Evidence map›Paper›PMID 34384615›Full record

ArticleJournal of electrocardiology

Transient recovery of epicardial and torso ST-segment ischemic signals during cardiac stress tests: A possible physiological mechanism.

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 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.6field-weighted citation impact, top 30% 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

4 citing papers in PubMed, 5 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

8 authors at 2 institutions 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 · USHarrison Medical Center · 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
Image Based Modeling, Simulation, and Visualization Summer Course for BiomedicalR25GM107009 · NIGMS · UNIVERSITY OF UTAH · PI MACLEOD, ROB S., WEISS, JEFFREY A. · 2013 to 2017
$764k
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 GM136986NIGMS NIH HHS R25 GM107009
6 · The paper itself

Abstract

backgroundAcute myocardial ischemia has several characteristic ECG findings, including clinically detectable ST-segment deviations. However, the sensitivity and specificity of diagnosis based on ST-segment changes are low. Furthermore, ST-segment deviations have been shown to be transient and spontaneously recover without any indication the ischemic event has subsided.

objectiveAssess the transient recovery of ST-segment deviations on remote recording electrodes during a partial occlusion cardiac stress test and compare them to intramyocardial ST-segment deviations.

methodsWe used a previously validated porcine experimental model of acute myocardial ischemia with controllable ischemic load and simultaneous electrical measurements within the heart wall, on the epicardial surface, and on the torso surface. Simulated cardiac stress tests were induced by occluding a coronary artery while simultaneously pacing rapidly or infusing dobutamine to stimulate cardiac function. Postexperimental imaging created anatomical models for data visualization and quantification. Markers of ischemia were identified as deviations in the potentials measured at 40% of the ST-segment. Intramural cardiac conduction speed was also determined using the inverse gradient method. We assessed changes in intramyocardial ischemic volume proportion, conduction speed, clinical presence of ischemia on remote recording arrays, and regional changes to intramyocardial ischemia. We defined the peak deviation response time as the time interval after onset of ischemia at which maximum ST-segment deviation was achieved, and ST-recovery time was the interval when ST deviation returned to below thresholded of ST elevation.

resultsIn both epicardial and torso recordings, the peak ST-segment deviation response time was 4.9±1.1 min and the ST-recovery time was approximately 7.9±2.5 min, both well before the termination of the ischemic stress. At peak response time, conduction speed was reduced by 50% and returned to near baseline at ST-recovery. The overall ischemic volume proportion initially increased, on average, to 37% at peak response time; however, it recovered to only 30% at the ST-recovery time. By contrast, the subepicardial region of the myocardial wall showed 40% ischemic volume at peak response time and recovered much more strongly to 25% as epicardial ST-segment deviations returned to baseline.

conclusionOur data show that remote ischemic signal recovery correlates with a recovery of the subepicardial myocardium, whereas subendocardial ischemic development persists.

Indexed as

ElectrocardiographyMyocardial IschemiaAnimalsHeartIschemiaSwineTorsoAcute myocardial ischemiaCardiac stress testExperimental modelST-segment changes

Identifiers

PMID34384615
PMCPMC8664997
OpenAlexW3185032683

What OpenQuestion holds

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Registered trials

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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.