Evidence map›Paper›PMID 40826103›Full record

Observational studyCritical care (London, England)2025

Heterogeneity in association of myocardial injury and mortality in sepsis or acute respiratory distress syndrome by subphenotype: a retrospective study.

Pablo Amador Sanchez, Sarah Obeidalla, V Eric Kerchberger, Andrew R Moore, Manoj V Maddali, Kirsten N Kangelaris, Carolyn M Hendrickson, Bruno Evrard, Kathleen D Liu, Julie A Bastarache and 3 more

Abstract readObservational Study
PubMed Full text at PMC Publisher
In one paragraph

Observational study in Critical care (London, England), 2025. 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
–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

3 citing papers in PubMed.

  1. Review
  2. Article
  3. mRedox biology · 2026
    Review
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

13 authors.

Pablo Amador SanchezDivision of Cardiology, Department of Medicine, University of California San Francisco, San Francisco, CA, USA. pablo.sanchez@ucsf.edu.
Sarah ObeidallaDivision of Allergy, Pulmonary, and Critical Care Medicine, Department of Medicine, Vanderbilt University Medical Center, Nashville, TN, USA.
V Eric KerchbergerDivision of Allergy, Pulmonary, and Critical Care Medicine, Department of Medicine, Vanderbilt University Medical Center, Nashville, TN, USA.
Andrew R MooreDivision of Pulmonary, Allergy and Critical Care Medicine, Department of Medicine, Stanford University, Stanford, CA, USA.
Manoj V MaddaliDivision of Pulmonary, Allergy and Critical Care Medicine, Department of Medicine, Stanford University, Stanford, CA, USA.
Kirsten N KangelarisDivision of Hospital Medicine, University of California San Francisco, San Francisco, CA, USA.
Carolyn M HendricksonDivision of Allergy, Pulmonary, and Critical Care Medicine, Department of Medicine, Zuckerberg San Francisco General Hospital and Trauma Center, San Francisco, CA, USA.
Bruno EvrardInserm CIC 1435, Dupuytren Teaching Hospital, 87000, Limoges, France.
Kathleen D LiuDivision of Nephrology, Department of Medicine, University of California San Francisco, San Francisco, CA, USA.
Julie A BastaracheDivision of Allergy, Pulmonary, and Critical Care Medicine, Department of Medicine, Vanderbilt University Medical Center, Nashville, TN, USA.
Michael A MatthayCardiovascular Research Institute, University of California San Francisco, San Francisco, CA, USA.
Angela J RogersDivision of Pulmonary, Allergy and Critical Care Medicine, Department of Medicine, Stanford University, Stanford, CA, USA.
Carolyn S CalfeeCardiovascular Research Institute, University of California San Francisco, San Francisco, CA, USA.

Funding

Precision Medicine in the Acute Respiratory Distress SyndromeR35HL140026 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI CALFEE, CAROLYN · 2018 to 2024
$6.8M
Advancing Precision Medicine for ARDS and SepsisR35HL177135 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI Carolyn Calfee · 2025 to 2026
$2.3M
The Sepsis ClinicAl Resource And Biorepository (SCARAB) ProjectR33GM144915 · NIGMS · VANDERBILT UNIVERSITY MEDICAL CENTER · PI BASTARACHE, JULIE A., WARE, LORRAINE B · 2024 to 2025
$1.5M
Tissue-specific functional genomics in the acute respiratory distress syndromeK01HL157755 · NHLBI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI KERCHBERGER, VERN ERIC · 2021 to 2025
$845k
Role of Cardiac Dysfunction and Injury in High-Risk Acute Respiratory Distress Syndrome SubphenotypesF32HL160103 · NHLBI · STANFORD UNIVERSITY · PI SANCHEZ, PABLO · 2022 to 2022
$61k
NHLBI NIH HHS F32 HL160103NHLBI NIH HHS K01 HL157755NHLBI NIH HHS R35 HL140026NHLBI NIH HHS R35 HL177135NIGMS NIH HHS R33 GM144915NIH HHS 1F32HL160103-01A1NIH HHS R33 GM144915NIH HHS R35 HL140026
6 · The paper itself

Abstract

rationaleMyocardial injury is common in acute respiratory distress syndrome (ARDS) and sepsis and associated with increased mortality. Two latent class analysis derived subphenotypes are associated with differential risk of mortality in these populations, though the association of troponin-I with mortality within each subphenotype is unknown.

methodsThe derivation (n = 597 in EARLI) and validation (n = 452 in VALID) cohorts consisted of patients with sepsis or ARDS admitted to the ICU and enrolled in two separate prospective observational studies. Patients with troponin-I measured between hospital presentation and within 24 h of ICU admission were included. A parsimonious classifier model using interleukin-8, soluble tumor necrosis factor receptor-1, and vasopressor use assigned patients to subphenotype. Association between peak troponin-I concentration and 60-day in-hospital mortality within each subphenotype was assessed through logistic regression adjusting for age, admission laboratory values, vasopressor use, invasive ventilation use, and cardiac comorbidities.

resultsMedian peak troponin-I was significantly higher in the hyperinflammatory vs hypoinflammatory subphenotype in both cohorts (0.07 vs 0.04 ng/mL and 0.17 vs 0.07 ng/mL, both p < 0.05). The association between peak troponin-I and mortality differed between inflammatory subphenotypes (p-interaction 0.004, EARLI). In EARLI, each doubling of peak troponin-I was associated with increased adjusted odds of 60-day mortality (aOR 1.14, 95% CI 1.02-1.28) in the hypoinflammatory subphenotype only. These findings were corroborated in VALID (aOR 1.11, 95% CI 1.03-1.21 in hypoinflammatory).

conclusionsAdmission peak troponin-I is significantly associated with 60-day mortality in patients with sepsis or ARDS. This association was distinctly driven by the hypoinflammatory subphenotype.

Indexed as

Respiratory Distress SyndromeSepsisAgedBiomarkersCohort StudiesFemaleHospital MortalityHumansIntensive Care UnitsMaleMiddle AgedPhenotypeProspective StudiesRetrospective StudiesTroponin IBiomarkersTroponin I

Identifiers

PMID40826103
PMCPMC12363128

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.