Evidence map›Paper›PMID 39652119›Full record

ArticleClinical research in cardiology : official journal of the German Cardiac Society2025

Eccentric hypertrophy impairs outcome after TAVR.

R Thalmann, V Obermeier, Dominik S Westphal, I Diebold, T Trenkwalder, C Pellegrini, G Buglio, H Seoudy, P Hoppmann, C Bradaric and 10 more

Abstract read
In one paragraph

Article in Clinical research in cardiology : official journal of the German Cardiac Society, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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

20 authors.

R Thalmann *Klinik Und Poliklinik Für Innere Medizin I, University Hospital Rechts Der Isar, School of Medicine and Health, Technical University of Munich, Ismaninger Str. 22, 81675, Munich, Germany.
V Obermeier *Klinik Und Poliklinik Für Innere Medizin I, University Hospital Rechts Der Isar, School of Medicine and Health, Technical University of Munich, Ismaninger Str. 22, 81675, Munich, Germany.
Dominik S Westphal *Klinik Und Poliklinik Für Innere Medizin I, University Hospital Rechts Der Isar, School of Medicine and Health, Technical University of Munich, Ismaninger Str. 22, 81675, Munich, Germany. dominik.westphal@mri.tum.de.ORCID http://orcid.org/0000-0003-4870-9863
I DieboldMGZ Medizinisch Genetisches Zentrum Munich, Munich, Germany.
T TrenkwalderDZHK (German Center for Cardiovascular Research), Partner Site Munich Heart Alliance, Munich, Germany.
C PellegriniDZHK (German Center for Cardiovascular Research), Partner Site Munich Heart Alliance, Munich, Germany.
G BuglioKlinik Und Poliklinik Für Innere Medizin I, University Hospital Rechts Der Isar, School of Medicine and Health, Technical University of Munich, Ismaninger Str. 22, 81675, Munich, Germany.
H SeoudyKlinik Für Innere Medizin III, University Hospital Schleswig-Holstein, Kiel, Germany.
P HoppmannKlinik Und Poliklinik Für Innere Medizin I, University Hospital Rechts Der Isar, School of Medicine and Health, Technical University of Munich, Ismaninger Str. 22, 81675, Munich, Germany.
C BradaricKlinik Und Poliklinik Für Innere Medizin I, University Hospital Rechts Der Isar, School of Medicine and Health, Technical University of Munich, Ismaninger Str. 22, 81675, Munich, Germany.
U SchönMGZ Medizinisch Genetisches Zentrum Munich, Munich, Germany.
E Holinski-FederMGZ Medizinisch Genetisches Zentrum Munich, Munich, Germany.
N LettmannKlinik Und Poliklinik Für Innere Medizin I, University Hospital Rechts Der Isar, School of Medicine and Health, Technical University of Munich, Ismaninger Str. 22, 81675, Munich, Germany.
H RugeDepartment of Cardiovascular Surgery, Institute Insure, German Heart Center Munich, School of Medicine and Health, Technical University of Munich, Munich, Germany.
M ErlebachDepartment of Cardiovascular Surgery, Institute Insure, German Heart Center Munich, School of Medicine and Health, Technical University of Munich, Munich, Germany.
C FuettererInstitute of AI and Informatics in Medicine, University Hospital Rechts Der Isar, School of Medicine and Health, Technical University of Munich, Munich, Germany.
K L LaugwitzKlinik Und Poliklinik Für Innere Medizin I, University Hospital Rechts Der Isar, School of Medicine and Health, Technical University of Munich, Ismaninger Str. 22, 81675, Munich, Germany.
M KraneDepartment of Cardiovascular Surgery, Institute Insure, German Heart Center Munich, School of Medicine and Health, Technical University of Munich, Munich, Germany.
D FrankKlinik Für Innere Medizin III, University Hospital Schleswig-Holstein, Kiel, Germany.
C KupattKlinik Und Poliklinik Für Innere Medizin I, University Hospital Rechts Der Isar, School of Medicine and Health, Technical University of Munich, Ismaninger Str. 22, 81675, Munich, Germany.

Funding

Deutsche Herzstiftung F/46/21Deutsches Zentrum für Herz-Kreislaufforschung 81X1600607
6 · The paper itself

Abstract

backgroundAortic stenosis (AS) induces cardiac remodeling upon chronic left ventricular (LV) pressure overload. Here, we analyzed the clinical outcome of patients undergoing transcatheter aortic valve replacement (TAVR) for symptomatic AS with regard to varying LV hypertrophy patterns. Moreover, we investigated the genetic influence on development of different hypertrophy patterns, measured by polygenic risk scores (PRS).

methods1703 patients with severe AS undergoing TAVR were categorized according to LV mass index and relative wall thickness in four subgroups: normal geometry (NG, n = 57), concentric remodeling (CR; n = 388), concentric hypertrophy (CH; n = 993) and eccentric hypertrophy (EH; n = 265). Data was analyzed retrospectively with regard to clinical outcome. In a substudy, 520 patients affected by CH (n = 237), EH (n = 139) or CR (n = 164) were analyzed using two PRS that have been previously associated with hypertrophic and dilated cardiomyopathy.

results1 year after TAVR, for EH, in contrast to the remaining groups (NG, CR, CH), a significant difference in all-cause mortality was observable (mortality 17.4% EH, 14.0% NG, 12.4% CR, 14.0% CH, p = 0.001). This difference was observed up to 4 years (mortality 41.9% EH, 26.9% CH, 28.1% CR, 26.4% NG, p = 0.001). Of note, higher percentiles in a PRS for hypertrophic cardiomyopathy were associated with a reduced likelihood of EH in patients with AS (p = 0.046).

conclusionsThe EH group had a statistically significant poorer 1-year and 5-year outcomes than the other groups. PRS might help predict myocardial reactions in patients with aortic stenosis in future.

Indexed as

Aortic Valve StenosisHypertrophy, Left VentricularTranscatheter Aortic Valve ReplacementVentricular Function, LeftVentricular RemodelingAgedAged, 80 and overEchocardiographyFemaleFollow-Up StudiesHumansMaleRetrospective StudiesRisk FactorsSeverity of Illness IndexTreatment OutcomeCardiomyopathyHypertrophyOutcomePolygenic risk scoreTAVRTranscatheter aortic valve replacement

Identifiers

PMID39652119
PMCPMC12540619

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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.