Sudden Cardiac Death in Sports: Pre-participation Screening of Athletes


Sudden death in sport (SD) is defined as natural death that occurs within one hour of onset of symptoms in a fit individual participating in, usually, an elite level sport. Sudden cardiac death contributes to 93% of all sudden deaths in sport. This apparently occurs in a person without previously recognized predisposing cardiovascular conditions. In some instances, pre-existing symptoms may already have been present, but the time and mode of death are unexpected. This excludes cerebrovascular, respiratory, traumatic and drug related causes which are the origin of the other 7% of sudden deaths”. A significant cause of death in contact sports is commotio cordis, which is referred to in one of my other articles.


The incidence of SD is estimated to be about one death in 1 in 200000 per year with an average of 300 deaths per year, but the incidence could be higher according to some European studies. An Italian study suggested an incidence of 1.6 – 2.3 per 100000 athletes per year (2.1 per 100000 per year due to cardiovascular causes) and 0.8. This clearly reflects an increased incidence in athletes.


most of cases are asymptomatic

in the rest, symptoms occurring prior to with SD are

i. angina (chest pain)

ii. dyspnoea (breathlessness)

iii. palpitations (awareness of one’s heart beating)

iv. pre syncope or syncope (light headedness or fainting)


Cardiovascular causes of sudden death

– Hypertrophic Cardiomyopathy (HCM)non obstructive, obstructive, ischemic, etc – Valvular disease: Aortic stenosis, Mitral Valve Prolapse

– Coronary artery disease

– Congenital anomalies of coronary arteries

– Idiopathic concentric left ventricular hypertrophy

– Aortic rupture

– Right ventricular dysplasia (ARVC)

– Myocarditis: viral, sarcoidosis, amyloidosis

– Arrhythmias and conduction defects Congenital heart disease: Marfan’s, WPW syndrome

– Pulmonary embolisation


– QT interval increasing: cisapride, domperidone,chlorpromazine, haloperidol, pimozide, erythromycin and clarithomycin

– epinephrine, ephedrine, cocaine, etc

– performance enhancing: erythropoietin (hyperviscocity & thrombogenesis) anabolics

Commotio cordis (CC)

sudden impact on the precordium, during a vulnerable period of the cardiac cycle cause ventricular fibrillation and sudden death without any visible injury to the sternum or ribs, e.g. contact sport. In 80% of cases of sudden cardiovascular death in athletes, the cause has been identified to be either hypertrophic cardiomyopathy or arrthymogenic right ventricular cardiomyopathy.

Age considerations

In general, in athletes > 35 years of age, atherosclerotic coronary arterial disease is the leading cause while in those < 35, it is often caused by HCM, a silent cardiac condition which gets unmasked during performance.

Geographic considerations in etiology

In the US, hypertrophic cardiomyopathy is the major cause of SD. In contrast, in Europe, cardiac arrhythmias and abnormal cardiac arterial anatomy is supposed to be the leading cause. An interesting statistic is that of all the sudden deaths in the US, 50% were found to be amongst athletes of Afro-American origin. In Asia, on the contrary, (the Philippines, Thailand, Japan), Brugada syndrome seems to be the most common cause of natural death in men younger than 50 years of age. This relates to cardiac arrest occurring during sleep or at rest and not during a sport performance . An importance observation is these cases had been the reports episodes of nightmares occurring prior to the event. This might suggest a role of the sympathetic nervous system.

Risk Stratification of Sudden Cardiovascular Death


a. Double apical impulse with each ventricular contraction

b. Carotid jerky double pulsation, called pulses bisferiens

c. Ejection systolic murmur

Laboratory Investigations


a. ECG: suggestive of LVH, in addition, there is ST segment depression, gross T wave inversions, pathologic Q waves, and suggestion of LBBB, left axis deviation

b. 2D Echocardiography: to measure the thickness of the Left ventricular wall, and the anatomical variations of the Mitral valve

c. Angio–CT

d. MRI

e. Doppler Study: to access the blood flow through the chambers

f. Ambulatory Holter monitoring Invasive Cardiac catheterization: to assess the pressure gradient between the LV and the ascending aorta, in normal heart there being no such difference

Pre-participation screening / exercise testing of athletes

Overwhelming majority of sports researchers agree on the need for preparticipation screening in sports. it is mandatory in the US and Italy. In Australia, it has been made compulsory in some sports. The American Heart Association has laid down specific recommendations for the screening of athletes. These state that ‘some form of pre- participation cardiovascular screening for high school and collegiate athletes is justifiable and compelling, based on ethical, legal and medical grounds’. Noninvasive testing can enhance the diagnostic potential of the standard history and physical examination; however it is not prudent to carry out routine use of tests as 12-lead ECG, echocardiography, or graded exercise for detection of CV disease in large populations of athletes. The Laussane recommendations have also laid down specific guidelines for pre-screening. However, guidelines by different bodies have given rise to a lot of debate and no single guideline can be considered satisfactory.


Usually, the underlying mechanism of sudden cardiovascular death is ventricular fibrillation; hence, as such can be treated with defibrillation. Thus in elite sport, up gradation of sport first aid infrastructure, with routine employment of automated external defibrillators (AEDs) is the need of the hour. Keeping in mind the ABC of resuscitation, the surviving sports person is then transported to a referral heath unit for investigation into the causes of the event. Admission to an ICU for observation or management is usually warranted.


In general, a lot of research has been done and a lot written about sudden cardiovascular death related to sport, but thanks to different outcomes of various studies, confusion still prevails about the exact definition of the condition, and indeed, what exactly causes it. Although, we know of conditions which may predispose to sudden death, we cannot as yet, on the basis of screening tests or procedures available, say for sure what condition(s) will definitely lead to sudden death. Hence, the major dilemma surrounding banning athletes from competition. On the one hand, there is the ethical issue of preventing risks that can lead to death, while on the other, there is the thought of banning the athlete when you are not sure if his/her heart condition is indeed a pathologic state. One may argue that taking risks is an inherent part of sports, esp. boxing, car racing, etc but life threatening risks should be a strict ‘no-no’. To conclude, exercise or sport may lead to sudden death but the benefits of exercise far outweigh the risks involved. Even in elite athletes, the risk-benefit ratio is to be taken into consideration when disqualifying him or her from competition. It is of paramount importance to judge whether the left ventricular wall thickness is a measure of physiologic adaptation to exercise or relates to a cardiac pathologic state. Physical exercise per say does not cause cardiovascular death. Does it, then, unmask a cardiac condition to cause a heart attack which otherwise would not have occurred had the person not been exercising or playing sport? That is the question for the medical community to answer. With a society dealing with ever increasing medical conditions associated with a sedentary lifestyle and unhealthy dietary habits, humanity can ill afford to be discouraged from participation in sport or exercising under any pretext unless irrefutable proof of exercise causing death exists.