Left-Dominant Arrhythmogenic Cardiomyopathy in a Young Athlete

Q: What is the clinical evidence from this study?

Study design: Case Report. Population: Arrhythmogenic left ventricular cardiomyopathy (n=1). Intervention: High-intensity exercise.

Q: What does this research mean for the field?

Arrhythmogenic left ventricular cardiomyopathy can mimic acute myocarditis with an inflammatory 'hot phase' and can be unmasked by exercise exposure, predisposing to life-threatening ventricular arrhythmias. Novelty: ClaimNovelty.INCREMENTAL. Consensus alignment: ConsensusAlignment.NEUTRAL.

Sofia Esteves; Daniel Inácio Cazeiro; Tatiana Guimarães; João R. Agostinho; João Abecasis; Tiago Pereira da Silva; Sância Ramos; Fausto J. Pinto; Nuno Cardim; Rui Plácido

doi:10.1016/j.jaccas.2026.108478

July 1, 2026JACC Case ReportsOpen Access

Left-Dominant Arrhythmogenic Cardiomyopathy in a Young Athlete

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Key result

Left-dominant arrhythmogenic cardiomyopathy can mimic myocarditis and worsen with high-intensity exercise in athletes.

n=1

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Graphical abstract published by JACC Case Reports — Graphical abstract · Published by JACC Case Reports · CC BY-NC-ND

Why the study?

Arrhythmogenic left ventricular cardiomyopathy may present with a myocarditis-like inflammatory hot phase and carries the risk of ventricular arrhythmias.

Key Points

To describe a case of left-dominant arrhythmogenic cardiomyopathy presenting as an inflammatory myocarditis-like hot phase complicated by cardioembolic stroke and exercise-triggered ventricular fibrillation.
Clinical and multimodality diagnostic evaluation of a 21-year-old athlete presenting with chest discomfort and paresthesia using electrocardiography, transthoracic echocardiography, and brain magnetic resonance imaging.
Longitudinal diagnostic reassessment at 3-month follow-up utilizing serial cardiac magnetic resonance imaging, endomyocardial biopsy, and comprehensive genetic testing.
Initial testing demonstrated high-sensitivity I troponin elevation (4,202 ng/L), left ventricular dilation (indexed left ventricular end-diastolic volume: 103 mL/m 2 ), preserved ejection fraction (61%), and an apical thrombus causing cerebral ischemic lesions.
Follow-up cardiac magnetic resonance at 3 months revealed progressive left ventricular remodeling (indexed left ventricular end-diastolic volume: 148 mL/m 2 , ejection fraction: 52%) with persistent late gadolinium enhancement, while genetic testing identified a pathogenic MYBPC3 variant (c.1484G>A; p.Arg495Gln).
During competitive physical activity, the patient experienced out-of-hospital cardiac arrest due to ventricular fibrillation requiring 3 shocks and 14 minutes to return of spontaneous circulation, followed by successful placement of a subcutaneous implantable cardioverter-defibrillator.

Study Design

Type

Case Report (n=1)

Structured PICO

P

Population

A 21-year-old male professional soccer player presenting with a myocarditis-like syndrome and cardioembolic stroke who was diagnosed with left-dominant arrhythmogenic cardiomyopathy.

E

Exposure

Anticoagulation with warfarin, exercise restriction, and subcutaneous implantable cardioverter-defibrillator (S-ICD) insertion.

Arrhythmogenic left ventricular cardiomyopathy can present as a myocarditis-like syndrome with cardioembolic stroke in young athletes, and premature return to high-intensity sports carries a critical arrhythmic risk.

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Implication

Alerts clinicians to ALVC in athletes with myocarditis-like illness; hypothesis-generating for exercise unmasking, needing prospective confirmation.

Abstract

BACKGROUND: Arrhythmogenic left ventricular cardiomyopathy (ALVC) may present with a myocarditis-like inflammatory "hot phase" and carries the risk of ventricular arrhythmias. CASE SUMMARY: A 21-year-old athlete presented with hemifacial and arm paresthesia and chest discomfort. He had parietal ischemic lesions, elevated high-sensitivity I troponin, left ventricle (LV) dilation, apical hypokinesia, apical thrombus, and multifocal nonischemic late gadolinium enhancement with edema. A cardioembolic stroke due to myocarditis with an LV thrombus was assumed. However, he had progressive LV remodeling with persistent late gadolinium enhancement. Endomyocardial biopsy showed low-grade inflammation. Genetic testing identified a pathogenic MYBPC3 variant. The patient declined exercise restriction and experienced exercise-triggered ventricular fibrillation. A subcutaneous implantable cardioverter-defibrillator was inserted, and he remained asymptomatic. DISCUSSION: The presentation and longitudinal course supported ALVC rather than myocarditis. TAKE-HOME MESSAGES: ALVC can mimic myocarditis and may be unmasked by exercise exposure. Serial cardiac magnetic resonance, endomyocardial biopsy, and genetic testing can confirm the diagnosis.

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Cite This Study

Esteves et al. (2026) conducted a case report in Arrhythmogenic left ventricular cardiomyopathy (n=1). High-intensity exercise was evaluated. Left-dominant arrhythmogenic cardiomyopathy can mimic myocarditis in young athletes and may be unmasked or exacerbated by high-intensity exercise exposure.

synapsesocial.com/papers/6a5b38f68167787360d24dd9 https://doi.org/10.1016/j.jaccas.2026.108478

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Left-Dominant Arrhythmogenic Cardiomyopathy in a Young Athlete

Figures

Key Points

Study Design

Structured PICO

Ask about this paper

Implication

Abstract

Discussion

Cite This Study

Left-Dominant Arrhythmogenic Cardiomyopathy in a Young Athlete

Figures

Key Points

Study Design

Structured PICO

Ask about this paper

Implication

Abstract

Discussion

Cite This Study

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