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Sudden death (SD) in athletes represents a cardiac ‘earthquake’ affecting apparently healthy and highly trained individuals. This is not due to excessive demands on a normal heart, as occurred to Phidippides in Marathon, because our body has built-in safeguard mechanisms—dyspnea, angina, fatigue—to protect us from physical exhaustion. Autopsy investigations reveal that SD in athletes occurs three times more often than in non-athletes, and is caused by concealed cardiovascular abnormalities, mostly structural, that are unmasked by activity-triggered electrical instability.1–5 The structural culprits may be any of the cardiovascular components, including aorta, coronary arteries, myocardium, valves, conduction system and ion channels.1 The ECG is often abnormal, and its implementation in Italy for obligatory preparticipation screening has resulted in progressive reductions by 90% of SD in athletes aged 12–35 years between 1979 and 20024 (figure 1). This was mostly attributable to identification and disqualification of people affected by cardiomyopathies.
Arrhythmogenic right ventricular cardiomyopathy—unknown until the 1980s—is the major cause of SD in Italian athletes (relative risk 5.4 compared with non-athletes), and can now be identified at preparticipation screening by application of specific diagnostic criteria. Hypertrophic cardiomyopathy, on the other hand, was a rare cause of athlete SD in Italy compared with the US.4 ,6 In fact, abnormalities of the screening 12-lead ECG prompted echocardiography, which was diagnostic in …