Abstract Background Sudden cardiac death (SCD) is a rare but tragic event which can involve young and apparently healthy individuals. Several heart conditions, such as hypertrophic cardiomyopathy (HCM), the most frequent cause of SCD in young adults, may not be diagnosed as early as needed. Therefore, proper screening methods and protocols are required for athletes and individuals who engage in chronic intense physical activity. Purpose Current guidelines recommend a screening for athletes and healthy individuals who engage in high-intensity physical activities based on patient history and symptoms, clinical examination and resting 12-lead electrocardiography (ECG). While trans-thoracic echocardiography (TTE) is an useful tool in showing and differentiating pathological patterns from physiological adaptive changes, there is not enough evidence to include it as a standard screening method. Therefore we conducted a study in which we evaluated the use of a complex screening protocol involving the afore-mentioned screening tools, together with TTE, with the aim of better highlighting potential life-threatening cardiac anomalies which may cause adverse events during physical activity. Materials and Methods In the years 2021–2023, we evaluated 25 male professional football players, all between the ages of 18 and 21. They underwent physical examination, resting 12-lead ECG, (TTE) examination, using the M-mode, Continuous wave Doppler (CWD) and the pulse wave Doppler (PWD), as well as serum biomarkers determinations (D-Dimers, Myoglobin, CK-MB, Troponin I and NT-proBNP), before and after cardiopulmonary exercise testing (CPET). Results All of the athletes' echocardiographies showed the "athlete's heart" pattern, with a slightly enlarged left ventricular cavity and mild concentric left ventricular hypertrophy (LVH). Additionally, the myocardium's contractility was within normal bounds and the ejection fraction was on upper limit of the normal values. Two of the examinations showed a mild tricuspid regurgitation, while other four displayed a mitral valve prolapse, regarded to be minor physiological variations in a well-trained individual. No aspects suggestive of dilated cardiomyopathy, hypertrophic cardiomyopathy or isolated left ventricular non-compaction were observed. Most correlations were between the myoglobin levels and the TTE parameters, showing how the overall changes comprising of left ventricular hypertrophy, enlarged cavities and increased cardiac performance may be translated also through the increased serum myoglobin levels in athletes, both at rest and after CPET. Conclusion TTE remains the most precise way to differentiate between physiological LVH and HCM among other pathological patterns. The "athlete's heart" pattern and the morpho-functional changes it encompasses in young individuals were correlated to increased levels of serum biomarkers such as myoglobin, both at rest and after CPET.
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