Sudden Cardiac Death in Athletes: Facts and Fallacies

Abstract

The benefits of exercise for cardiovascular and general health are many. However, sudden cardiac death (SCD) may occur in apparently healthy athletes who perform at the highest levels. A diverse spectrum of diseases is implicated in SCD in athletes, and while atherosclerotic coronary artery disease predominates in individuals of >35 years of age, primary cardiomyopathies and ion channelopathies are prevalent in young individuals. Prevention of SCD in athletes relies on the implementation of health policies aimed at the early identification of arrhythmogenic diseases (such as cardiac screening) and successful resuscitation (such as widespread utilization of automatic external defibrillators and training members of the public on cardiopulmonary resuscitation). This review will focus on the epidemiology and aetiologies of SCD in athletes, and examine fallacies in the approach to this controversial field. Furthermore, potential strategies to prevent these tragic events will be discussed, analysing current practice, gaps in knowledge and future directions.

Keywords: athlete’s heart; cardiomyopathy; channelopathy; sports cardiology; sudden arrhythmic death syndrome; sudden cardiac death.

Figure 1

Dehydration, adrenergic surge, electrolyte imbalance and acid/base disturbance are common physiological effects of intense exercise. While these are well tolerated by healthy athletes, they may cause potentially fatal arrhythmias in individuals with an underlying electrical, structural or genetic pathological cardiac substrate. This image of a heart at post-mortem is suggestive of HCM, and this is used as an example.

Figure 2

Aetiologies of SCD in athletes and age. Cardiomyopathies, channelopathies and congenital anomalies of the coronary arteries are prevalent causes in younger individuals. Atherosclerotic coronary artery disease is the most common cause of sudden cardiac death and sudden cardiac arrest in older individuals. The size of the circles relate to the relative frequency of SCD caused by the respective pathology. Age 35 has been used as a threshold as this is the most frequently used age in the literature; however, a clear line in terms of age is difficult to draw.

Figure 3

Summary of main studies describing the causes of SCD in athletes. Abbreviations: ARVC—arrhythmogenic right ventricular cardiomyopathy; CAD—coronary artery disease; DCM—dilated cardiomyopathy; HCM—hypertrophic cardiomyopathy; LAD—left anterior descending artery; LQT—long QT; LVH—left ventricular hypertrophy; MVP—mitral valve prolapse; NOS—not otherwise specified; SADS—sudden arrhythmic death syndrome; SUD—sudden unexplained death; WPW—Wolff–Parkinson–White [18,21,41,45].

Figure 4

Structural, electrical and functional physiological changes commonly observed in athletes. Physiological changes may overlap with cardiac conditions that may pose a risk of SCD, and therefore differential diagnosis is very important. Abbreviations: AV—atrioventricular; CO—cardiac output; EF—ejection fraction; GLS—global longitudinal strain; LV—left ventricle; LVH—left ventricular hypertrophy; RV—right ventricle; RVH—right ventricular hypertrophy; WT: wall thickness.