Sudden cardiac death in athletes: causes, mechanisms, prevention

Probably, you heard about the sudden cardiac death in athletes. Miklos Feher, a Hungarian soccer player, died while playing, was one of the most famous tragedies. The young soccer player died from a sudden cardiac death when he was 24 years old. Sudden cardiac death means unexpected death due to cardiac arrest within one hour of the onset of symptoms. The incidence of sudden cardiac death is higher in athletes compared to the general population.

The risk of male athletes is 9 times higher than in female athletes. In young athletes, sudden cardiac death is caused by inherited or acquired abnormalities. While in the older athletes coronary atherosclerosis is the main reason. Sudden cardiac death may be caused by congenital structural, electrical cardiac abnormalities and acquired abnormalities.

The electrical cardiac abnormalities include Wolff-Parkinson-White syndrome, long QT-syndrome, Brugada syndrome, catecholaminergic polymorphic ventricular tachycardia, early repolarization syndrome.

Structural cardiac abnormalities that may cause sudden cardiac death include hypertrophic cardiomyopathy, arrhythmogenic right ventricular cardiomyopathy, aortic dilation, mitral valve prolapse, aortic stenosis, coronary artery abnormalities and left ventricular hypertrophy. Also, infection, trauma, hypo- or hyperthermia, toxins, performance-enhancing drugs can lead to the sudden cardiac death. The main predictors are fainting, near-fainting, dizziness during exercise. Other risk factors include a family history of sudden cardiac death as well as palpitations, chest pain, excessive fatigue and dyspnea during exercise. But some athletes are fully asymptomatic.

The most common cause of sudden cardiac death in young athletes is hypertrophic cardiomyopathy. It’s primary myocardial disorder with an autosomal dominant type of inheritance. Usually sudden death occurs commonly in children and young adults. Often the patient is asymptomatic. Hypertrophic cardiomyopathy is characterized by significant left ventricular hypertrophy.

Often a dynamic left ventricular flow obstruction due to ventricular septum hypertrophy develops, it impedes normal stroke volume. Death occurs due to ventricular tachycardia or fibrillation upon exertions.

Cardiac arrest may be the first sign of this disease. This disease can be suspected by ECG. It reveals increased precordial voltage, mainly in V3-V4 leads, left ventricular strain, deep Q waves, T wave inversion in precordial leads.

Diagnosis is made when left ventricular thickness is 15 mm and more. Patient with previous cardiac arrest require an implanted cardioverter-defibrillator. Athletes with this diagnosis should be excluded from sports. Cardiac arrest may be caused by a blow to the heart area at a critical time during the cycle of a heartbeat.

Ventricular fibrillation occurs when the impact occurs in the ascending phase of the T-wave during myocardial relaxation.

Premature ventricular depolarization may trigger the ventricular fibrillation. Arrhythmogenic right ventricular dysplasia is characterized by a fibrofatty replacement of myocardium of the right ventricle which can cause ventricular tachycardia or fibrillation. ECG reveals epsilon wave, T wave inversion, prolonged S wave upstroke, rSr pattern. Previous cardiac arrest, syncope, or ventricular tachycardia are indications for implanted cardioverter-defibrillator. Brugada syndrome is a genetic disease which significantly increases the risk of ventricular fibrillation.

It’s sodium channelopathy, the disease of sodium cellular channels. ECG reveals incomplete right bundle branch block and coved ST-segment elevation. Sudden cardiac death results from polymorphic ventricular tachycardia of ventricular fibrillation.

Although cardiac death occurs usually at rest when the vagal tone is increased. Sport is not recommended because enhanced vagal tone in the athletes and hyperthermia may precipitate the cardiac arrest.

Sudden cardiac death in athletes: causes, mechanisms, prevention

Catecholaminergic polymorphic ventricular tachycardia is an inherited disease that may lead to cardiac arrest most often upon exertions or emotional stress when catecholamines are released. Usually, bidirectional ventricular tachycardia develops, it may terminate itself or transform in the ventricular fibrillation. Usually, patients have no symptoms, but some of them have a sudden loss of consciousness. In the case of catecholaminergic polymorphic ventricular tachycardia, ECG, echocardiography, MRI, CT reveal norm. During the exercise testing, ventricular ectopic beats may develop; it can progress to polymorphic ventricular tachycardia.

Sudden cardiac death can be prevented by beta-blockers, flecainide, verapamil and ICD implantation. Inherited long QT syndrome is the state when repolarization of the heart is affected.

There are many different genes responding to this disease. Some patients experience palpitation, chest pain, syncope, seizures. But some patients are completely asymptomatic, and the sudden cardiac death is unexpected.

Long QT syndrome is diagnosed when a corrected QT interval is 480 ms and more as well as 460 ms and more in a patient with unexplained syncope. Corrected QT interval is defined as QT interval divided by square root of RR interval. It can have an extracardiac manifestation: facial dysmorphism, paralysis, syndactyly, deafness, autism. Beta-blockers are the first-line drugs for sudden death prevention.

Wolff-Parkinson-White syndrome may be accompanied by the sudden cardiac death too.

Often it’s asymptomatic, but sometimes patients experience symptoms such as palpitation, abnormally fast heartbeat, breathlessness, syncope. Also, the cardiac arrest may occur. This syndrome is caused by functioning bundle of Kent, the accessory conduction pathway between the atria and ventricles. Impulses are conducted to ventricles without the participation of the atrioventricular node. ECG reveals shortening of the PR interval and delta-wave at ascending part of QRS complexes.

Radical treatment is radiofrequency catheter ablation when accessory conduction pathways are destroyed. Verapamil and beta-blockers should be avoided because they slow down conduction by a normal electrical pathway.

Often sudden cardiac death may be prevented. According to the risk of sudden death, the doctor should choose optimal treatment. In some cases, pharmacological treatment may be used.

But if the risk of sudden cardiac death is high, implanted cardioverter-defibrillator is the most reliable method of its prevention. In the case of ventricular tachycardia or ventricular fibrillation, it performs a shock conversing these arrhythmias into the normal rhythm also called sinus rhythm. Most of the listed above disease belong to contraindications for the sport. Although most of patient with the Wolff-Parkinson-White syndrome may continue physical exertions after successful ablation of the accessory conduction pathways. Antony Van Loo is a soccer player which survived sudden cardiac death on the field.

He had arrhythmogenic right ventricular dysplasia.

Cardioverter-defibrillator was implanted. He continued playing soccer. During the match, cardiac arrest occurred, but the cardioverter-defibrillator restored normal heart rhythm, and he survived ..

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