sudden cardiac death

Sudden cardiac death: how can clubs pick out those at risk ?

The cardiovascular benefits of regular exercise are well established: as well as improving stamina, regular exercise promotes weight reduction, controls blood pressure, regulates blood fats and enhances insulin sensitivity, thereby reducing the risk of coronary artery disease and sudden cardiac death. Young people (under-35s) who participate in regular physical training generally make up the healthiest segment of our society. However, a significant minority are at risk of sudden death, usually during or shortly after a bout of physical training(1,2).

Sudden cardiac death in young athletes is, fortunately, rare, although precise data on its incidence is lacking. Data compiled from long-standing endurance running events in the USA and the UK suggest an incidence range of 1 in 50,000-67,000(3,4). However, these are probably conservative estimates since the data is derived from highly scrutinised sporting events. With no systematic notification of sudden cardiac death in athletes, deaths associated with lower-profile events or recreational activities are not taken into consideration when compiling statistics.

While the commonest cause of sudden cardiac death in the over-35s is coronary artery disease(5), more than 80% of sudden deaths in young athletic individuals are due to inherited (congenital) defects of the heart, resulting in structural and/or functional abnormalities(1). For affected individuals, the surges of adrenal hormones that accompany competitive vigorous physical activity predispose them to fatal cardiac arrhythmias (rhythm disturbances) and sudden death. Most of these deaths occur in adolescent male athletes; according to one study from the US, the mean age of sudden cardiac death is 17.1 years(1).

Some athletic individuals harbouring these potentially lethal cardiac abnormalities are capable of incredibly high levels of performance. Sudden death has been reported in many sporting disciplines including rowing, running and cycling. But most reported deaths in the UK have been in footballers. In 1992, Daniel Yorath, the son of Terry Yorath (former Leeds United player and manager of the Welsh national team) died while playing football with his father in the garden. Daniel himself was a football player of great potential, who had just been signed, aged 15, by Leeds United.

This tragedy was followed by the deaths of Ian Bell (16), who had just signed for Hartlepool, John Marshall, also 16, a junior international who died the day after he signed for Everton, and Jason Erics, 17, a member of the Tottenham Hotspur youth team. The more recent death of Manchester City star and Cameroon international, Marc-Vivien Foe, aged 24, during a live televised international match in June 2003, was the most disturbing of all. All of these young men harboured a cardiac condition that proved fatal; and in all except one, that condition was hypertrophic cardiomyopathy (HCM) – pathological enlargement of the heart muscle.

In fact, HCM is the commonest cause of sudden cardiac death in athletes, accounting for almost one third of all sudden death in highly trained sportsmen. It is a familial heart muscle disorder, caused by gene mutations affecting contractile proteins of the heart(6). The condition has a prevalence of 1 in 500(7) and is characterised by unexplained left ventricular hypertrophy (LVH) of variable magnitude, coupled with a relatively small left ventricular cavity.

Affected individuals usually have impaired relaxation of the heart muscle, with a propensity to myocardial ischaemia (poor blood flow to the heart) and fatal arrhythmias during intensive physical activity. The disorder is variable in degree, with some people having only minimal ventricular hypertrophy. It is also variable in presentation, with some patients displaying severe symptoms and others being entirely asymptomatic.

The commonest manifestations of the disorder are central chest pain during exertion (angina), breathlessness that is disproportionate to the amount of exercise being performed, palpitation, and syncope (fainting). However, with entirely asymptomatic individuals, sudden death may be the first presentation of the problem.

Most people with HCM cannot boost their stroke volume (the amount of blood put out with each beat of the heart) during exercise at high work rates because of their small left ventricular cavity and impaired left ventricular filling (with blood). For this reason, most do not reach high levels in competitive sport. However, some are capable of high levels of athletic performance, particularly in sporting disciplines like football that are characterised by a ‘start-stop’ pattern of activity. Marc-Vivien Foe, for example was regarded by the managers of West Ham and Manchester City as fitter than most of his fellow squad members, and he never complained of any cardiac symptoms before to his death.

Hypertrophic cardiomyopathy is diagnosed by means of echocardiography (cardiac ultrasound) – a simple, non-invasive test that can be carried out in 15-20 minutes by a skilled technician or cardiologist. Although there is no cure for the condition, the risk of sudden death may be reduced by giving up vigorous physical activity. In patients at high risk of sudden death, the implantation of an internal cardiovertor defibrillator (which restores normal cardiac rhythm) has been shown to prevent sudden death(8).

There is a case for saying that if HCM can be diagnosed with relative ease in athletes, they should be screened for the condition. In the cases of sudden death referred to above, a diagnosis of HCM would have led to disqualification from football(9), which might have proved costly in psychological as well as financial terms, but might also have saved lives.

In Italy, all young athletes are required to produce an annual certificate of fitness based on a normal physical examination, ECG and a limited exercise test. And the systematic evaluation of sudden cardiac death victims in northern Italy reveals that HCM is a very rare cause of death in young athletes(10). This evidence contrasts with published reports from other countries, where HCM is by far the commonest cause of sudden cardiac death. One interpretation of this discrepancy is that Italian athletes with HCM are being identified early and excluded from sporting activities.

The argument against screening for HCM is that the condition has a very low prevalence of just 1-in-500 in the general population and probably even lower among athletes, since most people with HCM would find themselves unable to compete in sporting disciplines requiring vigorous physical activity at regional or national level. In order to identify the very small proportion of athletes with HCM, it would be necessary to screen many thousands of healthy individuals. Admittedly, such activity would not be cost-effective, but there is also an argument for saying that most Premier League clubs are sufficiently well-endowed to carry this cost if it has the potential to save young lives.

The death of Daniel Yorath in 1992 led Leeds United to organise pre-participation cardiovascular evaluation – comprising physical examination, ECG and echocardiography – for all junior recruits before accepting them onto the team. Everton adopted the same policy after the death of John Marshall. The steady trickle of sudden deaths in football has led the Premier League to invest substantial sums into screening all junior recruits with ECG and echocardiography over the past five years, although their results, in terms of detecting cases of HCM, have yet to be published.

Football is the most popular sport in the UK and, of course, Premier League players are merely the tip of a very large iceberg. However, large-scale screening for the general population participating in football and other sports is not currently considered a viable option. Since cost is a major issue, raising public awareness of the risk of sudden cardiac death in athletes and the warning signs and symptoms may be a more practical way forward.

Athletes suffering from exertional chest pain, disproportionate breathlessness, dizziness or fainting should be evaluated in specialist cardiology centres to exclude the possibility of underlying cardiovascular disease. Given that HCM is a familial disorder, athletes with a family history of the condition, or of unexplained sudden death under 40 should also be evaluated

Regular physical training is usually associated with modest increases in left ventricular wall thickness and cavity size(11). In the vast majority of athletes, the maximal left ventricular wall thickness is well within values for the normal population (less than 12 mm). A very small proportion of athletes, including football players, may develop relatively greater LVH, which is similar to that seen in mild HCM(12,13). However, a left ventricular wall thickness of more than 14 mm is most unusual in football players with non-pathological LVH. Furthermore, unlike people with HCM, athletes with this kind of benign LVH also tend to have large left ventricular cavities(14).

To summarise, sudden cardiac death in young football players is rare, but is most commonly due to HCM. The condition can be identified and sudden death can be prevented by discontinuing vigorous exercise. The steady trickle of deaths in football has led to mandatory screening for all junior recruits at Premier League clubs. However, most clubs cannot afford screening (which is not available on the NHS), and so efforts should be made to raise awareness of the symptoms of HCM amongst athletes, coaches and doctors in the hope that symptomatic athletes can be screened and premature deaths on the football pitch prevented.

Sanjay Sharma

References

  1. JAMA 1996; (3) 276: 199-204
  2. J Am Coll Cardiol 1986; 7: 204-14
  3. Tunstall-Pedoe D, Morbidity and mortality in the London marathon. In Marathon Medicine, Ed. Tunstall Pedoe D, Royal Society of Medicine Press Ltd, 2000; pp 197-207
  4. J Am Coll Cardiol 1996; 28:428-431
  5. Am J Cardiol 1980; 45:1292-300
  6. NEJM 1997; 336:775-85
  7. Circulation 1995; 92:785-789
  8. NEJM 2000; 342: 365-73
  9. J Am Coll Cardiology 1986; 6:1189-90
  10. NEJM 1998; 339:364-369
  11. Circulation. 2000; 101:336-344
  12. NEJM 1991; 324:295-301
  13. J Am Coll Cardiol 2002; 40:1431-1436
  14. Circulation 1995; 91:1596-1601
  15.  

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