Evidence map›Paper›PMID 38115713›Full record

ArticleTexas Heart Institute journal2023

Characterization of Myocardial Injury With High-Sensitivity Troponin.

Sant Kumar, Nayrana Griffith, Dylan Walter, Michael Swett, Venkatesh Raman, Jose D Vargas, Brototo Deb, Jiling Chou, Ayah Arafat, Monvadi B Srichai

Open access · diamondAbstract read
In one paragraph

Article in Texas Heart Institute journal, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.3field-weighted citation impact, top 17% 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

7 citing papers in PubMed, 6 citations in OpenAlex.

  1. Review
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  6. Review
  7. Upregulation of Serum miRNA-3615 Serves as a Biomarker to Predict Disease Onset and Prognosis in Acute Coronary Syndrome Patients.Clinical and applied thrombosis/hemostasis : official journal of the International Academy of Clinical and Applied Thrombosis/Hemostasis
    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

10 authors at 5 institutions in 1 country.

Sant KumarDepartment of Internal Medicine, MedStar Georgetown University Hospital, Washington, DC.
Nayrana GriffithDepartment of Internal Medicine, MedStar Georgetown University Hospital, Washington, DC.
Dylan WalterDepartment of Internal Medicine, MedStar Georgetown University Hospital, Washington, DC.
Michael SwettDepartment of Internal Medicine, MedStar Georgetown University Hospital, Washington, DC.
Venkatesh RamanDepartment of Cardiology, US Department of Veterans Affair Medical Center, Washington, DC.
Jose D VargasDepartment of Cardiology, US Department of Veterans Affair Medical Center, Washington, DC.
Brototo DebDepartment of Internal Medicine, MedStar Washington Hospital Center, Washington, DC.
Jiling ChouMedStar Health Research Institute, Hyattsville, Maryland.
Ayah ArafatMedStar Health Research Institute, Hyattsville, Maryland.
Monvadi B SrichaiDepartment of Cardiology, MedStar Georgetown University Hospital, Washington, DC.
Georgetown University · USMedStar Health · USUnited States Department of Veterans Affairs · USMedStar Georgetown University Hospital · USMedStar Washington Hospital Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundHigh-sensitivity troponin I, cardiac form (hs-cTnI) accelerates the assessment of acute coronary syndrome. Little has been documented about its performance, how it relates to different types of myocardial injury, and its impact on morbidity and mortality. This study sought to expand understanding of hs-cTnI by characterizing types of myocardial injury, the impact of comorbidities, and 30-day outcomes.

methodsThe study retrospectively evaluated 1,975 patients with hs-cTnI levels obtained in the emergency department or inpatient setting from June to September 2020. Troponin was considered elevated if it was higher than the 99th percentile for either sex. Charts were reviewed to determine the presence of myocardial injury. Troponin elevation was adjusted for demographics, comorbidities, and kidney dysfunction. Thirty-day mortality and readmission rates were calculated.

resultsOf 1,975 patients, 468 (24%) had elevated hs-cTnI, and 330 (17%) had at least 1 type of myocardial injury, type 2 myocardial infarction being the most frequent. Sensitivity and specificity using the 99th percentile as a cutoff were 99% and 92%, respectively. The average maximum hs-cTnI level was significantly higher for type 1 myocardial infarction (P < .001). Being male, Black, non-Hispanic, and a hospital inpatient were all associated with higher initial and peak hs-cTnI levels (P < .001). Elevated hs-cTnI level, age, heart disease, kidney dysfunction, and inpatient status were predictive of 30-day mortality on multivariate analysis.

conclusionElevated hs-cTnI levels in emergency department and inpatient settings occurs most commonly because of type 2 myocardial infarction. Maximum hs-cTnI level is associated with the patient's particular type of myocardial injury, certain demographics, and cardiovascular comorbidities, and it may be a predictor of 30-day outcomes.

Indexed as

Acute Coronary SyndromeAnterior Wall Myocardial InfarctionHeart InjuriesMyocardial InfarctionBiomarkersFemaleHumansMaleRetrospective StudiesTroponin ITroponin TBiomarkersTroponin ITroponin Tacute coronary syndromemortalitymyocardial infarctionTroponin

Identifiers

PMID38115713
PMCPMC10751476
OpenAlexW4390011519

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.