BackgroundProspective national registries examining the incidence and aetiology of sports-related sudden cardiac death (SrSCD) not only in competitive athletes but also in recreational sports participants are uncommon. In May 2012, a prospective registry on SrSCD was installed to examine the incidence and particularly the aetiology of such events in the general population in Germany.MethodsThe registry consists of a web-based platform to record SrSCD cases. Media-monitoring and cooperation with 15 institutes of forensic medicine complemented the search. SrSCD was defined as death occurring during sports activity or up to 1 hour after its cessation, regardless of successful resuscitation. We included subjects at all levels of competition as well as recreational athletes.ResultsAfter 30 months of observation, 144 SrSCDs were recorded (mean age 46.8 ± 16.2 years). The overall incidence was 1.2–1.5/million/year, with 97% being male. Most of the cases occurred in the context of non-elite competitive or recreational sports. Football and running were the most common disciplines. In subjects ≤35 years, myocarditis prevailed, whereas in athletes ≥35 years, CAD predominated by far. Few cardiomyopathies were observed.ConclusionsIn Germany, the largest proportion of SrSCDs occurs in middle-aged men during recreational sports or non-elite competitive sports. The distribution of cardiac diseases responsible for SrSCD seems to vary among European countries. Our findings may indicate the need for a larger focus on myocarditis prevention in the young as well as widening the screening scope to younger athletes below the ‘elite’ level and to senior athletes.

ObjectiveTo investigate the underlying causes and regional patterns of sudden death in football (soccer) players worldwide to inform and improve existing screening and prevention measures.MethodsFrom 2014 to 2018 cases of sudden cardiac death (SCD), survived sudden cardiac arrest (SCA) and traumatic sudden death were recorded by media monitoring (Meltwater), a confidential web-based data platform and data synchronisation with existing national Sudden Death Registries (n=16). Inclusion criteria were met when sudden death occurred during football-specific activity or up to 1 hour afterwards. Death during other activities was excluded.ResultsA total of 617 players (mean age 34±16 years, 96% men) with sudden death were reported from 67 countries; 142 players (23%) survived. A diagnosis by autopsy or definite medical reports was established in 211 cases (34%). The leading cause in players >35 years was coronary artery disease (76%) and in players ≤35 years was sudden unexplained death (SUD, 22%). In players ≤35 years the leading cause of SCD varied by region: cardiomyopathy in South America (42%), coronary artery anomaly in North America (33%) and SUD in Europe (26%). Traumatic sudden death including commotio cordis occurred infrequently (6%). Cardiopulmonary resuscitation (CPR) resulted in a survival rate of 85% with the use of an automated external defibrillator (AED) compared with 35% without.ConclusionsRegional variation in SCD aetiology should be verified by expansion of national registries and uniform autopsy protocols. Immediate access to an AED at training and competition sites, as well as CPR training for players, coaches and staff members, is needed to improve survival from SCA.

www.uniklinik-freiburg.de/zks/live/uklregister/Oeffentlich.html Identifier: UKF001272.

Background— It is under debate whether the cumulative effects of intensive endurance exercise induce chronic cardiac damage, mainly involving the right heart. The aim of this study was to examine the cardiac structure and function in long-term elite master endurance athletes with special focus on the right ventricle by contrast-enhanced cardiovascular magnetic resonance. Methods and Results— Thirty-three healthy white competitive elite male master endurance athletes (age range, 30–60 years) with a training history of 29±8 years, and 33 white control subjects pair-matched for age, height, and weight underwent cardiopulmonary exercise testing, echocardiography including tissue-Doppler imaging and speckle tracking, and cardiovascular magnetic resonance. Indexed left ventricular mass and right ventricular mass (left ventricular mass/body surface area, 96±13 and 62±10 g/m 2 ; P <0.001; right ventricular mass/body surface area, 36±7 and 24±5 g/m 2 ; P <0.001) and indexed left ventricular end-diastolic volume and right ventricular end-diastolic volume (left ventricular end-diastolic volume/body surface area, 104±13 and 69±18 mL/m 2 ; P <0.001; right ventricular end-diastolic volume/body surface area, 110±22 and 66±16 mL/m 2 ; P <0.001) were significantly increased in athletes in comparison with control subjects. Right ventricular ejection fraction did not differ between athletes and control subjects (52±8 and 54±6%; P =0.26). Pathological late enhancement was detected in 1 athlete. No correlations were found for left ventricular and right ventricular volumes and ejection fraction with N-terminal pro-brain natriuretic peptide, and high-sensitive troponin was negative in all subjects. Conclusions— Based on our results, chronic right ventricular damage in elite endurance master athletes with lifelong high training volumes seems to be unlikely. Thus, the hypothesis of an exercise-induced arrhythmogenic right ventricular cardiomyopathy has to be questioned.