Dilated cardiomyopathy (DCM) represents a diagnostic challenge in athletes due to the
significant overlap between physiologic cardiac remodeling and pathologic structural changes.
The differentiation between athlete’s heart and early or subclinical cardiomyopathy carries
critical implications, particularly given the risks of sudden cardiac death, arrhythmia, and long-
term ventricular dysfunction such as reduced ejection fraction in competitive sports. To clarify
this diagnostic intersection, we conducted a structured literature review using PubMed; of 53
identified articles, 22 met inclusion criteria.
Emerging evidence highlights imaging modalities—particularly echocardiography, electrocardiography, and cardiovascular magnetic resonance—as the most reliable tools for distinguishing physiologic remodeling from DCM. Key discriminators include left ventricular cavity size, systolic function at rest and with exercise, tissue characterization via CMR mapping, and electrocardiographic markers suggestive of underlying genetic or structural disease. Recent studies further emphasize the contribution of genetic variants, such as titin and lamin A/C mutations, which may predispose athletes to impaired systolic function despite high training loads. Sex-based differences and the role of clinical context also remain important considerations in risk stratification.
Overall, current literature underscores the complexity of differentiating benign adaptation from pathologic cardiomyopathy in athletes, necessitating a multimodal diagnostic approach that integrates imaging, genetics, and clinical evaluation. Improved recognition of these “gray zones” is vital to optimize risk assessment, guide safe return-to-play decisions, and prevent adverse outcomes in athletes.
Emerging evidence highlights imaging modalities—particularly echocardiography, electrocardiography, and cardiovascular magnetic resonance—as the most reliable tools for distinguishing physiologic remodeling from DCM. Key discriminators include left ventricular cavity size, systolic function at rest and with exercise, tissue characterization via CMR mapping, and electrocardiographic markers suggestive of underlying genetic or structural disease. Recent studies further emphasize the contribution of genetic variants, such as titin and lamin A/C mutations, which may predispose athletes to impaired systolic function despite high training loads. Sex-based differences and the role of clinical context also remain important considerations in risk stratification.
Overall, current literature underscores the complexity of differentiating benign adaptation from pathologic cardiomyopathy in athletes, necessitating a multimodal diagnostic approach that integrates imaging, genetics, and clinical evaluation. Improved recognition of these “gray zones” is vital to optimize risk assessment, guide safe return-to-play decisions, and prevent adverse outcomes in athletes.