athletes, and 19 inactive patients, the risk of VT or SCD was significantly higher among competitive athletes compared with either recreational athletes (hazard ratio [HR] 2.0, 95% CI 1.2-3.3) or inactive patients (HR 2.1, 95% CI 1.1-3.9) [51]. In addition, there are increasing data that repetitive extreme conditioning/exertion enhances disease progression [51,52]. Any activity, competitive or not, that causes symptoms of palpitations, presyncope, or syncope should be avoided. Marfan syndrome Athletes with Marfan syndrome can selectively participate in low and moderate static/low dynamic competitive sports (classes IA and IIA) ( figure 1) if they do not have one or more of the following: aortic root dilatation, moderate-to-severe mitral regurgitation, or family history of dissection or sudden death in a Marfan relative [53]. These athletes should have an echocardiographic measurement of aortic root dimension repeated every 6 to 12 months (depending upon the size of the aorta, rate of growth, etc) for close surveillance of aortic enlargement. (See "Management of Marfan syndrome and related disorders", section on 'Monitoring MFS'.) Athletes with Marfan syndrome, familial aortic aneurysm or dissection, or congenital bicuspid aortic valve with any degree of ascending aortic enlargement should not participate in sports that involve the potential for bodily collision. On the other hand, some moderate-intensity and many low-intensity recreational activities are generally considered to be safe, including stationary biking, hiking, doubles tennis, swimming laps, golf, and skating. However, intense static (isometric) exertion is associated with increased wall stress; therefore, activities such as weight training with either free weights or weight machines should be avoided. Marfan syndrome is an autosomal dominant condition that is one of the most common inherited disorders of connective tissue. The full phenotype is characterized by arachnodactyly, tall stature, pectus excavatum, kyphoscoliosis, and lenticular dislocation. Malignant arrhythmias are not common in Marfan syndrome, but the cardiovascular manifestations include aortic https://www.uptodate.com/contents/athletes-overview-of-sudden-cardiac-death-risk-and-sport-participation/print 12/28 7/6/23, 11:26 AM Athletes: Overview of sudden cardiac death risk and sport participation - UpToDate dissection, which can lead to sudden death. The genetics, epidemiology, diagnosis, and management of Marfan syndrome are discussed in detail separately. (See "Genetics, clinical features, and diagnosis of Marfan syndrome and related disorders" and "Management of Marfan syndrome and related disorders".) Myocarditis Persons with probable or definite evidence of myocarditis should be withdrawn from all competitive and recreational sports and undergo a prudent convalescent period of between three and six months following the onset of clinical manifestations [29,31]. Athletes may return to training and competition after this period of time if LV systolic function has returned to normal (based on echocardiography and/or CMR), clinically relevant arrhythmias such as frequent and/or complex repetitive forms of ventricular or supraventricular ectopic activity are absent on ambulatory Holter monitoring and graded exercise testing, and serum markers of inflammation and heart failure have normalized. The impact that persistent LGE on CMR represents following the apparent clinical resolution of myocarditis is still uncertain [29]. As patients with previous myocarditis are at increased risk of recurrence and/or silent progressive myocardial dysfunction, periodic clinical reevaluation (at least annually) is recommended, including clinical assessment and imaging testing [31]. Patients should be advised to seek medical attention for dyspnea on exertion, syncope, or arrhythmic events. Myocarditis has been reported in 6 to 7 percent of cases of SCD in competitive athletes and 20 percent of military recruits [16,25,42]. (See 'Etiology of sudden death' above.) The clinical presentation of myocarditis is quite broad, from subclinical cases with only mild reduction of physical performance or palpitation to more severe presentations with clinical findings of heart failure in an otherwise healthy young person. The ECG usually shows diffuse repolarization abnormalities, and global or regional wall motion abnormalities are present on cardiac imaging. Active myocarditis is associated with atrial and ventricular tachyarrhythmias, bradyarrhythmias, and SCD. Healed myocarditis leading to a dilated cardiomyopathy or persistent segmental abnormalities increases the risk of SCD, and this risk may be proportional to the degree of cardiac dysfunction and severity of clinical presentation. (See "Clinical manifestations and diagnosis of myocarditis in adults".) Myocarditis and other causes of myocardial injury in individuals with coronavirus disease 2019 (COVID-19), the risk of SARS-CoV-2 vaccine-associated myocarditis, and return to play after COVID-19 are discussed separately. (See "COVID-19: Cardiac manifestations in adults" and "COVID-19: Evaluation and management of cardiac disease in adults" and "COVID-19: Arrhythmias and conduction system disease" and "COVID-19: Vaccines", section on 'Myocarditis' and "COVID-19: Return to sport or strenuous activity following infection".) https://www.uptodate.com/contents/athletes-overview-of-sudden-cardiac-death-risk-and-sport-participation/print 13/28 7/6/23, 11:26 AM Athletes: Overview of sudden cardiac death risk and sport participation - UpToDate Congenital heart diseases The estimated prevalence of congenital abnormalities in the athlete is 0.2 percent. Recommendations for athletic activity in patients with congenital heart disease, which are based primarily on expert opinion, depend upon the nature of the abnormality [40]. The approach for exercise prescription in adolescents and adults with congenital heart disease should be individualized [54]. However, there is generally a prohibition of competitive sports in those who have: Significant pulmonary hypertension Cyanosis with an arterial saturation <80 percent Symptomatic arrhythmias Symptomatic ventricular dysfunction INHERITED ARRHYTHMIA SYNDROMES There is a partial divergence of opinions on competitive athletics for individuals with inherited arrhythmias, and specifically for long QT syndrome (LQTS) [55-58]. The 2015 American Heart Association/American College of Cardiology (AHA/ACC) Scientific Statement on Eligibility and Disqualification Recommendations for Competitive Athletes discusses participation in competitive events and training sessions in patients with channelopathies (namely, LQTS) as allowable if the patient is asymptomatic and an emergency action plan with an automated external defibrillator (AED) is immediately available on site. However, a different approach is dictated by the European guidelines, which advise precautionary restriction from competitive sports in these instances. Congenital long QT syndrome Guidelines for physical activity and sports participation in congenital LQTS are presented separately. (See "Congenital long QT syndrome: Treatment", section on 'Physical activity and LQTS'.) Brugada syndrome Professional society guidelines allow sports participation in patients with Brugada syndrome who are defined as low risk based on absence of symptoms and events after the clinician and patient participate in a fully informed discussion and shared decision-making process and take all appropriate precautionary measures [55]. In contrast to other inherited arrhythmia syndromes, most moderate- and low-intensity recreational, noncompetitive sports are considered safe for patients with Brugada syndrome or Brugada pattern ECG, except for those that would incur significant risk of trauma with impaired consciousness should syncope or presyncope result (eg, weightlifting with free weights, horseback riding, motor races, downhill skiing, scuba diving, or snorkeling). Moreover, patients https://www.uptodate.com/contents/athletes-overview-of-sudden-cardiac-death-risk-and-sport-participation/print 14/28 7/6/23, 11:26 AM Athletes: Overview of sudden cardiac death risk and sport participation - UpToDate should avoid triggering drugs [59], electrolyte imbalance, and increases in core temperature >39 C (eg, by avoiding saunas, steam rooms, and sports in warm/humid conditions, including prolonged endurance events such as marathons in unfavorable atmospheric conditions). Patients with Brugada syndrome have historically been advised to avoid most high-intensity competitive sports, including cycling, rowing, basketball, ice hockey, sprinting, and singles tennis. However, there is no evidence that exercise in patients with Brugada syndrome increases the risk of cardiac arrest. Brugada syndrome is characterized by the ECG findings of right bundle branch block (RBBB) pattern and ST-segment elevation in leads V1 to V3 ( waveform 1), and an increased risk of sudden death. Arrhythmic events generally occur between the ages of 22 and 65 and are more common at night than in the day and during sleep than while awake [60,61]. SCD in Brugada patients is usually not related to exercise [62]. (See "Brugada syndrome: Clinical presentation, diagnosis, and evaluation".) Catecholaminergic polymorphic ventricular tachycardia We agree with professional society recommendations that patients with catecholaminergic polymorphic VT (CPVT) who were previously symptomatic, and asymptomatic patients with exercise-induced ventricular premature beats in a pattern of bigeminy, couplets, or nonsustained VT, should be restricted from competitive sports with the exception of minimal contact, class IA activities ( figure 1) [55]. Among individuals with a genetic diagnosis of CPVT, but who remain asymptomatic with none of the clinical features of inducible VT (so-called genotype positive, phenotype negative patients), the natural history is not well defined. As such, no agreement exists in the guidelines, and specifically, a prudent precautionary restriction from competitive sports is advised by European recommendations with more uncertainty in the AHA/ACC Guidelines. CPVT occurs in the absence of structural heart disease or known associated syndromes. The disorder typically begins in childhood or adolescence, and affected patients may have a family history of juvenile sudden death or stress-induced syncope [63]. The disorder has been linked to mutations in the cardiac ryanodine receptor and calsequestrin 2 genes. (See "Catecholaminergic polymorphic ventricular tachycardia".) Affected patients present with life-threatening VT or ventricular fibrillation (VF) occurring during emotional or physical stress, with syncope often being the first manifestation of the disease [63]. Arrhythmic events during swimming, previously considered to be specific for LQTS type 1, have also been described with CPVT [64]. The VT may have a polymorphic appearance or may be a bidirectional VT that resembles the arrhythmia associated with digitalis toxicity. https://www.uptodate.com/contents/athletes-overview-of-sudden-cardiac-death-risk-and-sport-participation/print 15/28 7/6/23, 11:26 AM Athletes: Overview of sudden cardiac death risk and sport participation - UpToDate Short QT syndrome Short QT syndrome is an extremely rare inherited channelopathy associated with marked shortened QT intervals and SCD in individuals with a structurally normal heart. Based on expert opinion, short QT syndrome is managed similarly to other inherited arrhythmia syndromes (ie, LQTS), although there is a paucity of data regarding the risks of exercise in this condition. (See 'Inherited arrhythmia syndromes' above.) When an abnormally short QTc interval is identified in an athlete (QTc <320 milliseconds), causes of transient QT shortening (such as hypercalcemia, hyperkalemia, hyperthermia, acidosis, and some drugs [eg, digitalis, anabolic steroids]) must be ruled out. In the absence of acquired causes of short QT interval, the athlete may be referred for familial ECG clinical screening and molecular genetic evaluation. However, the limited specificity of a short QTc must be acknowledged; the vast majority of patients with a short QTc will not have the syndrome. The clinical features and management of short QT syndrome are discussed in detail separately. (See "Short QT syndrome".) Early repolarization syndrome The early repolarization syndrome is the combination of early repolarization pattern and arrhythmic symptoms and/or SCD, not just early repolarization pattern. At present, no data are available regarding the impact of regular exercise programs and sports participation on the natural outcome of the early repolarization syndrome, and a prudent precautionary attitude is advised. The term early repolarization has long been used to characterize a QRS-T variant with J-point elevation on the ECG. Two terms, distinguished by the presence or absence of symptomatic arrhythmias, have been used to describe patients with this ECG finding: the early repolarization pattern describes the patient with appropriate ECG findings in the absence of symptomatic arrhythmias, while the early repolarization syndrome applies to the patient with both appropriate ECG findings and symptomatic ventricular arrhythmias, typically VF. Recommendations regarding participation in athletics apply only to patients with the early repolarization syndrome. (See "Early repolarization".) Early repolarization pattern, meaning the presence of ST-segment elevation in precordial leads, usually preceded by J-point elevation, is a common finding in athletes and is associated with other typical features of the athlete's ECG, such as bradycardia, increased R/S wave voltages, and incomplete RBBB. Typically, early repolarization in athletes disappears during exercise. This ECG pattern is not associated with symptoms or family history of SCD and does not require additional testing for diagnosis. There are no sports restrictions for these individuals. CORONARY ARTERY DISEASE https://www.uptodate.com/contents/athletes-overview-of-sudden-cardiac-death-risk-and-sport-participation/print 16/28 7/6/23, 11:26 AM Athletes: Overview of sudden cardiac death risk and sport participation - UpToDate Our approach to participation Patients with clinically proven coronary artery disease (CAD) who are considered to be at low-risk for cardiac events after individual evaluation may be allowed to participate in competitive sports. As a measure of caution, in consideration of the high hemodynamic load and possible electrolyte imbalance, some restrictions may apply on an individual basis for sports with the highest cardiovascular demand, such as extreme power and endurance disciplines. Patients with clinically proven CAD who are considered to be at high risk should be temporarily restricted from competitive sports and receive appropriate management. In situations where full medical therapy has been implemented and persistent ischemia remains, revascularization may be considered on a case-by-case basis. After revascularization, the individual patient should be encouraged to start exercise programs without delay, as per the cardiac rehabilitation guidelines. In the early phase, exercise should be prescribed in a graduated fashion, starting with low-intensity exercise of limited duration and progressively increased. When the clinical situation is stable and the patient is asymptomatic, a more intense training and participation in competition should be considered after a graduated and progressive increase in rehabilitation training load. We recommend a minimum of three months after percutaneous coronary intervention before participation in competitive sports can be resumed. Participation in competitive sports may be selectively advised as per patients with CAD and well-treated risk factors if exercise is not associated with elements of high risk, such as critical coronary artery stenosis (>70 percent), LV dysfunction, inducible ischemia by exercise, or frequent, repetitive ventricular arrhythmias induced by exercise. Contact sports should be avoided while the patient is under dual antiplatelet therapy because of the risk of bleeding, but may be considered afterwards. (See "Cardiac rehabilitation: Indications, efficacy, and safety in patients with coronary heart disease".) In patients 35 years of age, the most frequent cause of exercise-related SCD is CAD. Ventricular arrhythmias can originate from myocardial scar (from prior MIs), or from acute ischemia. In addition, ischemia during exertion can result either from fixed, chronic coronary stenosis that precludes increased myocardial oxygen delivery during exercise (ie, demand ischemia), or from an acute coronary syndrome. Autopsy examination of adults with exercise-related SCD usually reveals advanced CAD and/or an acute coronary lesion [26]. (See "Pathophysiology and etiology of sudden cardiac arrest" and "Mechanisms of acute coronary syndromes related to atherosclerosis".) Risk assessment Prior to initiating systematic training or competition, athletes with previously documented CAD should have an assessment of LV function. Universal exercise testing is somewhat controversial, although many clinicians state it should be performed, both https://www.uptodate.com/contents/athletes-overview-of-sudden-cardiac-death-risk-and-sport-participation/print 17/28 7/6/23, 11:26 AM Athletes: Overview of sudden cardiac death risk and sport participation - UpToDate to assess exercise capacity to determine the possible induction of signs of ischemia and to ensure the absence of exercise-induced arrhythmias. Whenever possible, such testing should be performed while the patient is taking prescribed medications and should approximate the cardiovascular and metabolic demands of the planned athletic activity. The approach to screening is discussed in detail separately. (See "Screening to prevent sudden cardiac death in competitive athletes".) There are no data that directly relate the presence and severity of CAD to the risk of participating in competitive athletics. However, it is likely that the risk of a cardiac event during exercise increases with the presence of increasingly severe CAD, type of lesion (soft plaques are at higher risk of rupture), LV dysfunction, and ventricular arrhythmias, as well as with the intensity of the competitive sport and the individual's effort. As a result, risk assessment should involve a full evaluation of cardiac status in individual patients. Athletes with CAD are considered to be at low risk if all of the following are true [65]: LV ejection fraction 50 percent. Normal exercise tolerance for age. (See "Exercise and fitness in the prevention of atherosclerotic cardiovascular disease", section on 'Relation to fitness'.) No inducible ischemia with exercise testing. (See "Prognostic features of stress testing in patients with known or suspected coronary disease".) No sustained or nonsustained VT during exercise testing. No hemodynamically significant coronary artery stenosis (ie, no stenosis 70 percent in a major coronary artery and no stenosis 50 percent in the left main coronary artery) if angiography is performed. Patients who have had successful revascularization of prior stenosis are also considered to be at low risk. SUMMARY AND RECOMMENDATIONS Sudden cardiac death (SCD) associated with athletic activity is a rare but devastating event. Victims can be young and apparently healthy, and while many of these deaths are unexplained, a substantial number harbor underlying undiagnosed cardiovascular disease. The majority of SCD events in athletes are due to malignant arrhythmias, usually ventricular tachycardia degenerating into ventricular fibrillation (VF) or primary VF itself. (See 'Introduction' above.) https://www.uptodate.com/contents/athletes-overview-of-sudden-cardiac-death-risk-and-sport-participation/print 18/28 7/6/23, 11:26 AM Athletes: Overview of sudden cardiac death risk and sport participation - UpToDate The balance between the risks and benefits of athletic activity depends upon several factors, including baseline fitness level, the nature and intensity of athletic activity, the presence and extent of cardiac disease, and the psychologic and physical benefit from sport. Although there are exceptions, for most individuals, the overall benefits of regular exercise far outweigh the risks. (See 'Competitive versus recreational athletics' above.) The incidence of SCD among young athletes is actually quite low, estimated to be between 1:50,000 and 1:100,000 young athletes per year. This rate is notably higher in older adults, closer to 1:7000 healthy adult athletes per year. (See 'Incidence of sudden cardiac death' above.) The potential etiologies of SCD include certain structural heart diseases, inherited arrhythmia syndromes, and coronary heart disease; the exact distribution of etiologies varies according to age and geography. (See 'Etiology of sudden death' above and "Pathophysiology and etiology of sudden cardiac arrest".) Some level of activity restriction ( figure 1) is recommended for nearly all individuals with underlying heart disease. The precise restrictions vary depending on the underlying disease process and other comorbidities. (See 'Structural abnormalities associated with SCD' above and 'Inherited arrhythmia syndromes' above and 'Coronary artery disease' above.) Use of UpToDate is subject to the Terms of Use. REFERENCES 1. Maron BJ, Chaitman BR, Ackerman MJ, et al. Recommendations for physical activity and recreational sports participation for young patients with genetic cardiovascular diseases. Circulation 2004; 109:2807. 2. Franklin BA, Thompson PD, Al-Zaiti SS, et al. Exercise-Related Acute Cardiovascular Events and Potential Deleterious Adaptations Following Long-Term Exercise Training: Placing the Risks Into Perspective-An Update: A Scientific Statement From the American Heart Association. Circulation 2020; 141:e705. 3. Harmon KG, Drezner JA, Wilson MG, Sharma S. Incidence of sudden cardiac death in athletes: a state-of-the-art review. Br J Sports Med 2014; 48:1185. 4. Landry CH, Allan KS, Connelly KA, et al. Sudden Cardiac Arrest during Participation in Competitive Sports. N Engl J Med 2017; 377:1943. 5. Emery MS, Kovacs RJ. Sudden Cardiac Death in Athletes. JACC Heart Fail 2018; 6:30. https://www.uptodate.com/contents/athletes-overview-of-sudden-cardiac-death-risk-and-sport-participation/print 19/28 7/6/23, 11:26 AM Athletes: Overview of sudden cardiac death risk and sport participation - UpToDate 6. Maron BJ, Shirani J, Poliac LC, et al. Sudden death in young competitive athletes. Clinical, demographic, and pathological profiles. JAMA 1996; 276:199. 7. Van Camp SP, Bloor CM, Mueller FO, et al. Nontraumatic sports death in high school and college athletes. Med Sci Sports Exerc 1995; 27:641. 8. Maron BJ, Poliac LC, Roberts WO. Risk for sudden cardiac death associated with marathon running. J Am Coll Cardiol 1996; 28:428. 9. Phillips M, Robinowitz M, Higgins JR, et al. Sudden cardiac death in Air Force recruits. A 20- year review. JAMA 1986; 256:2696. 10. Mitchell JH, Haskell W, Snell P, Van Camp SP. Task Force 8: classification of sports. J Am Coll Cardiol 2005; 45:1364. 11. Belonje A, Nangrahary M, de Swart H, Umans V. Major adverse cardiac events during endurance sports. Am J Cardiol 2007; 99:849. 12. Hillis WS, McIntyre PD, Maclean J, et al. ABC of sports medicine. Sudden death in sport. BMJ 1994; 309:657. 13. Thompson PD, Funk EJ, Carleton RA, Sturner WQ. Incidence of death during jogging in Rhode Island from 1975 through 1980. JAMA 1982; 247:2535. 14. Vuori I. The cardiovascular risks of physical activity. Acta Med Scand Suppl 1986; 711:205. 15. Gibbons LW, Cooper KH, Meyer BM, Ellison RC. The acute cardiac risk of strenuous exercise. JAMA 1980; 244:1799. 16. Corrado D, Basso C, Schiavon M, Thiene G. Screening for hypertrophic cardiomyopathy in young athletes. N Engl J Med 1998; 339:364. 17. Maron BJ, Thompson PD, Ackerman MJ, et al. Recommendations and considerations related to preparticipation screening for cardiovascular abnormalities in competitive athletes: 2007 update: a scientific statement from the American Heart Association Council on Nutrition, Physical Activity, and Metabolism: endorsed by the American College of Cardiology Foundation. Circulation 2007; 115:1643. 18. Roberts WO, Stovitz SD. Incidence of sudden cardiac death in Minnesota high school athletes 1993-2012 screened with a standardized pre-participation evaluation. J Am Coll Cardiol 2013; 62:1298. 19. Harmon KG, Asif IM, Klossner D, Drezner JA. Incidence of sudden cardiac death in National Collegiate Athletic Association athletes. Circulation 2011; 123:1594. 20. Eckart RE, Shry EA, Burke AP, et al. Sudden death in young adults: an autopsy-based series of a population undergoing active surveillance. J Am Coll Cardiol 2011; 58:1254. https://www.uptodate.com/contents/athletes-overview-of-sudden-cardiac-death-risk-and-sport-participation/print 20/28 7/6/23, 11:26 AM Athletes: Overview of sudden cardiac death risk and sport participation - UpToDate 21. Maron BJ, Zipes DP, Kovacs RJ. Eligibility and Disqualification Recommendations for Competitive Athletes With Cardiovascular Abnormalities: Preamble, Principles, and General Considerations: A Scientific Statement From the American Heart Association and American College of Cardiology. J Am Coll Cardiol 2015; 66:2343. 22. Finocchiaro G, Papadakis M, Robertus JL, et al. Etiology of Sudden Death in Sports: Insights From a United Kingdom Regional Registry. J Am Coll Cardiol 2016; 67:2108. 23. Baggish AL, Battle RW, Beckerman JG, et al. Sports Cardiology: Core Curriculum for Providing Cardiovascular Care to Competitive Athletes and Highly Active People. J Am Coll Cardiol 2017; 70:1902. 24. Peterson DF, Kucera K, Thomas LC, et al. Aetiology and incidence of sudden cardiac arrest and death in young competitive athletes in the USA: a 4-year prospective study. Br J Sports Med 2021; 55:1196. 25. Eckart RE, Scoville SL, Campbell CL, et al. Sudden death in young adults: a 25-year review of autopsies in military recruits. Ann Intern Med 2004; 141:829. 26. Karam N, Pechmajou L, Dumas F, et al. Comprehensive Assessment of Coronary Artery Disease in Sports-Related Sudden Cardiac Arrest. Circulation 2018; 138:429. 27. Hausmann R, Hammer S, Betz P. Performance enhancing drugs (doping agents) and sudden death a case report and review of the literature. Int J Legal Med 1998; 111:261. 28. Kennedy MC, Lawrence C. Anabolic steroid abuse and cardiac death. Med J Aust 1993; 158:346. 29. Maron BJ, Udelson JE, Bonow RO, et al. Eligibility and Disqualification Recommendations for Competitive Athletes With Cardiovascular Abnormalities: Task Force 3: Hypertrophic Cardiomyopathy, Arrhythmogenic Right Ventricular Cardiomyopathy and Other Cardiomyopathies, and Myocarditis: A Scientific Statement From the American Heart Association and American College of Cardiology. J Am Coll Cardiol 2015; 66:2362. 30. Priori SG, Blomstr m-Lundqvist C, Mazzanti A, et al. 2015 ESC Guidelines for the management of patients with ventricular arrhythmias and the prevention of sudden cardiac death: The Task Force for the Management of Patients with Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death of the European Society of Cardiology (ESC). Endorsed by: Association for European Paediatric and Congenital Cardiology (AEPC). Eur Heart J 2015; 36:2793. 31. Pelliccia A, Solberg EE, Papadakis M, et al. Recommendations for participation in competitive and leisure time sport in athletes with cardiomyopathies, myocarditis, and pericarditis: position statement of the Sport Cardiology Section of the European Association of Preventive Cardiology (EAPC). Eur Heart J 2019; 40:19. https://www.uptodate.com/contents/athletes-overview-of-sudden-cardiac-death-risk-and-sport-participation/print 21/28 7/6/23, 11:26 AM Athletes: Overview of sudden cardiac death risk and sport participation - UpToDate 32. Ommen SR, Mital S, Burke MA, et al. 2020 AHA/ACC Guideline for the Diagnosis and Treatment of Patients With Hypertrophic Cardiomyopathy: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. Circulation 2020; 142:e558. 33. Dias KA, Link MS, Levine BD. Exercise Training for Patients With Hypertrophic Cardiomyopathy: JACC Review Topic of the Week. J Am Coll Cardiol 2018; 72:1157. 34. Gersh BJ, Maron BJ, Bonow RO, et al. 2011 ACCF/AHA guideline for the diagnosis and treatment of hypertrophic cardiomyopathy: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. Circulation 2011; 124:e783. 35. Authors/Task Force members, Elliott PM, Anastasakis A, et al. 2014 ESC Guidelines on diagnosis and management of hypertrophic cardiomyopathy: the Task Force for the Diagnosis and Management of Hypertrophic Cardiomyopathy of the European Society of Cardiology (ESC). Eur Heart J 2014; 35:2733. 36. Elliott PM, Poloniecki J, Dickie S, et al. Sudden death in hypertrophic cardiomyopathy: identification of high risk patients. J Am Coll Cardiol 2000; 36:2212. 37. Pelliccia A, Lemme E, Maestrini V, et al. Does Sport Participation Worsen the Clinical Course of Hypertrophic Cardiomyopathy? Clinical Outcome of Hypertrophic Cardiomyopathy in Athletes. Circulation 2018; 137:531. 38. Caselli S, Pelliccia A. The electrocardiogram and the phenotypic expression of hypertrophic cardiomyopathy. Eur Heart J 2019; 40:982. 39. Heidb chel H, Corrado D, Biffi A, et al. Recommendations for participation in leisure-time physical activity and competitive sports of patients with arrhythmias and potentially arrhythmogenic conditions. Part II: ventricular arrhythmias, channelopathies and implantable defibrillators. Eur J Cardiovasc Prev Rehabil 2006; 13:676. 40. Van Hare GF, Ackerman MJ, Evangelista JA, et al. Eligibility and Disqualification Recommendations for Competitive Athletes With Cardiovascular Abnormalities: Task Force 4: Congenital Heart Disease: A Scientific Statement From the American Heart Association and American College of Cardiology. J Am Coll Cardiol 2015; 66:2372. 41. Thompson PD, Myerburg RJ, Levine BD, et al. Eligibility and Disqualification Recommendations for Competitive Athletes With Cardiovascular Abnormalities: Task Force 8: Coronary Artery Disease: A Scientific Statement from the American Heart Association and American College of Cardiology. J Am Coll Cardiol 2015; 66:2406. https://www.uptodate.com/contents/athletes-overview-of-sudden-cardiac-death-risk-and-sport-participation/print 22/28 7/6/23, 11:26 AM Athletes: Overview of sudden cardiac death risk and sport participation - UpToDate 42. Maron BJ, Carney KP, Lever HM, et al. Relationship of race to sudden cardiac death in competitive athletes with hypertrophic cardiomyopathy. J Am Coll Cardiol 2003; 41:974. 43. Taylor AJ, Rogan KM, Virmani R. Sudden cardiac death associated with isolated congenital coronary artery anomalies. J Am Coll Cardiol 1992; 20:640. 44. Liberthson RR. Sudden death from cardiac causes in children and young adults. N Engl J Med 1996; 334:1039. 45. Liberthson RR, Dinsmore RE, Fallon JT. Aberrant coronary artery origin from the aorta. Report of 18 patients, review of literature and delineation of natural history and management. Circulation 1979; 59:748. 46. Taylor AJ, Byers JP, Cheitlin MD, Virmani R. Anomalous right or left coronary artery from the contralateral coronary sinus: "high-risk" abnormalities in the initial coronary artery course and heterogeneous clinical outcomes. Am Heart J 1997; 133:428. 47. Basso C, Maron BJ, Corrado D, Thiene G. Clinical profile of congenital coronary artery anomalies with origin from the wrong aortic sinus leading to sudden death in young competitive athletes. J Am Coll Cardiol 2000; 35:1493. 48. Thiene G, Nava A, Corrado D, et al. Right ventricular cardiomyopathy and sudden death in young people. N Engl J Med 1988; 318:129. 49. Blomstr m-Lundqvist C, Sabel KG, Olsson SB. A long term follow up of 15 patients with arrhythmogenic right ventricular dysplasia. Br Heart J 1987; 58:477. 50. Douglas PS, O'Toole ML, Hiller WD, Reichek N. Different effects of prolonged exercise on the right and left ventricles. J Am Coll Cardiol 1990; 15:64. 51. Ruwald AC, Marcus F, Estes NA 3rd, et al. Association of competitive and recreational sport participation with cardiac events in patients with arrhythmogenic right ventricular cardiomyopathy: results from the North American multidisciplinary study of arrhythmogenic right ventricular cardiomyopathy. Eur Heart J 2015; 36:1735. 52. James CA, Bhonsale A, Tichnell C, et al. Exercise increases age-related penetrance and arrhythmic risk in arrhythmogenic right ventricular dysplasia/cardiomyopathy-associated desmosomal mutation carriers. J Am Coll Cardiol 2013; 62:1290. 53. Braverman AC, Harris KM, Kovacs RJ, Maron BJ. Eligibility and Disqualification Recommendations for Competitive Athletes With Cardiovascular Abnormalities: Task Force 7: Aortic Diseases, Including Marfan Syndrome: A Scientific Statement From the American Heart Association and American College of Cardiology. J Am Coll Cardiol 2015; 66:2398. 54. Budts W, B rjesson M, Chessa M, et al. Physical activity in adolescents and adults with congenital heart defects: individualized exercise prescription. Eur Heart J 2013; 34:3669. https://www.uptodate.com/contents/athletes-overview-of-sudden-cardiac-death-risk-and-sport-participation/print 23/28 7/6/23, 11:26 AM Athletes: Overview of sudden cardiac death risk and sport participation - UpToDate 55. Ackerman MJ, Zipes DP, Kovacs RJ, Maron BJ. Eligibility and Disqualification Recommendations for Competitive Athletes With Cardiovascular Abnormalities: Task Force 10: The Cardiac Channelopathies: A Scientific Statement From the American Heart Association and American College of Cardiology. J Am Coll Cardiol 2015; 66:2424. 56. Zipes DP, Link MS, Ackerman MJ, et al. Eligibility and Disqualification Recommendations for Competitive Athletes With Cardiovascular Abnormalities: Task Force 9: Arrhythmias and Conduction Defects: A Scientific Statement From the American Heart Association and American College of Cardiology. J Am Coll Cardiol 2015; 66:2412. 57. Pelliccia A, Fagard R, Bj rnstad HH, et al. Recommendations for competitive sports participation in athletes with cardiovascular disease: a consensus document from the Study Group of Sports Cardiology of the Working Group of Cardiac Rehabilitation and Exercise Physiology and the Working Group of Myocardial and Pericardial Diseases of the European Society of Cardiology. Eur Heart J 2005; 26:1422. 58. Turkowski KL, Bos JM, Ackerman NC, et al. Return-to-Play for Athletes With Genetic Heart Diseases. Circulation 2018; 137:1086. 59. www.brugadadrugs.org (Accessed on December 11, 2019). 60. Antzelevitch C, Brugada P, Borggrefe M, et al. Brugada syndrome: report of the second consensus conference: endorsed by the Heart Rhythm Society and the European Heart Rhythm Association. Circulation 2005; 111:659. 61. Matsuo K, Kurita T, Inagaki M, et al. The circadian pattern of the development of ventricular fibrillation in patients with Brugada syndrome. Eur Heart J 1999; 20:465. 62. Corrado D, Basso C, Buja G, et al. Right bundle branch block, right precordial st-segment elevation, and sudden death in young people. Circulation 2001; 103:710. 63. Priori SG, Napolitano C, Memmi M, et al. Clinical and molecular characterization of patients with catecholaminergic polymorphic ventricular tachycardia. Circulation 2002; 106:69. 64. Choi G, Kopplin LJ, Tester DJ, et al. Spectrum and frequency of cardiac channel defects in swimming-triggered arrhythmia syndromes. Circulation 2004; 110:2119. 65. Borjesson M, Dellborg M, Niebauer J, et al. Recommendations for participation in leisure time or competitive sports in athletes-patients with coronary artery disease: a position statement from the Sports Cardiology Section of the European Association of Preventive Cardiology (EAPC). Eur Heart J 2019; 40:13. Topic 986 Version 36.0 https://www.uptodate.com/contents/athletes-overview-of-sudden-cardiac-death-risk-and-sport-participation/print 24/28 7/6/23, 11:26 AM Athletes: Overview of sudden cardiac death risk and sport participation - UpToDate GRAPHICS Classification of sports based on peak static and dynamic components during competition This classification is based on peak static and dynamic components achieved during competition; however, higher values may be reached during training. The increasing dynamic component is defined in terms of the estimated percentage of maximal oxygen uptake (VO max) achieved and results in an increasing cardiac output. The 2 increasing static component is related to the estimated percentage of maximal voluntary contraction reached and results in an increasing blood pressure load. The lowest total cardiovascular demands (cardiac output and blood pressure) are shown in the palest color, with increasing dynamic load depicted by increasing blue intensity and increasing static load by increasing red intensity. Note the graded transition between categories, which should be individualized on the basis of player position and style of play. https://www.uptodate.com/contents/athletes-overview-of-sudden-cardiac-death-risk-and-sport-participation/print 25/28 7/6/23, 11:26 AM Athletes: Overview of sudden cardiac death risk and sport participation - UpToDate Danger of bodily collision (refer to UpToDate content regarding sports according to risk of impact and educational background). Increased risk if syncope occurs. Reproduced from: Levine BD, Baggish AL, Kovacs RJ. Eligibility and disquali cation recommendations for competitive athletes with cardiovascular abnormalities: Task force 1: Classi cation of sports: Dynamic, static, and impact: A scienti c statement from the American Heart Association and American College of Cardiology. J Am Coll Cardiol 2015; 66:2350. Illustration used with the permission of Elsevier Inc. All rights reserved. Graphic 105651 Version 9.0 https://www.uptodate.com/contents/athletes-overview-of-sudden-cardiac-death-risk-and-sport-participation/print 26/28 7/6/23, 11:26 AM Athletes: Overview of sudden cardiac death risk and sport participation - UpToDate 12-lead electrocardiogram (ECG) from a patient with the Brugada syndrome shows downsloping ST elevation ST segment elevation and T wave inversion in the right precordial leads V1 and V2 (arrows); the QRS is normal. The widened S wave in the left lateral leads (V5 and V6) that is characteristic of right bundle branch block is absent. Courtesy of Rory Childers, MD, University of Chicago. Graphic 64510 Version 10.0 https://www.uptodate.com/contents/athletes-overview-of-sudden-cardiac-death-risk-and-sport-participation/print 27/28 7/6/23, 11:26 AM Athletes: Overview of sudden cardiac death risk and sport participation - UpToDate Contributor Disclosures