An estimated 1/200,000 apparently healthy young athletes develops abrupt-onset ventricular tachycardia or fibrillation and dies suddenly during exercise. Males are affected 10 times more often than females. Basketball and football players in the US and soccer players in Europe may be at highest risk.
In young athletes, sudden cardiac death has many causes (see Table 1: Causes of Sudden Cardiovascular Death in Young Athletes*), but the most common is
Commotio cordis (sudden ventricular tachycardia or fibrillation after a blow to the precordium) is a risk in athletes with thin, compliant chest walls 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.
Other causes include inherited arrhythmia syndromes (eg, long QT syndrome, Brugada syndrome). Some young athletes die of aortic aneurysm rupture (in Marfan syndrome).
In older athletes, sudden cardiac death is typically caused by
Occasionally, hypertrophic cardiomyopathy, mitral valve prolapse, or acquired valvular disease. is involved.
In other conditions underlying sudden death in athletes (eg, asthma, heatstroke, 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. In some cases, an implanted cardioverter-defibrillator may ultimately be required.
Cardiovascular Screening for Sports Participation
Athletes are commonly screened to identify risk before participation in sports, and they are reevaluated every 2 yr (if high school age) or every 4 yr (if college age or older).
Screening recommendations for all children, adolescents, and college-age young adults include
Screening for older adults also includes incremental symptom-limited exercise testing.
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.
Genetic testing for hypertrophic cardiomyopathy or long QT syndrome is not recommended or even feasible for the screening of athletes.
Athletes with a family history or symptoms or signs of hypertrophic cardiomyopathy (see Hypertrophic Cardiomyopathy), long QT syndrome (see Long QT Syndrome and Torsades de Pointes Ventricular Tachycardia), or Marfan syndrome (see Marfan Syndrome) require further evaluation, typically with ECG, echocardiography, or both. Confirmation of any of these disorders may preclude sports participation.
Athletes with presyncope or syncope should also be evaluated for anomalous coronary arteries (eg, by cardiac catheterization).
If ECG reveals Mobitz type II heart block, complete heart block, true right bundle branch block, or left bundle branch block, or there is clinical or electrocardiographic evidence of supraventricular or ventricular rhythm disorders, a search for cardiac disease is required.
If an enlarged aorta is detected on echocardiography (or incidentally), further assessment is needed.
Athletes should be counseled against use of illicit and performance-enhancing drugs. Patients with mild or moderate valvular heart disease may participate in vigorous activity; however, patients with severe valvular heart disease, particularly of the stenotic variety, should not participate in competitive sports.
Last full review/revision December 2014 by Robert S. McKelvie, MD, PhD, MSc
Content last modified December 2014