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HannuParikka

Athlete's Heart

Essentials

  • Intensive, prolonged training may slightly increase the size of the ventricles and thicken their walls.
  • An ECG may show sinus bradycardia, increased QRS voltage, early repolarisation and T wave changes.
  • Changes due to athlete's heart are always asymptomatic and will reverse during a training-free period.
  • Symptoms suggesting heart disease are an indication for further investigations.

Definition

  • Athlete's heart refers to the adaptations in the structure of the heart and its electrical activity that result from intensive and prolonged training.
    • The changes are the result of increased pressure and volume loads as well as vagal tone.
    • The changes are adaptive and therefore will reverse with time after intensive physical training stops.
    • The manifestation of the changes depends on the sport as well as on individual factors, such as the person's age, size, sex, ethnic background and the duration of the athlete career.

Structural changes

  • Increased ventricular chamber size, more pronounced in endurance athletes than in strength training athletes
  • Increased ventricular wall thickness, slightly more pronounced in strength training athletes than in endurance athletes
  • Increase in left ventricular muscle mass
  • Significant echocardiographic abnormalities are rarely present in male athletes, hardly ever in female athletes.
  • Both structural and electrical changes are more pronounced in athletes of black ethnicity.

Abnormalities in the ECG and rhythm

  • Sinus bradycardia, down to 30 bpm, especially in endurance athletes
  • Intermittent junctional escape rhythm
  • Prolonged PR interval and intermittent Wenckebach type atrioventricular block
  • Bradycardia invariably occurs only at rest and during the night, and reverses on exertion.
  • ECG meets the voltage criteria for ventricular hypertrophy, particularly for the left ventricle. This may be associated with a narrow but not deep Q wave, no strain pattern.
  • Early repolarisation with some ST elevation combined with J point elevation especially in the leads V1-V3, in black people also in V4, and a high T wave with slight terminal negativity in leads V1-V3 (picture ).
  • Repolarisation changes disappear on exertion.
  • Incomplete RBBB is very common.
  • Ventricular extrasystoles are encountered in some endurance athletes, despite the heart being structurally sound.
  • In endurance athletes, atrial fibrillation becomes more common from middle age onwards.

Differential diagnosis

  • The changes may raise a suspicion of heart disease even in the absence of symptoms.
  • The most significant problem in differential diagnostics is hypertrophic cardiomyopathy Hypertrophic Cardiomyopathy, and its exclusion warrants echocardiography, MRI of the heart and, in some cases, invasive investigations in specialist health care.
  • Other cardiomyopathies (picture ), myocarditis, ischaemic heart disease and ASD should also be borne in mind.
  • Diagnosis can be aided by comparing the ECG changes with an ECG recording taken during an asymptomatic phase or before the intensive training started.
  • Morphological changes will normalise if training is totally stopped for 2-3 months.
  • Frequent ventricular extrasystoles (for example > 100 ventricular extrasystoles in 24 hours or short salvos of ventricular extrasystoles) should always be investigated in specialist health care; they may signify incipient heart disease.
  • Sport-induced adaptive changes are always asymptomatic. If an athlete develops symptoms suggestive of heart disease careful investigations are indicated, often in specialist health care (echocardiography Echocardiography as an Outpatient Procedure, exercise ECG Exercise Stress Test, continuous ambulatory ECG monitoring Ambulatory ECG Monitoring, MRI of the heart, invasive investigations as indicated).

Significance

  • Morphological changes of the heart or rhythm disturbances in a person who, after engaging in athletic activities in his/her youth, has not been training for several years must always be interpreted as signs of heart disease or idiopathic arrhythmia, and further investigations are indicated.
  • Sport does not cause heart disease or sport-specific arrhythmias.
  • The very rare cases of sudden death that have occurred during sporting activities (1-2 cases /100 000 athletes) have always been the consequence of an undiagnosed myocardial disease (most commonly hypertrophic cardiomyopathy), complications of a known mild heart defect or an acute cardiac event (ischaemia especially in persons over 35 years of age, myocarditis).
  • The consensus panel of the European Society of Cardiology and the Medical Commission of the International Olympic Committee recommend that screening for heart disease of competitive active athletes for the prevention of sudden death should start at the age of 12-14 and continue until the age of 35 1.
    • Complete personal and family history (particularly sudden death in family members), physical examination and an ECG
    • The health status should be monitored regularly every 2 years or as guided by findings.
    • The evaluation should be carried out by a physician with specific training.
  • Mild, asymptomatic heart disease with a benign prognosis does not necessarily prevent the continuation of elite sporting activities, but several heart diseases (structural or electrical; including significant valve disease, cardiomyopathies, ischaemic heart disease, myocarditis, Marfan syndrome, long QT syndrome) necessitate the recommendation to abstain from competitive sports. Such decisions call for expertise in cardiology.

References

  • Corrado D, Pelliccia A, Bjørnstad HH et al. Cardiovascular pre-participation screening of young competitive athletes for prevention of sudden death: proposal for a common European protocol. Consensus Statement of the Study Group of Sport 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(5):516-24. [PubMed]