Arrhythmogenic right ventricular cardiomyopathy (ARVC) is an inherited myocardial disorder characterized by fibrofatty infiltration predominantly of the right ventricle (RV), predisposing to ventricular arrhythmias and sudden cardiac death (SCD). Differentiating early ARVC from physiological athletic remodeling poses a significant diagnostic dilemma, particularly in asymptomatic adolescents engaged in high-level sports.[1] Evolving diagnostic criteria, including the 2020 Padua revisions, emphasize tissue characterization and electroanatomic mapping, especially in early or concealed forms.2] The intersection between athletic cardiac adaptation and arrhythmogenic syndromes remains an active area of investigation in sports cardiology.[3] We report the case of a competitive young footballer with suspected ARVC, highlighting the challenges of diagnosis and management within the context of modern sports cardiology.

A 15-year-old male footballer underwent routine cardiac screening. He was asymptomatic, reported no family history of cardiomyopathy or SCD, and engaged in high-intensity football training for approximately four hours daily. Physical examination was normal. Resting electrocardiography (ECG) demonstrated normal sinus rhythm with isolated T-wave inversion in lead V1 [Figure 1]. No epsilon waves or terminal activation delays were observed.

Transthoracic echocardiography (TTE) revealed mild RV enlargement with preserved biventricular function. No septal defects or significant valvular abnormalities were identified. Cardiac magnetic resonance imaging (CMR) demonstrated minor regional RV wall motion abnormalities in the basal free wall with mildly reduced RV ejection fraction (46%) [Figure 2]. No late gadolinium enhancement (LGE) was detected. Indexed RV volumes were borderline elevated.

Twenty-four-hour Holter monitoring and exercise treadmill testing revealed no ventricular ectopy or arrhythmias. Cardiac biomarkers (NT-proBNP and troponin-T) were within normal limits.

The findings fulfilled only a single minor criterion for ARVC per 2010 Task Force Criteria and 2020 Padua revisions. The presence of isolated T-wave inversion confined to V1 is considered a normal variant in adolescent athletes and did not contribute diagnostic weight. The CMR evidence of subtle regional dyskinesia and mild RV dysfunction warranted concern but was insufficient alone for definitive diagnosis.

The differential diagnosis included early-stage ARVC versus pronounced physiological RV remodeling due to endurance athletic training. The absence of arrhythmias and normal exercise testing results favored a benign athletic adaptation.

Diagnosing ARVC in athletes remains challenging, particularly when only minor structural abnormalities are present. Athletic remodeling often leads to RV dilatation without associated regional wall motion abnormalities.[4] The finding of localized dyskinesia on CMR heightened suspicion for pathology.

High-intensity endurance exercise has been associated with exacerbation of ARVC phenotypes and may accelerate disease progression in predisposed individuals.[5] Conversely, athlete's heart typically shows global chamber dilation with preserved or supranormal systolic function.[4]

Current consensus advocates for the use of multimodal evaluation - including ECG, echocardiography, CMR, Holter monitoring, and genetic testing - to stratify risk.[6,7] Revised diagnostic frameworks, including the 2020 Padua criteria, seek to improve sensitivity in borderline cases and distinguish athletic remodeling from concealed cardiomyopathy.[2] The role of sports cardiology manuals, such as the IOC Manual, further reinforces structured approaches to screening and athlete evaluation.[3]

In this case, management prioritized risk minimization. Competitive sports participation was restricted pending further genetic analysis and serial imaging reassessment. A period of detraining was advised to assess reversibility of RV changes.

Shared decision-making was emphasized, involving the athlete and family in the understanding of diagnostic uncertainty and potential SCD risks. Regular follow-up with surveillance imaging and arrhythmia monitoring was instituted.

This case underscores the diagnostic complexity of suspected ARVC in adolescent athletes. Isolated minor imaging abnormalities require cautious interpretation within clinical context. Comprehensive evaluation, risk stratification, and individualized, multidisciplinary management — centered on shared decision-making - are paramount. Restriction from competitive sports pending definitive diagnosis is a prudent strategy in such borderline cases.

1. Corrado D, Zorzi A. Arrhythmogenic right ventricular cardiomyopathy and sports activity: From molecular pathways to athletic heart mimicry. Eur Heart J 2021;42:1231-43.
2. Corrado D, van Tintelen PJ, McKenna WJ, et al. Arrhythmogenic right ventricular cardiomyopathy: evaluation of the current diagnostic criteria and differential diagnosis. Eur Heart J 2020;41:1414-29.
3. Drezner JA, Sharma S, Wilson MG, eds. IOC Manual of sports cardiology. 1st edn. Oxford: Wiley Blackwell 2017.
4. D'Ascenzi F, Pisicchio C, Caselli S, et al. Right ventricular remodeling induced by exercise training in competitive athletes. Eur Heart J Cardiovasc Imaging 2016;17(3):301-7.
5. Sawant AC, Calkins H. Relationship between exercise and arrhythmogenic right ventricular dysplasia/cardiomyopathy. Trends Cardiovasc Med 2014;24:129-36.
6. Pelliccia A, Sharma S, Gati S, et al. 2020 ESC guidelines on sports cardiology and exercise in patients with cardiovascular disease. Eur Heart J 2021;42:17-96.
7. Drezner JA, Sharma S, Baggish AL, et al. International criteria for electrocardiographic interpretation in athletes: Consensus statement. Br J Sports Med 2017;51:704-31.