Evidence map›Paper›PMID 41355854›Full record

ArticleEuropean heart journal. Case reports2025

Running the risk: extreme right ventricular remodelling in an endurance athlete-a case report.

Jonathan S Ahn, Elizabeth H Dineen, Kristina H Haugaa, Bassam Yaghmour, Jennifer Xu

Abstract readCase Reports
In one paragraph

Article in European heart journal. Case reports, 2025. 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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0cells of the map it votes in
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

5 authors.

Jonathan S AhnDepartment of Medicine, Loma Linda University, 11234 Anderson St., Room 1503, Loma Linda, CA 92354, USA.ORCID https://orcid.org/0000-0002-2358-5246
Elizabeth H DineenDepartment of Cardiovascular Medicine, Mayo Clinic Florida, 4500 San Pablo Road, Jacksonville, FL 32224, USA.ORCID https://orcid.org/0000-0002-4704-4495
Kristina H HaugaaProCardio Center for Innovation, Department of Cardiology, Oslo University Hospital, Postboks 4950 Nydalen, 0424 Oslo, Norway.ORCID https://orcid.org/0000-0002-4900-0453
Bassam YaghmourDivision of Pulmonary Diseases & Critical Care Medicine, Department of Medicine, University of California, Irvine, 333 City Blvd. West, Suite 400, Orange, CA, USA.ORCID https://orcid.org/0000-0002-5812-6904
Jennifer XuDivision of Cardiology, Department of Medicine, University of California, 333 City Blvd. West, Suite 400, Orange, CA, USA.ORCID https://orcid.org/0009-0006-1462-4529

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Distinguishing physiological cardiac adaptation from pathological remodelling in endurance athletes is challenging. While the athletic heart typically demonstrates balanced biventricular enlargement, extreme exercise may rarely trigger disproportionate right ventricular (RV) changes that challenge diagnostic classification. Case summary: A 47-year-old male ultra-endurance athlete presented with exertional symptoms 3 months after recovery from a pulmonary embolism (PE). Initial post-PE echocardiography was normal. After resuming extreme training, he developed severe RV dilation (basal diameter 5.7 cm on echocardiography; RV volume index 92 cc/m² on cardiac magnetic resonance imaging) disproportionate to the left ventricle, with preserved systolic function and no late gadolinium enhancement. Cardiopulmonary exercise testing revealed significant chronotropic incompetence with below-expected peak oxygen uptake for his elite training status. Symptoms and ventricular ectopy improved with detraining, but severe RV dilation persisted. Evaluation excluded arrhythmogenic cardiomyopathy and significant pulmonary vascular sequelae. Discussion: This case illustrates disproportionate RV remodelling precipitated by the resumption of extreme exercise in a susceptible athlete post-PE. The temporal dissociation from the PE and absence of residual clot burden implicate exercise-related haemodynamic stress as the primary driver, challenging the boundary between physiological adaptation and maladaptation. These findings highlight a potential maladaptive response to extreme exercise, possibly potentiated by a prior vascular insult, and underscore the value of integrated functional assessment and monitored detraining in athletes with borderline findings.

Indexed as

Athletic heartCardiac remodellingCase reportExercise-induced cardiomyopathyRight ventricular dilation

Identifiers

PMID41355854
PMCPMC12677944

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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.