascular dysfunction during exercise and its absence during dobutamine stress may explain these differences.

Indexed as

ElectrocardiographyMyocardial IschemiaAnimalsDobutamineExercise TestIschemiaPericardiumSwineDobutamineAcute myocardial ischemiaCardiac stress testExperimental modelST-segment changes

Identifiers

PMID34339897
PMCPMC8490320
OpenAlexW3185602405

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.