Evidence map›Paper›PMID 41910533›Full record

ArticleEuropean journal of clinical investigation2026

CMR-derived skeletal muscle T1 time and extracellular volume as novel diagnostic markers for cardiac amyloidosis.

Christina Kronberger, Katharina Mascherbauer, Michael Poledniczek, Lena Marie Schmid, Carolina Donà, Matthias Koschutnik, Laura Lunzer, René Rettl, Franz Duca, Christina Binder and 11 more

Abstract read
In one paragraph

Article in European journal of clinical investigation, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0citing papers in PubMed
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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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

21 authors.

Christina KronbergerDivision of Cardiology, Department of Internal Medicine II, Medical University of Vienna, Vienna, Austria.ORCID https://orcid.org/0000-0002-3866-3710
Katharina MascherbauerDivision of Cardiology, Department of Internal Medicine II, Medical University of Vienna, Vienna, Austria.ORCID https://orcid.org/0000-0001-9681-1833
Michael PoledniczekDivision of Cardiology, Department of Internal Medicine II, Medical University of Vienna, Vienna, Austria.ORCID https://orcid.org/0000-0002-6091-9823
Lena Marie SchmidDivision of Cardiology, Department of Internal Medicine II, Medical University of Vienna, Vienna, Austria.
Carolina DonàDivision of Cardiology, Department of Internal Medicine II, Medical University of Vienna, Vienna, Austria.
Matthias KoschutnikDivision of Cardiology, Department of Internal Medicine II, Medical University of Vienna, Vienna, Austria.ORCID https://orcid.org/0000-0001-6164-8773
Laura LunzerDivision of Cardiology, Department of Internal Medicine II, Medical University of Vienna, Vienna, Austria.
René RettlDivision of Cardiology, Department of Internal Medicine II, Medical University of Vienna, Vienna, Austria.
Franz DucaDivision of Cardiology, Department of Internal Medicine II, Medical University of Vienna, Vienna, Austria.
Christina BinderDivision of Cardiology, Department of Internal Medicine II, Medical University of Vienna, Vienna, Austria.
Christian NitscheDivision of Cardiology, Department of Internal Medicine II, Medical University of Vienna, Vienna, Austria.
Nikita ErmolaevDivision of Cardiology, Department of Internal Medicine II, Medical University of Vienna, Vienna, Austria.
Gözde CelebiDivision of Cardiology, Department of Internal Medicine II, Medical University of Vienna, Vienna, Austria.
Varius DannenbergDivision of Cardiology, Department of Internal Medicine II, Medical University of Vienna, Vienna, Austria.ORCID https://orcid.org/0000-0001-5722-4281
Dietrich BeitzkeDivision of Cardiovascular and Interventional Radiology, Department of Biomedical Imaging and Image-Guided Therapy, Medical University of Vienna, Vienna, Austria.
Roza Badr EslamDivision of Cardiology, Department of Internal Medicine II, Medical University of Vienna, Vienna, Austria.
Jutta Bergler-KleinDivision of Cardiology, Department of Internal Medicine II, Medical University of Vienna, Vienna, Austria.
Julia MascherbauerKarl Landsteiner University of Health Sciences, Department of Internal Medicine 3, University Hospital St. Pölten, Krems, Austria.
Johannes KastnerDivision of Cardiology, Department of Internal Medicine II, Medical University of Vienna, Vienna, Austria.
Christian HengstenbergDivision of Cardiology, Department of Internal Medicine II, Medical University of Vienna, Vienna, Austria.
Andreas Anselm KammerlanderDivision of Cardiology, Department of Internal Medicine II, Medical University of Vienna, Vienna, Austria.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionCardiac amyloidosis (CA) is a progressive cardiomyopathy caused by amyloid deposition, leading to heart failure and increased mortality. Cardiac magnetic resonance (CMR) identifies myocardial involvement via elevated native T1 relaxation time and extracellular volume (ECV). Although amyloid infiltration has also been observed in thoracic skeletal muscle, the diagnostic and prognostic relevance of thoracic skeletal muscle T1 time and ECV remain unclear.

aimTo compare native thoracic skeletal muscle T1 time and ECV between CA patients and controls and assess their diagnostic and prognostic value.

methodsIn a prospective CMR registry, consecutive CA patients and controls underwent CMR with T1-mapping. Native and post-contrast T1 relaxation time and ECV were quantified in myocardium and thoracic skeletal muscles. Diagnostic performance was evaluated using ROC analysis and associations with mortality were assessed using Cox regression.

resultsAmong 1976 participants (267 CA, 1709 controls), CA patients showed significantly higher native myocardial T1 time and ECV, as well as elevated native thoracic skeletal muscle T1 time (919.4 vs. 868.5 ms, p < 0.001) and ECV (16.4 vs. 12.9%, p < 0.001). Native thoracic skeletal muscle T1 time demonstrated moderate diagnostic performance for CA (AUC = 0.70), with an optimal cutoff of 895 ms yielding a sensitivity of 61% and specificity of 59%. Higher native thoracic skeletal muscle T1 time predicted increased mortality (HR = 1.65 per 100 ms, p < 0.001), and this association remained significant after adjusting for age, sex and ventricular function (HR = 1.21 per 100 ms, p = 0.008).

conclusionNative skeletal muscle T1 relaxation time and ECV indicate systemic amyloid involvement and provide additional diagnostic and prognostic information beyond myocardial assessment, potentially supporting improved detection and risk stratification in CA.

Indexed as

AmyloidosisCardiomyopathiesMuscle, SkeletalAgedCase-Control StudiesFemaleHumansMagnetic Resonance ImagingMaleMiddle AgedMyocardiumPrognosisProspective StudiesROC Curvecardiac amyloidosisdiagnosisECVnative T1 timeT1‐mapping

Identifiers

PMID41910533
PMCPMC13034890

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