Pre-participation screening in young elite athletes: Towards a new algorithm?

Currently, history, clinical assessment, electrocardiogram (ECG) and conventional echocardiography are the cornerstones of the pre-participation athletic evaluation. The Association for European Pediatric Cardiology recommends that cardiovascular screening should be performed on athletes when they start their competitive activity.1 In 1996, the English Football Association introduced a mandatory cardiovascular screening program including ECG and echocardiography in all youth academy players from 15 to 17 years of age. In a recent study from Maholtra et al.,2 there were 46 cases of high-risk cardiovascular disease in 11,168 players of this highly trained cohort. During a mean follow-up period of 10.6 years, there were eight deaths due to cardiac disorders, all of which were sudden and occurred during exercise. Cardiomyopathies accounted for seven of eight (88%) sudden cardiac deaths. Six athletes (75%) with sudden cardiac death had normal cardiac screening results in ECG and conventional echocardiography.2 Nowadays, in European elite junior football, competitive sports start at a younger age. Players receive a scholar contract with a view to progressing to a professional senior career at an age of 12–13 years. Therefore, there is a high interest in sports cardiology for an effective screening algorithm to detect cardiovascular abnormalities as early as possible. Intense physical training is associated with changes in cardiac morphology, called the “athlete’s heart”. A small proportion of athletes do exhibit structural changes that overlap with subtle forms of cardiomyopathy. In pre-pubertal athletes, even intense and regular physical training does not largely affect the size or mass of the left ventricle, as measured by two-dimensional echocardiography or magnetic resonance imaging (MRI).3 The current advanced echocardiographic techniques and MRI have begun to clarify the mechanism involved in adaptive processes in pre-pubertal athletes. They may help to differentiate between the physiological adaptation to exercise and early stages of cardiomyopathies.4 Hypertrophic cardiomyopathy (HCM) is a primary myocardial disease caused predominantly by mutations within genes encoding sarcomeric contractile proteins. It is characterized by a hypertrophied left ventricle, which usually becomes evident during adolescence or early adulthood. The diagnosis of cardiomyopathy relies on cardiac imaging studies, although a large proportion of affected patients also demonstrate electrocardiographic abnormalities. Most athletes with HCM show an asymmetric pattern of left ventricular (LV) hypertrophy and reveal normal indices of diastolic transmitral filling. LV systolic function is usually within the range of normality in both athletes and HCM patients. Only subtle differences in myocardial mechanics may be detected by the LV strain assessment.5 Also, abnormalities of the relaxation pattern of tissue doppler imaging (TDI) may be present in the early stage of the disease.6 Usually, MRI is used as a secondary screening test for athletes who had a primary screening test with unclear results.7 The proposal that has been suggested is to carry out routine MRI screening of high-risk individuals, especially in athletes.8 Cardiovascular MRI has unrivalled value in excluding localized hypertrophy, in segments that cannot be visualized adequately with echocardiography, such as the LV apex or the antero-lateral segments.5 Recently, Małek et al.9 analyzed whether prolonged and regular physical training in children leads to changes in myocardial systolic deformation and rotational mechanics. For that purpose, cardiac MRI feature tracking was performed retrospectively in pre-adolescent male soccer players and matched controls. They did not find changes in global strain, but LV twist and apical rotation were greater in soccer players, which add to the features of pediatric athlete’s heart.9 STE measures motion against a fixed external point in space (i.e. the transducer) and has the advantage of being able to measure this motion in any direction within the image plane.10 STE assesses LV mechanics by quantifying deformation in the longitudinal, circumferential and radial planes, as well as rotation and twist. When using STE to measure LV twist, image quality of basal LV short-axis recordings can be a limitation. This is due, in part, to acoustic problems related to the depth of the basal part of the ventricle and to the wide sector angle that is necessary to visualize the entire LV base. Although slightly lower ejection fraction of the LV might be found in athletes, the adaptive cardiac remodeling shows normal or even supranormal values by TDI and normal values of longitudinal strain assessed by STE.4 Beaumont et al.11 have now compared LV structure, function and mechanics by advanced STE techniques in highly trained pre-adolescent soccer players and age-matched controls. The major findings from their study are that pre-pubertal soccer players showed greater circumferential strains, twist and faster diastolic lengthening in the absence of differences in wall thickness.11 LV rotation or twisting motion has an important role in LV systolic and diastolic function. Patients with HCM show variability in the extent of LV twist and untwisting, depending on the extent and distribution of hypertrophy and obstruction.12 But there are still some technical problems associated with STE. Dobrovie et al.13 evaluated the impact of abnormal myocardial shapes, such as regional hypertrophy, on longitudinal strain measurements with different tracking approaches. Bulged segments significantly influenced global longitudinal strain measurements, mostly in the endocardial layer. Global longitudinal strain values obtained with the straight region of interest correlated better with longitudinal fractional shortening of the LV.13 The study of the athlete’s heart is essential, not only to understand how cardiac adaptation contributes to improved athletic performance, but also to differentiate the athlete’s heart from important diseases that may share similar morphologic features. Advanced STE technologies are a promising tool for the early detection of subtle changes in myocardial mechanics in pre-pubertal athletes. To better understand these changes, we will need longitudinal data and also age-, race- and sex-specific normative values. If we continue embedding artificial intelligence technologies like machine learning and deep learning in sonographic cardiovascular imaging, we might overcome actual technical obstacles of STE. But even with the most comprehensive pre-participation screening program, there are still cardiac abnormalities that cause malignant arrhythmia, which cannot be prevented (e.g. commotio cordis or myocarditis).14 Therefore, it is advisable to also put efforts into the enhancement of possibilities for promptly starting cardiopulmonary resuscitation in the case of cardiac arrest in athletes. The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article. The author(s) received no financial support for the research, authorship, and/or publication of this article.