Contemporary sports reporting has secretly been enriched with a facet that has inevitably and unpleasantly become noticeable for long-time observers of the section. This is about the abnormal accumulation of sudden and unexpected deaths in connection with cardiac events, which should actually be completely atypical in an age cohort of young and excellently trained organisms. Unfortunately, it is also significant that the writers in the mainstream press report these cases but completely ignore the research into the causes. Anyone who has closely followed the defamation and sanctioning of dissidents in recent years [1] will probably be aware that their colleagues prefer to ignore the sensitive topic through collective self-censorship before they get into serious problems with the editorial board or other higher authorities. This is, with all due respect, particularly cowardly and precarious because it involves active education to prevent further potential victims, which could be prevented if the causes were known.
The concise headlines in the relevant media prove that there are obviously significant perception indicators that verify the previously noted phenomenon of the disproportionate number of cases of athletes who were injured or died at an early stage [2]. A very young gymnast [3], a professional soccer player as well as the reigning Swiss marathon champion in his prime [4], a world-class pole vaulter [5] or a health influencer [6] are “caught” because, as shown, there is no information about the causal consequences of death be shown. These are not isolated cases, as various meta-analyses clearly show [7]. The progressive symptoms are therefore obvious, but what is the underlying cause?
Of course, this requires a retrospective excursus on cardiac pathophysiological symptoms in the context of high-performance sports activities. First of all, it should be noted that long-term repetitive maximum cardiovascular stress alone can cause subclinical cardiac damage, with resulting focal myocardial necrosis or fibrosis [8]. The measurement of cardiac troponins (cTnI) in sports practice is a particularly suitable, easy-to-measure blood parameter for the stress-induced pathomorphological changes in myocardial texture. This basal risk factor of potential overload can be addressed using responsible training methods adapted to the athletes’ individual resilience and dosed competitions should be eliminated as far as possible. Unfortunately, in the profit-oriented professional sports business, this is just wishful thinking and is intended more as an appeal to those responsible. As an indication of how seriously the caring environment should take this advice, the rare but highly dramatic cases can be cited as examples, which clearly document the time delay factor in triggering a fatal cardiac crisis [9]. The dramatic Nicolas Portal case in particular demonstrates the treacherous dynamics mentioned above. After a year of rest, the athlete initially completed a long professional career [10], but then died 12 years after the initial diagnosis, long after he had ended his active career [11]. Saarland University has written an excellent review article [12] to estimate the incidence of sudden cardiac death in competitive sports and has introduced a corresponding register [13].
Another dominant aspect for acute cardiac events during stress is the genetic predisposition to congenital cardiac or coronary anomalies. The most common correlation is with hypertrophic and dilated cardiomyopathy. Particular susceptibility also exists in the case of conduction disorders, such as pre-excitation in Wolff-Parkinson-White syndrome, Brugada syndrome, arrhythmogenic right ventricular dysplasia (ARVD) or catecholaminergic polymorphic ventricular tachycardia (CPVT). These can often be treated with minimally invasive intervention such as ablation or the implantation of a defibrillator. The Turgis brothers are a prominent example of how such cardiac degenerations can also be inherited in families [14]. Possible causal gene polymorphisms in this regard could be identified using, among other things, the molecular genetic predictor HPA-2 Met [15]. Further morphological abnormalities, such as mitral valve prolapse, atypical coronary branches or atrial or ventricular septal defects, such as those that occurred in the world-class professional cyclists Roger Kluge (with a persistent foramen ovale) and Loïc Vlieder [16], expand the unpleasant cardiac risk spectrum. As part of the routine medical check-ups by racing teams and clubs, as well as by major organizers (e.g. the mandatory initial examinations for major cycling tours) in accordance with the UCI guidelines [17], ECG, echocardiography and cardiac magnetic resonance imaging [18] are suitable for preventive exclusion diagnostics.
