SEMS-journal

Arrhythmias and sudden cardiac death in athletes

paulburri64

Wilhelm Matthias

Centre for Rehabilitation & Sports Medicine, Inselspital, Bern University Hospital, University of Bern, Switzerland

Abstract

This case-based review provides an overview of the most relevant supraventricular and ventricular arrhythmias in athletes, elucidating their connections with intensive exercise and sports and the risk of sudden cardiac arrest. It highlights typical symptoms and key diagnostic characteristics of these arrhythmias. Additionally, it discusses potential treatment strategies, aligning them with the latest guidelines and recommendations. It aims to enhance sports physicians’ understanding of arrhythmias in athletes and to provide practical guidance on their management.

Résumé

Cette étude de cas donne un aperçu des arythmies supraventriculaires et ventriculaires les plus pertinentes chez les athlètes, en élucidant leurs liens avec l’exercice intensif et le sport, ainsi que le risque de mort subite cardiaque. Il met en évidence les symptômes typiques et les principales caractéristiques diagnostiques de ces arythmies. En outre, il aborde les stratégies de traitement potentielles, en les alignant sur les dernières lignes directrices et recommandations. Il vise à améliorer, chez les médecins du sport, la compréhension des arythmies chez les athlètes et à fournir des conseils pratiques sur leur prise en charge.

Mots-clés: Arythmies, mort cardiaque subite, cas cliniques, ECG

Zusammenfassung

Diese fallbasierte Übersichtsarbeit gibt einen Überblick über die wichtigsten supraventrikulären und ventrikulären Arrhythmien bei Sportlern und beleuchtet deren Zusammenhang mit intensiver körperlicher Betätigung und Sport sowie das Risiko eines plötzlichen Herzstillstands. Es werden typische Symptome und wichtige diagnostische Merkmale dieser Arrhythmien hervorgehoben. Darüber hinaus werden mögliche Behandlungsstrategien erörtert und mit den neuesten Leitlinien und Empfehlungen in Einklang gebracht. Ziel des Buches ist es, das Verständnis der Sportmediziner für Herzrhythmusstörungen bei Sportlern zu verbessern und praktische Anleitungen für deren Behandlung zu geben.

Schlüsselwörter: Arrhythmien, plötzlicher Herztod, klinische Fälle, EKG

Introduction

Assessing athletes with arrhythmias, discerning between benign and malignant forms, and preventing sudden cardiac death represent significant challenges in the field of sports medicine. Collaboration among sports physicians, cardiologists, and electrophysiology specialists is crucial. [1] Sports physicians, who often are the first point of contact for athletes, must recognize red flags in an athlete’s personal and family history, during examinations, and in electrocardiogram (ECG) interpretations to ensure timely referrals for specialist evaluation. [2] Given the relatively low prevalence of arrhythmias in athletes, establishing a knowledge base solely on personal experiences proves challenging. The aim of this review is to provide a case-based summary of major cardiac arrhythmias, tailored to the needs of sports physicians to enhance their personal experience and complement textbook knowledge (Table 1). [3,4]

Table 1: Overview of supraventricular and ventricular arrhythmias

It is important to acknowledge that despite our best efforts to prevent life-threatening arrhythmias through pre-participation cardiovascular evaluations, sudden cardiac arrest can still be the first manifestation of an underlying cardiac condition. [5] Therefore, sports physicians responsible for sporting events should also develop comprehensive medical action plans to ensure the proper application of cardiopulmonary resuscitation and the widespread availability and use of auto­mated external defibrillators (AEDs) to improve survival rates from sudden cardiac arrest on the field. [6]
The cases selected for this review were presented at the 2023 Sport & Exercise Medicine Switzerland (SEMS) educational course in Nottwil.

Case 1 – A track and field athlete with ­palpitations

Case presentation

A 28-year-old track and field athlete was referred to the sports cardiology clinic for short episodes of palpitations during training and competitions. During these episodes, he observed a heart rate of 215 beats per minute (bpm) on his heart rate monitor. He reported no additional symptoms, no personal or family history of cardiovascular diseases, no recent infections, no drug abuse, and no medication use. The resting electrocardiogram (ECG) showed neither pre-excitation nor other abnormalities. Standard laboratory tests were normal, including the thyroid-stimulating hormone levels. An exercise test on a treadmill (Bruce Protocol) revealed excellent exercise capacity (18 metabolic equivalents, METs) and a normal heart rate profile in sinus rhythm (maximum 192 bpm). A 24-hour Holter monitoring was uneventful. Transthoracic echocardiography indicated slightly enlarged heart chambers, typical of an athlete’s heart, but was otherwise normal. A customized treadmill exercise test, simulating conditions of training and competition, induced two non-sustained supraventricular tachycardias with rapid onset and cessation, accompanied by palpitations (Figures 1 and 2). An electrophysiological study confirmed the diagnosis of AV nodal re-entrant tachycardia (AVNRT). A slow pathway ablation procedure was successfully performed, and the athlete was symptom-free afterward.

Figure 1: Individualized treadmill protocol for a 28-year-old track and field athlete experiencing palpitations. The red curve represents the heart rate profile. The two arrows indicate episodes of non-sustained AV nodal re-entrant tachycardia, as shown in Figure 2.

 

Figure 2: ECG of non-sustained AV nodal re-entrant tachycardia in a 28-year-old track and field athlete with palpitations, induced during an individualized exercise test on a treadmill (Figure 1). The arrows indicate start and end of the AV nodal re-entrant tachycardia.

What do the guidelines recommend?
Participation in all sports activities is possible in athletes with paroxysmal supraventricular tachycardias without pre-excitation (Class IC). [1]
In competitive athletes, curative treatment by ablation should be considered (Class IIaC). [1]

Key messages
Paroxysmal supraventricular tachycardias, such as AVNRT, are generally benign. While sports activities may trigger the arrhythmia, leading to symptoms like palpitations and potential loss of performance, the condition is often challenging to detect since routine exercise tests may appear normal. ­Tailored exercise testing protocols or heart rate monitoring during exercise can aid in identifying the condition.

Example from professional sports
A notable Swiss athlete who was diagnosed with AVNRT and successfully treated with an ablation procedure is Carlo Janka. [7]

Case 2 – A marathon runner with loss of ­performance and dizziness

A 48-year-old marathon runner was admitted to the emergency room with a symptomatic broad complex tachycardia, as depicted in Figure 3A. The patient’s running partner had alerted emergency services after observing a significant decline in the patient’s performance and episodes of dizziness during a leisurely jog. The ECG displayed a fast, broad, and irregular (FBI) pattern, indicative of atrial fibrillation in the presence of an accessory pathway (Wolff-Parkinson-White, WPW Syndrome). Consequently, electrical defibrillation was administered. Subsequent examination during the electrophysiological study confirmed the presence of a left posterior accessory pathway, as shown in Figure 3B. Ablation therapy was successfully performed, as illustrated in Figures 3C and D.

What do the guidelines recommend?
Ablation of the accessory pathway is recommended in competitive and recreational athletes with pre-excitation and documented arrhythmias (Class IC). [1]
In healthy individuals aged>35 years, cardiac screening with family history, symptoms, physical examination, and 12-lead ECG should be considered for competitive athletes (Class IIaC). [1]

Figure 3: Clinical studies on a 48-year-old marathon runner experiencing performance loss and dizziness. A – ECG in the emergency room displays a fast, broad, and irregular (FBI) pattern suggestive of atrial fibrillation with an accessory pathway. B – ECG in the electrophysiology laboratory following electrical defibrillation. It shows sinus rhythm and a delta wave, indicative of a left posterior accessory pathway. C – ECG during ablation: The first beat shows a short PR duration and a QRS complex with a delta wave. The second beat displays a normal PR duration and a smaller QRS complex without the delta wave. The newly observed T wave inversions in the inferolateral leads are typical transient patterns following posterior pathway ablation. D – Left anterior oblique fluoroscopic view of the heart. The upper image displays a diagnostic catheter within the coronary sinus, highlighted using contrast media. The lower image reveals three more diagnostic catheters positioned in the left atrium, ventricle, and near the bundle of His, along with the ablation catheter in the left posterior position.

Key messages
Middle-aged endurance athletes are at an elevated risk of developing atrial fibrillation, as high-volume endurance activities are associated with atrial structural and electrical remodeling. [8] When an accessory pathway is present, atrial fibrillation may manifest as a rapid, wide, and irregular form of supraventricular tachycardia. This condition is considered an emergency, and prompt electric defibrillation should be administered early to terminate the arrhythmia. This urgency is due to the risk of the arrhythmia deteriorating into ventricular fibrillation, potentially leading to cardiac arrest. Ablation of the accessory pathway can effectively cure the condition and allows for the safe continuation of competitive sports. A normal resting ECG rules out the presence of an accessory pathway with antegrade conduction capabilities. Pre-participation cardiovascular evaluation, including an ECG, could have identify pre-excitation conditions in this runner. [2] However, there is ongoing debate regarding whether recreational athletes who also compete in events such as marathons should undergo regular screening, considering the relatively low incidence of fatalities and high number of athletes that would have to be screened. [2,9]

Case 3 – A young soccer player with syncope

A 12-year-old soccer player visited the cardiology clinic following two fainting episodes during training sessions. The resting ECG was normal. An exercise test performed on a bicycle elicited a non-sustained monomorphic ventricular tachycardia, which led to syncope, as illustrated in Figure 4. Subsequent transthoracic echocardiography and cardiac magnetic resonance imaging did not reveal any structural heart disease. The presentation of left bundle branch block morphology and inferior axis indicated a likely right ventricular outflow tract tachycardia. This diagnosis was confirmed through an electrophysiological study, and the arrhythmia was successfully ablated. The patient remained symptom-free and continued to play soccer. However, at the age of 15, he experienced fainting spells again while playing soccer. Upon repeating the ECG and cardiac imaging, arrhythmogenic cardiomyopathy (ACM) with involvement of the right outflow tract was diagnosed. An implantable cardio­verter-defibrillator (ICD) was implanted. [10] A shared decision-making discussion was held with the family, where it was communicated that, due to his particular condition, the potential risks linked to engaging in high-intensity exercise and competitive sports are likely to surpass the advantages. [1,10]

Figure 4: ECG showing monomorphic ventricular tachycardia in a 12-year-old soccer player who experienced syncope, induced during a bicycle exercise test.

What do the guidelines recommend?
Participation in high-intensity recreational exercise and sports or any competitive sports is not recommended in individuals with ACM, including those who are gene positive but phenotype negative (Class III B). [1]
An ICD is not recommended as a substitute for disease-
related recommendations when these mandate sports restriction (Class IIIC). [1]

Key messages
Ventricular arrhythmias can sometimes be the initial sign of structural heart disease, which might not be apparent in cardiac imaging studies. ACM stands out as a cardiac condition where intense exercise can play a role in the expression of the phenotype and the progression of the disease, warranting a definitive recommendation against such activities. [1,5,10]
A resting ECG, included in the pre-participation cardiovascular assessment, is highly sensitive in identifying cardio­myopathies, including ACM. [2] Nevertheless, early stages of the condition may not be detected immediately, as was the situation in this case. This warrants repetitive screening. Soccer, a sport characterized by frequent starts and stops, places a significant cardiovascular strain on players, potentially facilitating arrhythmias in those with underlying structural heart disease.
Examples from professional sports
Tragic instances involving association football players where ACM led to sudden cardiac death include Matt Gadsby, aged 27, of Hinckley United, who passed away in 2006 during a Conference North game, and Antonio Puerta, aged 22, of Sevilla, who died in 2007 during a match against Getafe. [11]

Case 4 – A soccer player with sudden cardiac death on the pitch

A 27-year-old amateur soccer player participated in a soccer tournament organized by his employer. He was a healthy young man with no symptoms during intensive exercise, a non-smoker, with no history of drug abuse or medication use. His father had passed away suddenly at the age of 49 for unknown reasons. During the soccer match, he suffered a sudden cardiac arrest. The first responder team immediately initiated cardiopulmonary resuscitation, and upon the ambulance’s arrival, advanced life support was administered. The automatic external defibrillator (AED) detected ventricular fibrillation, but multiple attempts at external defibrillation were unsuccessful (Figure 5). The patient was then transported to a tertiary hospital where emergency cardiac catheterization was performed. A thrombotic occlusion of the left anterior descending (LAD) coronary artery was identified and successfully managed with balloon angioplasty and stent placement (Figure 6A and B). Despite successful revascularization, the patient died in cardiogenic shock. An autopsy later revealed coronary artery disease with a ruptured plaque in the LAD and a significant transmural myocardial infarction of the interventricular septum and the anterior wall as the cause of the ventricular fibrillation (Figure 6C and D). Given the family history, familial hypercholesterolemia was suspected to be the cause of the early atherosclerosis and the sudden cardiac death.

Figure 5: ECG from an automated external defibrillator (AED) of a 27-year-old man taken after a sudden cardiac arrest occurred during a soccer match. The ECG shows ventricular fibrillation that was not terminated by a 200 J shock from the AED.

 

Figure 7: ECG from an AED used on a 39-year-old female leisure-time mountain biker who experienced sudden cardiac arrest at rest while working in the office. The upper row displays ventricular fibrillation, while the lower row shows a successful restoration of a regular rhythm following a 120 J shock. The time from detection to successful intervention was 50 seconds.

 

What do the guidelines say?
Individuals with a history of premature cardiovascular death deserve early screening for cardiovascular risk factors (Class IC). [12]

Key messages
Coronary artery disease (CAD) may occur also in young individuals at risk, predisposing them to exercise-induced plaque rupture, myocardial infarction, and sudden cardiac death. In the Swiss Registry of Athletic Related Deaths, which encompassed all autopsy-confirmed sudden cardiac deaths between 1999 and 2010, CAD was identified as the most common cause of death among both recreational and competitive athletes aged 35 and younger. [13] This contradicts the perception that cardiomyopathies and channelopathies are the most common causes of sudden cardiac death (SCD) in young athletes. The variation is likely due to regional differences in the prevalence of cardiac conditions and differences in referral strategies and methods used for their detection. [5,14] A family history of unexplained sudden death should prompt an evaluation, regardless of age, that includes the cardiovascular risk profile, since early CAD is not detectable on an ECG. [12]

Example from professional sports
FC Porto’s goalkeeper, Iker Casillas, experienced a sudden cardiac arrest at the age of 38 due to a myocardial infarction caused by a blockage in the right coronary artery during a routine training session. He was successfully resuscitated. [15]
Swiss Marathon runner Adrian Lehmann suffered a myocardial infarction at the age of 34 while training for the Zurich Marathon and tragically died two days later in hospital. [20]

Case 5 – A mountain biker with sudden cardiac arrest unrelated to sports

A 39-year-old female leisure time mountain biker suffered a cardiac arrest while at the office. She was successfully resuscitated by first responders. An AED restored her normal heart rhythm within 50 seconds, with the total downtime being less than 5 minutes (Figure 7). She survived the incident without any neurological sequelae. A cardiac examination showed hypertrophic obstructive cardiomyopathy (HOCM) as the likely cause of the arrhythmia, and an ICD was subsequently implanted. Notably, despite having a resting left ventricular outflow tract (LVOT) gradient of 55 mmHg, she had experienced no symptoms while engaging in sports. She took part in a cardiac rehabilitation program and improved her exercise capacity from 90% of the predicted level to 109%. She was advised to engage in low- to moderate-intensity recreational exercises and purchased an electric mountain bike to continue cycling with her peers. Within six months, no exercise-related ventricular arrhythmias were detected by the ICD, and the continuation of mountain biking was encouraged. Nine months after the ICD was implanted, she experienced a fainting episode unrelated to exercise, caused by another episode of ventricular fibrillation, which was successfully terminated by her ICD (Figure 8).

Figure 7: ECG from an AED used on a 39-year-old female leisure-time mountain biker who experienced sudden cardiac arrest at rest while working in the office. The upper row displays ventricular fibrillation, while the lower row shows a successful restoration of a regular rhythm following a 120 J shock. The time from detection to successful intervention was 50 seconds.

 

Figure 8: ECG from an ICD in a 39-year-old female mountain biker diagnosed with hypertrophic obstructive cardio­myopathy after experiencing sudden cardiac arrest. The first row displays a normal sinus rhythm. The second row shows the onset of ventricular fibrillation. Notably, the arrhythmia occurred at rest, and not during exercise. The third row depicts the successful intervention of the ICD with the restoration of a regular rhythm.

 

What do the guidelines say?
Participation in low- or moderate-intensity recreational exercise, if desired, may be considered for individuals who have any markers of increase risk (cardiac symptoms or history of cardiac arrest or unexplained syncope, moderate ESC risk score (≥4%) at 5 years, LVOT gradient at rest ≥ 30 mmHg, abnormal blood pressure response to exercise, exercise-induced arrhythmias) following expert assessment (Class IIbC). [1]

Key messages
Hypertrophic cardiomyopathy (HCM) is a heterogeneous group of structural heart diseases with varying risks for life-threatening arrhythmias. Athletes may be asymptomatic when LVOT obstruction is present, even during exercise. Sudden cardiac arrest may be the first manifestation of the disease. Exercise in not the only trigger for life-threatening arrhythmias in athletes with HCM. [14,16]

Examples from professional sports
Gerald Asamoah, a former German soccer player originally from Ghana was diagnosed with HCM at the age of 20 years. Despite doctors advising against continuing his career in professional sports, Asamoah decided to play on. He went on to compete in the German Bundesliga and represented Germany in the World Cups of 2002 and 2006. In 2007, he founded the Asamoah Foundation for children with heart diseases. [17] Remarkably, he never experienced a life-threatening arrhythmia. In stark contrast to Asamoah’s story is the tragic case of Marc-Vivien Foé from Cameroon, who collapsed during a match at the 2003 FIFA Confederations Cup and later died in the hospital. Posthumously, HCM was identified as the cause. [11] Another case is that of Anthony Van Loo, a player from KSV Roeselare, who also has HCM but was equipped with an ICD. During a game, he suffered a sudden cardiac arrest, and his ICD successfully terminated the ventricular fibrillation. [18] This incident intensified the ongoing debate about whether athletes with structural heart diseases, who are equipped with an ICD, should be allowed to par­ticipate in competitive sports. It highlights the importance of shared decision-making. [1,19]

Figure Copyrights

The author holds the copyright for all images, except for images C and D of figure 6, which are courtesy of the Institute of Pathology at the University Hospital of Erlangen. Informed consent was obtained from all patients for the use of their data. For case 4, the family of the deceased patient consented to the educational use of the images.

Corresponding author

Matthias Wilhelm, Prof. Dr. med.
Chefarzt und Ärztlicher Leiter
Zentrum für Rehabilitation & Sportmedizin Inselspital
Universitätsspital Bern, Freiburgstrasse, CH-3010 Bern
matthias.wilhelm@insel.ch

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