Back to Sports MedicineSudden cardiac death (SCD) is a catastrophic event that affects young athletes too, however it is a rare episode being much more prevalent in the elderly and in unconditioned people. One case of SCD during a intercollegiate basketball game began a large discussion about this issue. Hank Gather was a American basketball player at Loyola Marymount University in Los Angeles who collapsed and died on the basketball court during a game in March 1990.
Gather had experienced an episode of collapse 3 months before his death during a basketball game were he was immediately taken to hospital and given a complete cardiovascular screening . Complex ventricular tachyarrhythmias were diagnosed by ECG and a Beta blocker therapy was introduced. Three weeks later, Gather was allowed to play again since he was compliant with therapy . Unfortunately, he died soon after and a pathological diagnosis of Hypertrophic Cardiomyopathy was made the likely cause of his SCD. Was this event preventable ? Likely yes if the screening had been done more carefully and his previous symptoms had been taken seriously.
· Hypertrophic Cardiomyopathy (HCM) , is responsible for 50% of all SCD in young athletes. This is an Autossomal dominant condition with variable penetration. The mechanism causing SCD is not completely understood, but it is known that bradyarrhythymias and supraventricular arrhythmias (with or without accessories pathways ) are involved. The first symptom of this condition can be syncope or thoracic pain , but sometimes SCD is the first one. The clinical criteria for diagnosis is a hypertrophic left ventricle without systemic or obstructive alteration ( hypertension , aortic stenosis). Because it is a hereditary characteristic, the familiar history must be appreciated, looking for cases of HCM or SCD in the family. This condition can be manifested only in adolescence, with no earlier manifestations . The definitive diagnosis is made by echocardiografic exam, but there are some clues in physical examination and other complementary exams that are very important to think in HCM (systolic murmur increased by Valsalva and decrease by Handgrip maneuver, S4 , ECG modifications , Cardiomegalyc image in chest film).
· Congenital Anomalous Coronary circulation is responsible for almost 15 % of all SCD in young athletes according Maron et al search. The principal abnormality found in these athletes is the left coronary arising from right Valsalva sinus. This fact causes a isquemic heart making easier the initiation of electrical disturbances.
Dilated Cardiomyopathy (DCM) - Normally this is caused by a viral infections , in 50 % of cases Coxackie B is involved. In the most of cases, it is asymptomatic until signs and symptoms of Congestive Heart Failure appear. Before these symptoms , DCM can cause ventricular arrhythmias and SCD making the diagnosis difficult .
Marfan’s Syndrome - This congenital syndrome is responsible for cardiovascular problems like aortic dissection, Mitral valve prolapse, aortic insufficiency or arrhythmias.
Long QT Syndrome is a congenital disease where Torsades de pointes syndrome may occur and is thought to be caused by EAD (early afterdepolarization). As result , polymorphic ventricular tachycardia may be present and lead to SHD.
Mitral Valve Prolapse and Aortic Stenosis, are other conditions that also have relation with SCD but they are less prevalent in provoking arrhythmias.
Until now, there is not a specific routine of procedures to identify this group and ,what is more, there is not a definition about when a athlete should be disqualified or allowed to competite.
Based on two American studies with universitary athletes (Maron et al. and Lewis et al.) , a complete sequence of exams that involve clinial history , physical examination, ECG and ECHO only will be able to disqualify 1 athlete when 200000 athletes had been carefully examinated . The cost per athlete examinated was estimated at 400 dollars, what makes this kind of screening impractical.
The most common sreening practice recommended today is based on (1) a familiar history of HCM , SCD, Long QT Syndrome or syncopes episodes of indeterminated cause and (2) the characteristic signs an symptoms listed below :
1. Syncope. This may or not be associated with heart disfunction. Sometimes it is consequence of HCM, but it is often caused by an abrupt interruption of exercise that promotes a sudden fall in the cardiac output.
2. Chest pain. In the most of cases occurs because musculoskeletal lesions, although HCM , Isquemic deseases and cocaine use can cause pain as well.
3. Palpitations. It is very common in athletes after exercises, but special attention must be given when it occurs for enlarged period after a physical exercise.
4. Dyspnea. Must be valorizated only when signs of HCM are present.
Others points that should be valorizated in the clinical history are the drug abuse , the use of anabolic steroids, recent virus infections (DCM) and very tall athletes with arachnodactily or arm span greater than height.
This is a non pathological disease where anatomical and physiological changes can be detect in the heart of a very well conditioned athlete. It is very important to identify these benign alterations because false diagnosis of HCM can disqualified a health athlete for ever. The comparison between AHS and HCM are listed on the table below.
| Athletic Heart Syndrome | Hypertrophic Cardiomyopathy | |
|---|---|---|
| Increase in Heart weight | + | + |
| Decrease in LV cavity | +/0 | + |
| Hypertrophic LV | + | + |
| Asymmetric Septal Hypertrophy | 0 | + |
| Thickening of anterior MV leafleat | 0 | + |
| Myocite Desorganization | 0 | + |
| Anomalous CA | 0 | + |
In addition, a decreased heart rate , a splitting second sound, a third and fourth heart sound or ST modifications are very often found in AHS and mustn’t be confused with pathological conditions.
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