Evidence map›Paper›PMID 40594668›Full record

ArticleScientific reports2025

Left ventricular global longitudinal strain and diagnostic yield of genetic testing in hypertrophic cardiomyopathy in a multicenter registry analysis.

Viktoria Santner, Viktoria Höller, Maria Ungericht, Nora Schwegel, David Zach, Heidelis Tichy, Gert Waltl, Richard Belciug, Markus Wallner, Johannes Gollmer and 9 more

Abstract readMulticenter Study
In one paragraph

Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Review
  2. 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

19 authors.

Viktoria SantnerDivision of Cardiology, Department of Internal Medicine, University Heart Center, Medical University of Graz, Graz, Austria.
Viktoria HöllerDivision of Cardiology, Department of Internal Medicine, University Heart Center, Medical University of Graz, Graz, Austria.
Maria UngerichtDepartment of Internal Medicine III, Cardiology & Angiology, Medical University of Innsbruck, Innsbruck, Austria.
Nora SchwegelDivision of Cardiology, Department of Internal Medicine, University Heart Center, Medical University of Graz, Graz, Austria.
David ZachDivision of Cardiology, Department of Internal Medicine, University Heart Center, Medical University of Graz, Graz, Austria.
Heidelis TichyInstitute of Human Genetics, Medical University of Graz, Graz, Austria.
Gert WaltlDivision of Cardiology, Department of Internal Medicine, State Hospital (LKH) Graz II, Graz, Austria.
Richard BelciugDivision of Cardiology, Department of Internal Medicine, University Heart Center, Medical University of Graz, Graz, Austria.
Markus WallnerDivision of Cardiology, Department of Internal Medicine, University Heart Center, Medical University of Graz, Graz, Austria.
Johannes GollmerDivision of Cardiology, Department of Internal Medicine, University Heart Center, Medical University of Graz, Graz, Austria.
Ewald KolesnikDivision of Cardiology, Department of Internal Medicine, University Heart Center, Medical University of Graz, Graz, Austria.
Peter P RainerDivision of Cardiology, Department of Internal Medicine, University Heart Center, Medical University of Graz, Graz, Austria.
Dirk von LewinskiDivision of Cardiology, Department of Internal Medicine, University Heart Center, Medical University of Graz, Graz, Austria.
Klemens AblasserDivision of Cardiology, Department of Internal Medicine, University Heart Center, Medical University of Graz, Graz, Austria.
Sabine Rudnik-SchönebornInstitute of Human Genetics, Medical University of Innsbruck, Innsbruck, Austria.
Gerhard PölzlDepartment of Internal Medicine III, Cardiology & Angiology, Medical University of Innsbruck, Innsbruck, Austria.
Ellen HeitzerInstitute of Human Genetics, Medical University of Graz, Graz, Austria.
Andreas ZirlikDivision of Cardiology, Department of Internal Medicine, University Heart Center, Medical University of Graz, Graz, Austria.
Nicolas VerheyenDivision of Cardiology, Department of Internal Medicine, University Heart Center, Medical University of Graz, Graz, Austria. nicolas.verheyen@medunigraz.at.

Funding

Österreichische Kardiologische Gesellschaft Project-related Grant 2024
6 · The paper itself

Abstract

In this multicenter study we investigated whether echocardiography-derived left ventricular global longitudinal strain (LV GLS), an indicator of myocardial fibrosis, independently predicts a positive genotype in hypertrophic cardiomyopathy (HCM). We performed a cross-sectional analysis including HCM patients with genetic testing results and echocardiographic data from two Austrian HCM registries. Echocardiographic parameters were measured in post-processing analysis by a blinded investigator. Among 125 patients with HCM, a positive genotype was present in 39%. Worse LV GLS was associated with a positive genotype in univariate analysis (Odds Ratio [OR] 95% CI 1.141, 1.018-1.279, p = 0.023). In multivariate regression analysis adjusted for genotype predictors (age at diagnosis < 45 years, arterial hypertension, positive family history of HCM, maximal to posterior wall thickness [MWTH: PWTH], reverse curve septal phenotype), the reverse curve septal phenotype remained as a single independent predictor of genotype-positive HCM (OR 6.948, 2.342-20.614, p < 0.001). Adding LV GLS to established Toronto and Mayo genotype prediction scores did not improve their performance. To conclude, worse LV GLS was not independently associated with genotype-positive HCM and did not improve the diagnostic yield of genetic testing in HCM in a multivariate model. Our study highlights the reverse curve septal phenotype as the strongest genotype predictor in HCM.

Indexed as

Cardiomyopathy, HypertrophicGenetic TestingHeart VentriclesAdultAgedAustriaCross-Sectional StudiesEchocardiographyFemaleGenotypeGlobal Longitudinal StrainHumansMaleMiddle AgedPhenotypeRegistriesEchocardiographyGenetic testingGenotypeHypertrophic cardiomyopathyMyocardial fibrosisStrain

Identifiers

PMID40594668
PMCPMC12216254

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.