Evidence map›Paper›PMID 36462758›Full record

ArticleThe Canadian journal of cardiology2023

Differentiation of COVID-19-Associated Multisystem Inflammatory Syndrome From Kawasaki Disease With the Use of Cardiac Biomarkers.

Michael D Fridman, Paul Tsoukas, Aamir Jeewa, Rae S M Yeung, Beth D Gamulka, Brian W McCrindle

Open access · bronzeAbstract read
In one paragraph

Article in The Canadian journal of cardiology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
3.1field-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

12 citing papers in PubMed, 14 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 1 institution in 1 country.

Michael D FridmanDepartment of Pediatrics, University of Toronto, Toronto, Ontario, Canada; Labatt Family Heart Centre, Hospital for Sick Children, Toronto, Ontario, Canada.
Paul TsoukasDepartment of Pediatrics, University of Toronto, Toronto, Ontario, Canada; Division of Rheumatology, Hospital for Sick Children, Toronto, Ontario, Canada; Department of Immunology and Institute of Medical Science, University of Toronto, Toronto, Ontario, Canada.
Aamir JeewaDepartment of Pediatrics, University of Toronto, Toronto, Ontario, Canada; Labatt Family Heart Centre, Hospital for Sick Children, Toronto, Ontario, Canada.
Rae S M YeungDepartment of Pediatrics, University of Toronto, Toronto, Ontario, Canada; Division of Rheumatology, Hospital for Sick Children, Toronto, Ontario, Canada; Department of Immunology and Institute of Medical Science, University of Toronto, Toronto, Ontario, Canada.
Beth D GamulkaDepartment of Immunology and Institute of Medical Science, University of Toronto, Toronto, Ontario, Canada; Division of Paediatric Medicine, Hospital for Sick Children, Toronto, Ontario, Canada.
Brian W McCrindleDepartment of Pediatrics, University of Toronto, Toronto, Ontario, Canada; Labatt Family Heart Centre, Hospital for Sick Children, Toronto, Ontario, Canada. Electronic address: brian.mccrindle@sickkids.ca.
University of Toronto · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundMultisystem inflammatory syndrome in children (MIS-C) after COVID-19 shares clinical similarities to Kawasaki disease (KD). We sought to determine whether cardiac biomarker levels differentiate MIS-C from KD and their association with cardiac involvement.

methodsSubjects included 38 MIS-C patients with confirmed prior COVID-19 and 32 prepandemic and 38 contemporaneous KD patients with no evidence of COVID-19. Patient, clinical, echocardiographic, electrocardiographic, and laboratory data timed within 72 hours of cardiac biomarker assessment were abstracted. Groups were compared, and regression analyses were used to determine associations between biomarker levels, diagnosis and cardiac involvement, adjusting for clinical factors.

resultsMIS-C patients had fewer KD clinical features, with more frequent shock, intensive care unit admission, inotrope requirement, and ventricular dysfunction, with no difference regarding coronary artery involvement. Multivariable regression analysis showed that both higher N-terminal pro-B-type natriuretic peptide (NT-proBNP) and cardiac troponin I (TnI) were associated with MIS-C vs KD, after adjusting for significant covariates. Receiver operating characteristic curves for diagnosis showed that any detectable TnI greater than 10 ng/L was predictive of MIS-C vs KD with 91% sensitivity and 76% specificity. NT-proBNP > 2000 ng/L predicted MIS-C vs KD with 82% sensitivity and 82% specificity. Higher TnI but not NT-proBNP was associated with lower LV ejection fraction. Neither biomarker was associated with coronary artery involvement.

conclusionsPositive TnI and higher NT-proBNP may differentiate MIS-C from KD, which may become more relevant as evidence of prior COVID-19 becomes more challenging to determine. Cardiac biomarkers may have limited associations with cardiac involvement in this setting.

Indexed as

COVID-19Mucocutaneous Lymph Node SyndromeBiomarkersChildEchocardiographyHumansNatriuretic Peptide, BrainPeptide FragmentsSystemic Inflammatory Response SyndromeBiomarkersNatriuretic Peptide, BrainPeptide Fragments

Identifiers

PMID36462758
PMCPMC9711900
OpenAlexW4311035620

What OpenQuestion holds

Textmetadata
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.