Reviews

Sudden cardiac death in athletes: a guide for emergency physicians

Carl A. Germann MD*, Andrew D. Perron MD

Department of Emergency Medicine, Maine Medical Center, Portland, ME 04102, USA

Received 4 September 2004; revised 4 September 2004; accepted 12 September 2004

Abstract A conditioned athlete is usually regarded as a member of the healthiest segment of society, and exercise itself is looked upon as a means to improve health. Although extremely uncommon, Sudden Cardiac Death in Young athletes is a devastating medical event to all involved (patient, family, community, team, and caregivers). Most etiologies of SCD in athletes result in the same final common denominator (cardiac arrest) on presentation to an emergency physician. There are, however, certain historic, physical examination, and Electrocardiographic features of many of these disease processes that emergency physicians should have a working knowledge of to try to identify them before they result in SCD. This review examines the clinical presentation, diagnostic techniques, and management options applicable to Emergency practitioners.

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Introduction

The first proposed case of sudden cardiac death (SCD) in an athlete involved Pheidippides in 490 bc. This trained runner was reported to have collapsed and died after running to Athens from Marathon with the news of the military defeat of Persia [1]. More recent accounts of athletes dying suddenly include Loyola Marymount basketball player Hank Gathers (1990), marathon runner Jim Fixx (1984), US Olympic volleyball player Flo Hyman (1986), former professional basketball players Pete Maravich (1980) and Reggie Lewis (1993), and Olympic figure skater Sergei Grinkov (1995). All these professional athletes suffered from presumed SCD.

T Corresponding author. Tel.: +1 207 842 7015; fax: +1 207 842 7054.

E-mail address: [email protected] (C.A. Germann).

Conditioned athletes are regarded to constitute the healthiest segment of the society while exercise itself is considered a means of improving personal health and decreasing the chance of cardiovascular disease. Although relatively uncommon, the sudden death of an athlete can have a tragic and devastating impact on the family, community, and medical staff involved. For many years, the lack of understanding regarding the causes of such catastrophes was reflected by vague descriptions of these events such as sudden death syndrome [2]. Over the past decade, however, a greater comprehension of the under- lying cardiovascular processes of SCD in athletes has been achieved.

The role of emergency physicians (EPs) in this setting is primarily to attempt resuscitation and stabilization of the patients. However, it is helpful for EPs to be aware of the demographics, risk factors, etiologies, and current preven- tive strategies regarding SCD.

0735-6757/$ – see front matter D 2005 doi:10.1016/j.ajem.2004.09.036

Definition

There is no universally accepted definition for SCD. One popular definition is that of a nontraumatic and unexpected sudden cardiac arrest that occurs within 6 hours of a previously normal state of health [3]. Other definitions limit the time frame in relation to sport participation and symptoms anywhere from within 1 to 24 hours [4-6].

The term athlete implies involvement in a regimented exercise program with participation in a team or individual sport. To better differentiate the etiology of SCD, athletes are often classified as byoungQ or bold.Q Although open for debate, for the purpose of this review, the term young athlete will refer to those aged younger than 35 years because most studies in this arena have defined it as such.

Hypertrophic cardiomyopathy“>Epidemiology

Sudden cardiac death in young athletes is rare. The exact prevalence is not known because there is no national database to track the death of athletes. The largest available studies estimate the incidence among high school and collegiate athletes to be between 1 per 100000 and 1 per 300 000, respectively, each year [7-10]. An estimated number of 50 to 100 cases occurs annually in the United States [7,9,11].

The overall estimate of incidence may be low given that fatal arrhythmias associated with subtle structural abnor- malities or a normal heart would be difficult or impossible to identify on postmortem examination. Also, often it is a coroner’s priority to exclude foul play rather than establish a precise cardiovascular diagnosis [12]. Likewise, lack of a national registry for SCD in athletes might lead to an underestimation. There is often reliance on media coverage rather than on voluntary or mandatory reporting for identifying cases of SCD.

Despite the overall low incidence of SCD, it represents 30% of all nontraumatic deaths, with one third of victims younger than 65 years [13]. For young athletes, SCD remains a significant cause of nontraumatic exercise-related death. The incidence of Cardiovascular collapse as the cause of athletic fatalities in high school and college athletes outnumbers death caused by trauma by nearly 2 to 1 [11,14]. Most (N80%) cases of SCD in young athletes occur either during or immediately after Strenuous exercise [15]. This suggests that physical activity may be a trigger for cardiac arrhythmias in those with certain cardiac disease. Athletes suffering from SCD participate in a large variety of sports, most frequently basketball and football (about 68%) [15]. Most cases of SCD occur in men with a ratio ranging from 5:1 to 9:1 [8,15]. This may be because of the lower participation rate of women in competitive sports in addition to the higher incidence of hypertrophic cardiomy- opathy (HCM) among men [15]. A considerable proportion of SCD occurs in African American athletes [16]. Although

African Americans constitute only about 12% of the US population, this subset represents a large portion (N40%) of individuals experiencing SCD. This fact is probably a result of a disproportional level of participation in certain competitive sports.

Causes of SCD in athletes

Sudden death in young athletes is predominantly caused by structural non-atherosclerotic heart disease [17]. Sudden cardiac death is caused by the combination of exercise and underlying heart disease rather than by exercise alone, which usually leads to the final common pathway of Lethal arrhythmia [11,18-20]. By far, the most common reason for SCD is HCM, accounting for at least 36% of deaths [15]. The second most frequent cause of death, encountered in 17% to 19% of deaths, is congenital coronary anomalies [11,15]. The next most common cause of SCD in young athletes is idiopathic left ventricular hypertrophy (ILVH), accounting for 9% to 10% of cases [11,15]. Infrequent causes include aortic rupture, arrhythmogenic right ventric- ular dysplasia, aortic valve stenosis, prolonged QT syn- drome, mitral valve prolapse (MVP), Commotio cordis, Wolff-Parkinson-White (WPW) syndrome, and atheroscle- rotic coronary artery disease.

On the other hand, in mature athletes (those older than 35 years), coronary artery disease is found in most cases of SCD [3,5,21,22]. In fact, atherosclerotic heart disease is found to be the cause of SCD in anywhere from 73% to 95% of this patient population [5,6,10,23,24].

Hypertrophic cardiomyopathy

By and large, HCM is the predominant cause of sudden death in young athletes, occurring in more than one third of all cases [15]. The estimated prevalence of HCM in the general population is about 1 in 500 [11], although many cases may go undetected during a patient’s lifetime.

The diagnostic criteria for HCM include a left ventricle that is hypertrophied but not dilated in the absence of other cardiac or systemic diseases that would produce left ventricular hypertrophy [23]. This pathological hypertrophy contributes to decreased ventricular compliance and diastol- ic dysfunction with impaired filling. The left ventricular outflow obstruction and possibly small lumen intramural vessels may potentiate myocardial ischemia. Arrhythmias arise in the context of an electrically unstable myocardial substrate caused by cardiac muscle cell disorganization, replacement fibrosis, or myocardial ischemia [24].

Hypertrophic cardiomyopathy is genetically transmitted as an autosomal dominant condition with variable expres- sion because it may not manifest itself until adolescence or young adulthood [23,25]. If a family history of HCM is confirmed, it is recommended that all first-degree relatives be examined with echocardiography [23,26]. It may be difficult, however, to distinguish mild HCM from

the normal cardiac hypertrophy that occurs in highly trained athletes [27].

Unfortunately, often the first clinical manifestation of HCM is sudden death. In a series of SCD occurring during exercise in patients with HCM, only 35.7% had a previous cardiac evaluation for risk factors that included syncope, family history, murmurs, fatigue, or ventricular tachycardia on exercise testing [17]. In another study, 21% of athletes who died from HCM had symptoms of cardiovascular disease before their death [15]. Symptoms may include chest pain, exertional dyspnea, lightheaded- ness, or syncope.

Hypertrophic cardiomyopathy should be suspected in any patient in whom a harsh systolic ejection murmur is heard on examination. The characteristic murmur increases in intensity with maneuvers that decrease venous return such as Valsalva’s maneuver. Examination may also reveal the presence of a fourth heart sound or a rapid initial upstroke of the carotid pulse. These patients will also demonstrate signs of left ventricular enlargement electro- cardiographically and radiographically. If HCM is suspected clinically, the diagnosis should be confirmed by echocardi- ography. If seen in the ED, patients should be proscribed from exertion or exercise until they can have an echocar- diogram and cardiology consultation.

Coronary artery abnormalities

Second in frequency to HCM as a cause of SCD in this population is congenital coronary abnormalities. These congenital abnormalities are also infrequently diagnosed during life. The most common coronary anomaly associated with SCD in athletes is a left main artery arising from the right sinus of Valsalva [28,29]. Coronary anomalies presumably lead to myocardial hypoperfusion during exercise; however, the precise mechanism is often unknown. Possible reasons for ischemia in anomalous coronary artery include a slit-like ostium that narrows with aortic dilatation during exercises, an acute-angled takeoff, and compression of the artery as it passes between the aorta and pulmonary trunk [3,9,15,23]. Other coronary anomalies include origin of the right coronary artery from the left sinus of Valsalva or from the pulmonary artery, presence of a single coronary artery, and coronary aneurysm [3,8,9,15].

Some individuals with coronary artery anomalies may demonstrate symptoms such as syncope or angina before an event. Among athletes who died of this disorder, 31% were found to have symptoms before death [15]. A high index of suspicion in conjunction with an echocardiogram may help suggest the presence of an anomaly in order for angiography to be obtained and to confirm this often surgically correctable abnormality [6]. It should be noted that recent research have shown that both magnetic resonance imaging and computed tomographic coronary angiography have demonstrated promise in detecting coronary artery anomalies [30,31].

Idiopathic left ventricular hypertrophy

This condition accounts for approximately 10% of all SCD in young athletes [11,15]. Idiopathic left ventricular hypertrophy is a symmetric, concentric hypertrophy where the left ventricular mass exceeds that of physiological hypertrophy. Unlike HCM, ILVH is not associated with genetic transmission and there is no cellular disarray microscopically. However, it is uncertain whether some cases of ILVH represent mild morphological expressions of HCM, unusual instances of exercise-induced cardiac hyper- trophy (bathlete’s heart syndromeQ) with nonbenign con- sequences, or possibly examples of undetected right ventricular dysplasia with mild left ventricular hypertrophy [27,30-32]. The precise mechanism of death is poorly established but thought to be similar to that of HCM.

Less common causes of SCD

Myocarditis

This inflammatory condition of the myocardium is frequently the result of a viral infection most commonly caused by either coxsackievirus or echovirus. Characteristic symptoms of myocarditis include a prodromal Viral illness followed by progressive exercise intolerance and congestive symptoms of dyspnea, cough, and orthopnea. On physical examination, an audible S₃ gallop or soft apical murmur as well as signs of congestive heart failure may be present. The electrocardiogram (ECG) may show low-voltage com- plexes, diffuse ST-segment and T-wave changes, and sinus tachycardia. Sudden cardiac death may occur in the presence of either active or healed myocarditis [9]. Thus, a convalescent period of at least 6 months is recommended before a return to sports [9,33].

Mitral valve prolapse

Idiopathic MVP is the most common valvular disorder, occurring in approximately 5% of the population [28,34]. Although sudden death from MVP has been reported, it is extremely rare and most athletes with MVP are totally asymptomatic. Physical examination of patients with MVP may reveal a midsystolic click and a late systolic murmur. If an athlete with known MVP develops syncope, exertional chest pain, or moderate-to-severe Mitral regurgitation, it is recommended that athletic participation be restricted [33].

Aortic rupture

Aortic rupture makes up 5% to 7% of sudden death in young athletes according to investigations by Maron et al [3,15]. Half of these cases occur in athletes with the Marfan syndrome, which is an autosomal dominant disorder with a prevalence in the general US population of 1 per 10000 [9,35]. In the Marfan syndrome, the aortic media are deficient in the number of elastic fibers, which leads to

Brugada syndrome“>weakening of the aortic wall and predisposes the individual to aortic dissection and death. A diagnosis of Marfan syndrome is based on clinical features as well as family history. Common manifestations involve the skeletal, ophthalmologic, and cardiovascular systems [35]. Skeletal features include tall stature with arm span greater than height, arachnodactyly, hyperextensible joints, scoliosis, a high-arched palate, and pectus excavatum. Ophthalmologic examination may show myopia and ocular lens subluxation, and echocardiography may reveal a dilated aortic root or MVP. Patients with suggestive physical features or a family history of Marfan syndrome may undergo clinical and echocardiographic evaluation or DNA testing to confirm the diagnosis.

Wolff-Parkinson-White syndrome“>long QT syndrome“>Arrhythmogenic right ventricular dysplasia

Arrhythmogenic right ventricular dysplasia was found to be the most common cause of sudden death in young athletes in the Veneto region of Northern Italy [36]. However, this disease appears to be much less prevalent in the United States, occurring in approximately 3% of SCD cases [15]. Right ventricular dysplasia is an autosomal dominant condition leading to fibrosis and fatty infiltration of the right ventricle.

This process results in the thinning and dilatation of the right ventricular wall and leads to recurrent and intractable Ventricular tachyarrhythmias. Diagnosis of this disease often proves difficult. If echocardiography does not demonstrate Right ventricular dilation and dysfunction, a magnetic resonance imaging can be diagnostic in demonstrating fatty infiltrates of the myocardium [11,37].

Wolff-Parkinson-White syndrome

The WPW syndrome is an abnormality of the cardiac Conduction system whereby an additional electrical pathway can lead to tachycardia and, rarely, SCD [11,37,38]. This conduction abnormality is relatively rare, affecting only 0.15% to 0.2% of the general population, and has a very small risk of sudden death (b0.1%) [11]. These individuals may have various symptoms including palpitations, synco- pe, and lightheadedness. The mechanism of SCD is the development of atrial fibrillation with rapid atrioventricular conduction via the bypass tract, resulting in rapid ventricular response and subsequent ventricular fibrillation [38]. The resting ECG may demonstrate an initial slurred upstroke of the QRS complex (delta wave), short PR interval, and wide QRS complex.

Long QT syndrome

The long QT syndrome is an abnormality of the electrical conduction system characterized by prolonged repolarization of the ventricle with an associated high risk of SCD [11]. This syndrome can be congenital, pharmaco- genic, or metabolic. It is often defined as a corrected QT

interval of more than 440 milliseconds. The mechanism of SCD is the development of wide, polymorphic tachycardia (ie, Torsades de pointes) [11,39]. These potential fatal rhythms can be provoked by exercise-related tachycardia; thus, anyone with this condition should be restricted from competitive sports.

Commotio cordis

Commotio cordis is an electrophysiological event caused by precordial chest impact that occurs in individuals free from structural cardiac disease. The mechanism of SCD appears to be ventricular fibrillation that is produced when the chest impact is delivered within a narrow, electrically vulnerable period of the cardiac cycle [40]. Specifically, the susceptible time is during repolarization, just before the peak of the T wave. Resuscitation of these victims is possible with prompt cardiopulmonary resusci- tation and defibrillation. A US commotio cordis registry has reported a 10% survival rate, with 2.8% experiencing Full recovery [41].

Brugada syndrome

The Brugada syndrome, described as a syndrome of SCD caused by unpredictable episodes of recurrent ventricular tachycardia, is also postulated to be a possible etiology of death in this patient population. It is characterized as a syndrome of SCD in individuals with a structurally normal heart and no evidence of atherosclerotic coronary artery disease. Patients are noted (if identified before their event) to have a distinct set of ECG abnormalities that include a complete or incomplete Right bundle branch block with ST- segment elevation in the Right precordial leads. Originally thought to be a disease primarily of men from Southeast Asia, it is now identified in women, children, and non- Asian ethnic groups. Patients may present with self- terminating episodes of ventricular tachycardia during exertion. If the diagnosis is supported by ECG findings, referral should be made for EP testing and consideration of automated implantable cardiac defibrillator placement.

Atherosclerotic coronary artery disease

Acquired coronary artery disease is occasionally respon- sible for sudden death in young athletes. Atherosclerotic coronary artery disease is thought to be responsible for approximately 2% of SCD cases in young athletes [15]. However, atherosclerotic disease is responsible for the vast majority of SCD cases in mature athletes (N35) [6,23].

Medications

Sudden cardiac death has been attributed to proarrhyth- mic drugs such as epinephrine, ephedrine, cocaine, and related sympathetic medications. Deaths have also been linked to performance-enhancing agents such as erythro-

poietin and anabolic steroids [5,23]. Anabolic steroids may cause cardiac hypertrophy, myocardial fibrosis, and accel- erated atherosclerosis that could promote cardiac necrosis and ischemia.

Emergency department management

The role of EPs is primarily to attempt resuscitation of patients experiencing SCD events. Although few athletes are electrocardiographically monitored at the time of death, most sudden deaths are thought to be caused by ventricular arrhythmias in the setting of an underlying heart disease. In one population of 16 athletes who survived cardiac arrest, 2 were found to have long QT syndrome, 5 had WPW syndrome, 8 had ventricular tachycardia or ventricular fibrillation, and 1 athlete had atrial fibrillation with heart block [42,43]. Treatment of these rhythms is established by advanced cardiac life support based on American College of Cardiology/American Heart Association recommendations and continued data from ongoing studies. Individuals experiencing successful resuscitation require a complete cardiac workup including echocardiogram, cardiac catheter- ization, and electrophysiological testing.

Emergency physicians should maintain a high index of suspicion when syncope or near-syncope occurs in the presence of exercise. Exertional syncope is a distinct red flag and all patients with this symptom should be excluded from participation until they have a complete cardiac evaluation. Likewise, the evaluation of athletes is similar to that of other patients with possible symptoms and signs of arrhythmic disorders. Symptoms of arrhyth- mias in athletes are similar to those in nonathletes and range from brief palpitations to syncope and resuscitated sudden death [42]. The key elements of the evaluation include the severity of the symptoms, the presence of structural heart disease, and the family medical history. In one study, 18% of athletes with SCD were known to have had symptoms judged to be cardiovascular in origin during the 36 months preceding death [15]. These symp- toms included chest pain, syncope, exertional dyspnea, and dizziness. A family history of congenital heart disease, syncope, or unexpected death at an early age may indicate an underlying cardiac abnormality. The physical examina- tion may elicit evidence of Marfan syndrome, aortic stenosis, MVP, HCM, or ILVH. When findings of the physical or historic evaluation suggest a syndrome associ- ated with high risk for SCD, further diagnostic testing is necessary. This will include an ECG and usually an echocardiogram. Likewise, long-term ECG monitoring with a Holter monitor can be useful in patients who present with frequent or reproducible symptoms. Investigative work and further risk stratification will usually be performed or followed up by a primary care physician. Participation in high-risk sports activity should remain forbidden until this workup is complete.

Conclusion

Sudden cardiac death rarely occurs in athletes with a structurally normal heart. Therefore, an assessment for structural heart disease is essential in evaluating athletes with possible cardiac signs or symptoms. Because certain SCD patients will lack a history of symptoms and physical findings, not all patients at risk will be identified. However, by knowing how to guide history and physical examination, potential diagnostic clues may help identify most patients at risk for SCD. Once cardiac arrest has occurred in patients, most of them may initially appear the same and death may not be preventable. In many cases, however, warning symptoms, a suggestive family history, clinical findings, or underlying Conduction abnormalities will be present.

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