Exercise as it relates to Disease/Sudden cardiac death in athletes
First ever reported sudden cardiac death (SCD) in an athlete occurred as early as 490 BC, when a trained runner called Pheidippides collapsed and died after running from Marathon to Athens. Recent athletes who were victims of SCD includes basketball players Hank Gathers (in 1990), Pete Maravich (in 1988) and Reggie Lewis (in 1993), marathon runner Jim Fixx (in 1984), US Olympic volleyball player Flo Hyman (in 1986), and Olympic figure skater Sergei Grinkov (in 1995). There is no universally accepted definition for SCD. It is broadly defined as non traumatic and unexpected cardiac arrest that occurs within 6 hours of a previously normal state of health. It is important to identify the athletes those who are at risk, however, unfortunately sudden death could be the first symptom in an athlete with a recognisable and potentially preventable etiology.
Mechanisms behind SCD is not fully understood. However, it is believed SCD in athletes is resulted by combination of factors such as increased myocardial oxygen demand, aortic rupture, shortened diastole and coronary perfusion time, alteration in sympathetic and parasympathetic tone, release of thromboxane A2 (a potent vasoconstrictor), enhanced blood coagulability, lactic acidosis, intracellular and extracellular electrolyte derangement, and increased blood temperature during intense exercise.
SCD is a rare condition, though true incidence is not verified. Epidemiological studies show that athletic population is at 2.8 times greater risk of SCD compared to non-athletic counterpart. Estimated incidence amongst athletes worldwide varies between 2 per 100000 and 1 per 300000. There are 50 to 100 cases reported annually in USA. Despite the low incidence SCD represents 30% of all non-traumatic deaths amongst athletes. Significantly higher proportion of men have suffered from SCD compared to women and the risk increases with age. About 68% of the cases were reported in basketball and soccer.
SDC is predominantly caused by structural non-atherosclerotic heart diseases. It is understood that combination of high intensity exercise and underlying heart disease triggers SCD rather than by exercise alone. Common causes can be categorised into structural,electrical and acquired cardiac abnormalities.
|Structural cardiac abnormalities||Electrical cardiac abnormalities||Acquired cardiac abnormalities|
- Pre-participation screeninɡ
- Family and personal history
- Physical examination
- Twelve-lead electrocardiogram (ECG)
- Pre-participation screening should be carried out in all competitive athletes.
- External defibrillators and advanced cardiac life support units should be present at competitive events and training venues.
- Young athletes who present with chest pain, dizziness and syncope during or after exercise should seek medical attention.
- Young athletes diagnosed with hypertrophic cardiomyopathy should only participate in low intensity sports whether patients are symptomatic or asymptomatic.
- Patients diagnosed with coronary abnormalities should not participate in any competitive sports. Patients treated with surgical intervention can participate in sports after 6 months after the operation if ischemia is not present during maximal exercise testing.
- Patients with Arrhythmogenic right ventricular cardiomyopathy should not participate in any competitive sports.
- Athletes thought to have myocarditis should be withdrawn from sports for 6 months. Before returning to sport, thorough investigation is warranted.
- Participation restriction in sports for patients diagnosed with congenital heart disease is dependent on the severity of the condition and medical clearance is required.
- Participating in recreational (low to moderate intensity) activity is encouraged to maintain physical and mental health, even when participating in competitive sports is restricted.
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