Evidence map›Paper›PMID 38842289›Full record

ArticleJournal of the American Heart Association2024

Individual and Joint Associations of High-Sensitivity Troponin I and High-Sensitivity Troponin T with Cardiac Phenotypes and Outcomes in the General Population: An Analysis From the Dallas Heart Study.

Rebecca Vigen, Colby Ayers, Jarett Berry, Anand Rohatgi, Vijay Nambi, Christie M Ballantyne, Torbjorn Omland, Christopher R de Filippi, James de Lemos

Abstract read
In one paragraph

Article in Journal of the American Heart Association, 2024. 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
–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

4 citing papers in PubMed.

  1. Article
  2. Article
  3. Sex Differences in Heart Failure: A Step Forward.Interventional cardiology (London, England) · 2025
    Review
  4. 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

9 authors.

Rebecca VigenDivision of Cardiology Department of Internal Medicine University of Texas Southwestern Medical Center Dallas TX USA.ORCID 0000-0001-7590-3341
Colby AyersDivision of Cardiology Department of Internal Medicine University of Texas Southwestern Medical Center Dallas TX USA.ORCID 0000-0003-2060-2263
Jarett BerryDepartment of Internal Medicine University of Texas at Tyler Health Science Center Tyler TX USA.ORCID 0000-0002-5004-8155
Anand RohatgiDivision of Cardiology Department of Internal Medicine University of Texas Southwestern Medical Center Dallas TX USA.ORCID 0000-0003-0164-2382
Vijay NambiDepartment of Medicine and Center for Cardiometabolic Disease Prevention Baylor College of Medicine Houston TX USA.ORCID 0000-0002-4237-0267
Christie M BallantyneDepartment of Medicine and Center for Cardiometabolic Disease Prevention Baylor College of Medicine Houston TX USA.ORCID 0000-0002-6432-1730
Torbjorn OmlandK.G. Jebsen Center of Cardiac Biomarkers Institute of Clinical Medicine University of Oslo Oslo Norway.ORCID 0000-0002-6452-0369
Christopher R de FilippiInova Heart and Vascular Institute Inova Fairfax Medical Campus Falls Church VA USA.ORCID 0000-0002-0660-4943
James de LemosDivision of Cardiology Department of Internal Medicine University of Texas Southwestern Medical Center Dallas TX USA.ORCID 0000-0003-2211-7261

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundHigh-sensitivity troponin I (hs-cTnI) and T (hs-cTnT) provide complementary information regarding cardiovascular disease risk. The explanation for their distinct risk profiles is incompletely understood. METHODS AND

resultshs-cTnI and hs-cTnT were measured in Dallas Heart Study participants. Associations of hs-cTnI and hs-cTnT with demographics and phenotypes were assessed using linear regression. Associations with incident heart failure, atherosclerotic cardiovascular disease, global cardiovascular disease, and cardiovascular and all-cause mortality were assessed using Cox models. Among 3276 participants (56% women, 50% Black persons, median age 43 years), the correlation between hs-cTnI and hs-cTnT was modest (Spearman rho=0.35). Variables associated with hs-cTnI but not hs-cTnT included hypertension, higher body mass index and total cholesterol, and lower high-density lipoprotein and cholesterol efflux capacity. Older age, male sex, and diabetes were positively associated, and smoking was negatively associated, with hs-cTnT but not hs-cTnI. Hs-cTnI and hs-cTnT were associated with heart failure (hazard ratio [HR] per SD log hs-cTnI 1.53 [95% CI, 1.30-1.81] and HR per SD log hs-cTnT 1.65 [95% CI, 1.40-1.95]), global cardiovascular disease (HR, 1.22 [95% CI, 1.10-1.34] and HR, 1.27 [95% CI, 1.15-1.32]), and all-cause mortality (HR, 1.12 [95% CI, 1.01-1.25], and HR, 1.17 [95% CI, 1.06-1.29]). After adjustment for N-terminal pro-B-type natriuretic peptide and the alternative troponin, both remained associated with heart failure (HR per SD log hs-cTnI 1.32 [95% CI, 1.1-1.58] and HR per log hs-cTnT 1.27 [95% CI, 1.06-1.51]).

conclusionsHs-cTnI and hs-cTnT are modestly correlated, demonstrate differential associations with cardiac and metabolic phenotypes, and provide complementary information regarding heart failure risk.

Indexed as

BiomarkersPhenotypeTroponin ITroponin TAdultCardiovascular DiseasesFemaleHeart FailureHumansIncidenceMaleMiddle AgedPredictive Value of TestsPrognosisRisk AssessmentRisk FactorsBiomarkersTroponin ITroponin Tcardiovascular diseasehigh‐sensitivity troponinsrisk prediction

Identifiers

PMID38842289
PMCPMC11255706

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LicenceCC BY-NC-ND
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.