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An estimated 1/200,000 apparently healthy young athletes develops abrupt-onset ventricular tachycardia or fibrillation and dies suddenly during exercise. Males are affected 9 times more often; basketball and football players in the US and soccer players in Europe may be at highest risk.
Sudden cardiac death in young athletes has many causes (see Table 1: Sports and the Heart: Causes of Sudden Cardiac Death in Young Athletes* ), but the most common is undetected hypertrophic cardiomyopathy. Athletes with thin, compliant chest walls are at risk of commotio cordis (sudden ventricular tachycardia or fibrillation after a blow to the precordium) even when no cardiovascular disorder is present. The blow may involve a moderate-force projectile (eg, baseball, hockey puck, lacrosse ball) or impact with another player during a vulnerable phase of myocardial repolarization. Some young athletes die of aortic aneurysm rupture (in Marfan syndrome).
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Table 1
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Causes of Sudden Cardiac
Death in
Young Athletes*
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Obstructive hypertrophic cardiomyopathy
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Commotio cordis
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Coronary artery anomalies (eg, anomalous left main coronary artery origin, anomalous right coronary artery origin, coronary arterial hypoplasia)
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Increased cardiac mass
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Myocarditis
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Ruptured aortic aneurysm
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Arrhythmogenic right ventricular dysplasia
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Tunneled left anterior descending coronary artery
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Aortic stenosis
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Premature atherosclerotic coronary artery disease
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Dilated cardiomyopathy
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Myxomatous degeneration of mitral valve
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Long QT syndrome
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Brugada syndrome
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Wolff-Parkinson-White syndrome (anterograde conduction only)
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Catecholaminergic polymorphic tachycardia
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Right ventricular outflow tract tachycardia
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Coronary vasospasm
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Cardiac sarcoidosis
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Cardiac trauma
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Ruptured cerebral artery aneurysm
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*Causes are listed in approximate order of frequency.
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Sudden cardiac death in older athletes is generally caused by coronary artery disease. Occasionally, hypertrophic cardiomyopathy, mitral valve prolapse, or acquired valvular disease is involved.
In other conditions underlying sudden death in athletes (eg, asthma, heat stroke, illicit or performance-enhancing drug-related complications), ventricular tachycardia or fibrillation is a terminal, not a primary event.
Symptoms and signs are those of cardiovascular collapse; diagnosis is obvious. Immediate treatment with advanced cardiac life support is successful in < 20%; the percentage may increase as distribution of community-based, automated external defibrillators expands. For survivors, treatment is management of the underlying condition.
Screening
Before participation in sports, athletes are commonly screened to identify risk. Screening recommendations for all children, adolescents, and college-age young adults include a medical and family history and physical examination (including BP and supine and standing cardiac auscultation). Family history or symptoms or signs of hypertrophic cardiomyopathy or of Marfan syndrome require further evaluation; confirmation of either disorder may preclude sports participation. Athletes with presyncope or syncope should be evaluated for anomalous coronary arteries. Athletes should be counseled against use of illicit and performance-enhancing drugs. History and examination are neither sensitive nor specific; false-negative and false-positive findings are common because prevalence of cardiac disorders in an apparently healthy population is very low. Use of screening ECG or echocardiography would improve disease detection but would produce even more false-positive diagnoses and is impractical at a population level.
Last full review/revision November 2005
Content last modified November 2005
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