Postmortem data on SCD in athletes reveal that 25% to 40% are autopsy- negative, suggesting a role for genetic molecular dis- orders in these victims S10.1-4,S10.1-10,S10.1-11 and for family Another limitation of SCD data analysis in ath- letes centers on noncardiac causes, some of which mimic cardiac events. Noncardiac causes include acute neurological disorders, drug abuse, heat stroke, rhabdomyolysis, sickle cell disorders, suicides, and Nonetheless, arrhythmias in ath- letes remain the most common medical cause of death and many occur as the first cardiac event. The most common structural cause of SCAs and SCDs in athletes in the United States is HCM, fol- lowed by anomalous origins of coronary arteries, with myocarditis contributing a smaller but significant Beyond these, the other inherited disorders contribute to the distribution of causes of a SCD in athletes, many of which can be suspected or identified by a careful family history and preparticipa- tion ECGs. In general, management of arrhythmias in athletes follows that in nonathletes. In regard to interventions, it is now generally recommended that AEDs be available at training and facilities for competitive athletes,S10.1-16 with less specific statements for AED availability at ven- ues (eg, tennis courts) or circumstances (eg, jogging or small group runs) in which recreational athletics are oc- curring. Many athletes who have had corrective procedures (repair of congenital or developmental defects such as anomalous origins of coronary arteries)S10.1-17,S10.1-18 are on therapy for inherited disordersS10.1-19 or have ICD im- and are able to participate in athletics de- pending on the nature and severity of the disease and with appropriate precautions and counseling regarding potential residual risks.S10.1-19,S10.1-20 For example, ath- letes with acquired disorders such as myocarditis are advised against exercise for at least 3 to 6 months after disease resolution. 