ArticleJACC. Case reports2026
Reclassification of Exercise-Induced Arrhythmogenic Cardiomyopathy: Detection of a Pathogenic PKP2 Variant in a Male Athlete.
Article in JACC. Case reports, 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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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.
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Abstract
backgroundArrhythmogenic cardiomyopathy (ACM) is predominantly a genetic disease. Endurance exercise acts as a disproportionate trigger in gene-elusive ACM. CASE SUMMARY: A 52-year-old male endurance athlete with stable coronary artery disease and no family history of ACM presented with premature ventricular contractions, right ventricular dilatation, and subtricuspid dyskinesia. After multimodality evaluation, "borderline" biventricular ACM was diagnosed. Genetic testing was negative, leading to a working diagnosis of exercise-induced ACM. Repeat genetic testing after 3 years using novel analytical methods identified a deep intronic pathogenic variant of PKP2. DISCUSSION: The identification of a pathogenic variant is relevant for family screening, risk stratification, and exercise counseling because most available outcome data apply to desmosomal ACM. Periodic genetic retesting is advised in gene-elusive ACM. TAKE-HOME MESSAGES: Periodic genetic retesting and readjudication is crucial for the management of gene-elusive ACM. Robust evidence-based data to guide personalized exercise recommendations in ACM are lacking.
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