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What is Sudden Death in Athletes?
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Definition of Sudden Death in an Athlete
Causes of Sudden Death in Athletes
Incidence and Prevalence of Sudden Death in Athletes
Distribution of Sudden Death Events in Athletes
Proposed Mechanisms of Sudden Death in Athletes
Definition of Sudden Death in an Athlete
Sudden death has been defined as "an abrupt unexpected death of cardiovascular cause, in which the loss of
consciousness occurs within 1 to 12 hours of onset of symptoms" (1, 2). The majority of sudden deaths in
athletes occur during or immediately after exercise (game, conditioning, training, etc). However, some deaths
occur at rest or during sleep. Autopsy is very useful in making a definitive diagnostic determination of the
cause of sudden death. Certain conditions (i.e., Long QT Syndrome, Brugada Syndrome) require detailed postmortem biochemical and sometimes genetic studies.
In studies of sudden deaths in athletes, individuals that participated in organized competitive sports, and
those that exercised regularly and vigorously and had an active lifestyle including sports, and sometimes
physically conditioned military personnel were considered "athletes." Individuals that lead a sedentary lifestyle
and exercise infrequently have not routinely been included into the definition of “athlete.”
Causes of Sudden Death in Athletes
The diseases responsible for sudden deaths on the athletic field have now been identified. For the most part,
they include a variety of cardiovascular abnormalities as shown in figure 1. The precise disease responsible for
the sudden death differs considerably with regards to age. For example, in young athletes, congenital
malformations of the heart and/or vascular system cause the majority of deaths. In contrast, in older athletes
who died suddenly, there is usually the evidence of atherosclerotic disease of coronary arteries.
Hypertrophic cardiomyopathy (HCM) is a genetic disease which manifests itself by the thickening of the
ventricular septum and/or other segments of the left ventricle with or without a partial obstruction to the
blood flow out of the left side of the heart. HCM has consistently been the single most common cardiovascular
cause of sudden death. HCM is relatively common in the general population (1:500 people) (3). HCM is usually
diagnosed by an imaging test (echocardiography or magnetic resonance imaging [MRI]). Electrocardiogram
(ECG) is often abnormal in patients with HCM. For a schematic representation of ECG and echocardiographic
image of a patient with HCM, click here. HCM is a diverse disease with various representations on the
echocardiography. For a series of representations, click here.
Congenital coronary anomalies, mostly a wrong origin of the left main coronary artery, are the second
most frequent cause of athletic field deaths. These anomalies may be more common than previously regarded
(4). For a schematic representation of anomalous coronary origins, click here. These anomalies are usually
diagnosed by echocardiography, MRI and/or coronary angiogram.
A diverse composition of approximately 15 other diseases of the heart account for the remaining athletic
field deaths due to cardiovascular disease. These include rupture of the aneurysm of the aorta as a component
of Marfan’s syndrome, arrhythmogenic right ventricular dysplasia/cardiomyopathy, rare anomalies of coronary
artery development ("bridging" of a coronary artery, congenital absence of one or more coronary artery, etc),
degeneration of the structures of mitral valve (mitral valve prolapse), aortic stenosis, dilated cardiomyopathy,
myocarditis, and other pathologies. Each of these is responsible for a minor portion of sudden deaths in
athletes, and presents a challenge for a physician to diagnose in the absence of symptoms.
Occasionally, athletes that die suddenly do not demonstrate any evidence of structural heart disease on
autopsy (5). Such deaths may be associated with the disorders of the conduction system of the heart,
such as Wolff-Parkinson-White (WPW) syndrome, Long QT Syndrome, Brugada Syndrome, and arrhythmias
related to exertion, such as catecholaminergic polymorphic ventricular tachycardia (CPVT) (5). In other
instances, exercise-induced coronary spasm, a heart block or asystole with loss of consciousness (6) may be
the cause of death.
There are a number of other causes of sudden death in athletes that are not related to cardiovascular
disease (7, 8). These are:
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Exercise-induced asthma and respiratory arrest
Exercise-induced anaphylaxis
Sarcoidosis
Malignant hyperthermia
Heat stroke
Sickle cell trait
Gastrointestinal bleeding
Rhabdomyolysis
Head trauma
Spine trauma (in pole vaulting)
Non-penetrating neck blow with rupture of cerebral artery (ice hockey)
Several deaths of athletes have been related to drug abuse. Although it is not possible to mention all
drugs that have been causally linked with sudden death in athletes, the most important (9) of them are:
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Ephedrine (Ma-Huang or herba ephedra)
Cocaine
Amphetamines
Anabolic steroids (oxymesterone, methandrostenolone, stanozol, etc)
Erythropoetin
Alcohol
Ergotamine derivatives
"Energy" drinks
There have been reports of sudden cardiac deaths related to vigorous exercise and starvation, semi-starvation
and liquid protein diets (9). It is believed that in those cases, severe weight loss results in a decrease of the
skeletal and the heart mass. Accompanying inflammation and also deficiencies in magnesium and potassium
may make the myocardium more susceptible to arrhythmias. An increase in sudden death and in QT interval
was associated with a liquid protein diet in a recent study (10). However, the rates of sudden death did not
increase in a medically supervised weight loss program.
Commotio Cordis or Innocent Chest Blow
A relatively modest and non-penetrating blow to the chest, in the absence of underlying cardiovascular disease
or injury to the chest wall itself may result in sudden cardiac death (5,11,12). On the athletic field, such an
event, referred to as Commotio Cordis (which means "disturbed or agitated heart motion"), is produced by an
object (i.e., ball) or by bodily collision with another athlete. A common scenario is that of a baseball player
struck in the chest while batting by a pitched ball thrown at approximately 40 mph from a distance of 40 feet
or farther. Catastrophes similar to this have occurred in a variety of sports (baseball, ice hockey, softball,
football, karate, lacrosse, boxing, rugby and soccer), including recreational activities at home and on the
playing field.
The precise mechanism responsible for the sudden death as the outcome of Commotio Cordis is not known
with complete certainty, but a recently developed animal model helped answer several key questions (13).
The model showed that a low-energy chest blow, when timed appropriately, creates devastating consequences
by triggering ventricular fibrillation. A very narrow window of 15-30 ms prior to the peak on the ascending side
of the T-wave on the ECG is a vulnerable phase of repolarization, and when the impact occurs in that interval,
or ventricular fibrillation develops instantaneously and reproducibly. When the impact occurs on the QRS
complex, transient or complete heart block, ventricular tachycardia develops.
Commotio Cordis is not uniformly fatal, and approximately 10% of the victims are known to have survived,
usually with prompt cardiopulmonary resuscitation and defibrillation. The Minneapolis Heart Institute
Foundation together with US Consumer Product Safety Commission (Dr. Susan B. Kyle, Ph.D.) maintains the
US Commotio Cordis Registry. If you have a case of Commotio Cordis that you would like to report to The
Registry, please click here. If you know of such a case, or know of a survivor of Commotio Cordis, please click
here to send an alert. For recent research in Commotio Cordis, click here.
Incidence and Prevalence of Sudden Death in Athletes
The precise frequency with which sudden death in athletes occurs remains unresolved. In the past, some
authors have suggested that the annual incidence of sudden deaths in young athletes is probably as low as 20
per year (14). These low estimates have placed a major obstacle on putting sudden death in athletes in its
proper perspective. The most recent survey of collections of newspaper articles for the year 2000 indicates
that the occurrence of these catastrophes is at least 7-10 times higher than previously believed. Estimates
range from 1 in 15,000 joggers to 1 in 50,000 marathoners, representing 1 death per 50,000 to 375,000 manhours of exercise (15). There are approximately 10 million joggers in the United States. Therefore, the number
of deaths related to jogging could potentially be several hundreds per year. In addition, surveying media may
grossly underestimate the true prevalence of this phenomenon, since the recognition of these events is not
systematic and mostly accounts for elite or well-known athletes and those in high-visibility sports, as well as
events that occur at athletic contests and draw the attention of the community. In contrast, deaths of nonelite athletes in many circumstances are probably less likely to achieve public recognition in the mainstream
press and are more likely to escape reporting.
To approach estimating the prevalence of these events over several years in a systematic way and to better
determine the causes of sudden death in athletes, along with other observations relating to these events, the
Minneapolis Heart Institute Foundation, with the support of the sponsors has established The US National
Registry of Sudden Death in Athletes. For more on The Registry, click here.
Distribution of Sudden Death Events in Athletes
Observations of distribution of sudden death in athletes are derived from the article by Barry J. Maron, MD;
Jamshid Shirani, MD; Liviu C. Poliac, MD; Robert Mathenge, MD; William C. Roberts, MD; Frederick O. Mueller,
PhD entitled "Sudden Death in Young Competitive Athletes" published in the Journal of the American Medical
Association in 1996 (JAMA 1996;276:199-204). A total of 158 sudden deaths that occurred in young
competitive athletes from 1985 to 1995 was analyzed. The athletes were identified from the news media
reports, the National Center for Catastrophic Sports Injury Research Registry, the Cardiovascular Pathology
Registry of Baylor University Medical Center, and reports from high school and colleges. In this study, only
15% of the athletes were female. This fact may be explained by lower participation rates of females and/or
less intensive demands of training, but could also originate from a lesser recognition of HCM in women (16).
You can view the occurrence of sudden cardiac death in athletes by the type of sport, hour of day and month
of year.
The article by Barry J. Maron, MD; Kevin P. Carney, BS; Harry M. Lever, MD; Jannet F. Lewis, MD; Ivan Barac,
MD; Susan A. Casey, RN and Mark Sherrid, MD entitled "Relationship of Race to Sudden Death in Competitive
Athletes with Hypertrophic Cardiomyopathy" and published in the Journal of the American College of
Cardiology (J Amer Coll Cardiol 2003;41:974-80) reported the relationship of race to the prevalence of
cardiovascular disease causing sudden death and compared the findings with a representative multi-center
hospital-based cohort of patients with HCM. You can view that information by clicking here.
Proposed Mechanisms of Sudden Death in Athletes
Exercise in general, and regular short-term exercise in particular, produce a significant increase in heart rate,
contractility of the heart and increase cardiac output and oxygen consumption. Numerous research studies
showed that regular exercise has multiple health benefits that go beyond increase in fitness (i.e.,
improvements in lipid profile, weight loss, reduction of insulin resistance and the risk of type 2 diabetes,
cardiovascular disease in general, including the risk of myocardial infarction, heart failure, and death caused
by cardiovascular disease). The National Institute of Health recommends a goal of 30 minutes of moderate
activity every day of the week (17). Regular physical activity has been put forward as one of the critical
components of the Healthy People 2010 initiative.
However, systemic training in endurance (dynamic, aerobic) or isometric sports (static, power) has been
known to increase cardiac mass and dimensions, and trigger structural remodeling in many athletes (18-22).
This form of hypertrophy is physiologic and is regarded as an adaptation to systematic athletic training, and
therefore was termed "athlete’s heart." The changes include enlargement of left and right ventricles and left
atrium; however the function of the heart remains preserved. Physiologic increases in cardiac mass vary in
magnitude according to sporting discipline. For example, the most extreme cavity dimensions and/or wall
thickness have been reported with rowing, cross-country skiing, cycling and swimming. Weight lifting and
wrestling have been associated with abnormal increases in left ventricular wall thickness disproportionate to
cavity size. Comparative chart guides the diagnosis between HCM and athlete’s heart. Extreme alterations in
cardiac dimensions evident in some athletes have unavoidably raised concern of whether such exercise-related
adaptations are truly physiologic, especially when present for the long periods of time. For example,
approximately 15 percent of trained athletes have striking left ventricular cavity enlargement. A longitudinal
echocardiographic study showed incomplete reversal with substantial residual chamber dilatation on 20
percent retired, deconditioned athletes (21). While firm evidence is presently lacking, one cannot exclude with
certainty that such extreme ventricular remodeling due to intense conditioning may have adverse
consequences over long time periods (20, 23).
In hypertrophic cardiomyopathy, intense training and the strain of competition, which increase physiologic
demands on the heart, produce alterations in electrolytes, blood volume and levels of hydration and
together increase sympathetic tone and withdrawal of parasympathetic tone. Multiple interactions of those
factors with the hypertrophied myocardium and the disarray of myocardial fibers act as triggers for potentially
lethal ventricular arrhythmias (24). Also, increased myocardial mass and insufficient regional perfusion during
high-intensity exercise cause myocardial ischemia, and over time, replacement fibrosis, both of which may act
as independent triggers of arrhythmias. In fact, patients with HCM that survived a sudden death had a very
high incidence of inducible ischemia on thallium stress-testing (25). In addition, lack of appropriate blood
pressure and heart rate response to exercise may act as the initial event cascading into a hemodynamic
collapse with loss of consciousness. Finally, partial obstruction present at rest may increase twice as high with
intense physical exercise compared to levels at baseline (26), which can potentially result in myocardial
ischemia, hemodynamic compromise and arrhythmias. Autopsy, histological and microscopic studies, and
sometimes biochemical tests establish a post-mortem diagnosis of HCM. To see a representational sample of a
gross heart specimen and histological studies, click here.
In congenital anomalies, each variation of normal anatomy may have its specific mechanism of induction of
hemodynamic compromise and/or lethal arrhythmias. There are several common mechanisms. For example, in
coronary anomalies, either the expansion of the aorta or pulmonary arteries from the increased stroke volume
changes the take-off angle of the artery and, as a consequence, the artery may become compressed
(2,22,27). The compression of the arterial lumen may only be present at vigorous exercise. Anatomic variance
known as “bridging” has largely similar mechanics, except the exact location is more distal in the vessel but
not at the origin. The events in the myocardium responsible for sudden death in these pathologies are rather
complex. However, myocardial ischemia, especially if it occurs repeatedly, is believed to play a major role
(2,22,27). Absence of a coronary artery results in decreased perfusion of the myocardium and prolonged
episodes of acute ischemia, which are sufficient enough to trigger ventricular fibrillation.
Sudden death in Marfan’s syndrome most commonly arises as a result of complications of the disease, such
as rupture of the ascending aorta. In arrhythmogenic right ventricular cardiomyopathy, CPVT and
selective cases of MVP, although heterogeneous from the standpoint of molecular pathophysiology, electrical
instability of the myocardium at peak exercise may induce ventricular fibrillation and then sudden death.
WPW, Brugada and Long QT syndromes may be responsible for sudden death with or without exercise. For
example, in WPW syndrome, the most frequent complication is rapid atrial fibrillation with a rapid ventricular
response, which may lead to cardiac arrest. Ventricular tachycardia and fibrillation may be easily inducible in
individuals with Brugada syndrome, especially under the influence of elevated body temperature, cocaine and
some other illicit drugs (28). Long QT syndromes resulted in sudden death, which related to exercise, although
forms that were linked to emotional stress, and also unrelated to either have been reported (29).
Myocarditis is associated with inflammatory infiltration of the myocardium, and sometimes with systemic
inflammation. Illicit drug use is sometimes associated with myocarditis. Dilated cardiomyopathy with
reduced cardiac function can result from myocarditis. With either myocarditis or dilated cardiomyopathy, small
vessel ischemia resulting from decreased regional perfusion may be an excellent substrate for ventricular
arrhythmias which can cause sudden death.
Exercise can induce coronary vasospasm, which can cause acute coronary syndrome with subsequent
arrhythmias leading to hemodynamic collapse and sudden death, all unfolding in a matter of minutes. As the
artery dilates with exercise, some segments that have atherosclerotic plaque rupture under high sheer stress
and coronary occlusion develops secondary to platelet aggregation. In some individuals exhibiting a
particularly augmented blood pressure response to exercise, platelets may hyper-aggregate in response to
increased circulating norepinephrine. The result of a coronary occlusion is acute myocardial ischemia, which
then may serve as a substrate for a lethal arrhythmia. Sudden deaths in athletes that are linked to acute
coronary syndrome in presence of coronary artery disease occur mostly in older (over the age of 35) athletes
and rarely happen in individuals younger than 30 years of age. The scenario of a sudden death related to
coronary artery disease and/or coronary spasm is especially real in men over 45 years of age with concomitant
hypertension and obesity that subject themselves to episodic high-intensity exercise and do not participate in
regular, medically supervised exercise programs. However, recent associations of cocaine use and acute
coronary syndrome (30) steer towards recognition of coronary complications of illicit drugs in younger
individuals.
Abnormalities of the conduction system, which include fibrosis and fatty infiltration within very small regions of
the myocardium or reside in the pericardium may be responsible for various heart blocks and
bradyarrhythmias, which occasionally may result in cardiac arrest, collapse, loss of consciousness and
death.
Changes that trigger sudden death related to drug abuse are in most cases specific to the class of drugs
involved. However, most commonly, increase in heart rate, blood pressure, contractility and oxygen demand,
together with induced prolongation of the QT interval and interference with repolarization, have the ability to
trigger ventricular tachycardia or Torsades de Pointes transforming into ventricular fibrillation. Such a scenario
holds true for abuse of ephedrine, cocaine, amphetamine- and cannabinoid- derivatives and “energy” drinks.
Acute coronary syndrome (see above) has also been associated with cocaine and anabolic steroid use,
although the former is more predominant than the latter. Anabolic steroids have been reported to increase
myocardial mass and induce hypertension, probably secondary to mineralocorticoid effect. In addition,
hyperaggregation of platelets and subsequent thrombosis were described (31-33).
The mechanisms associated with dieting combined with prolonged exertion resulting in sudden death are
not completely understood at the present time. Deficiency of magnesium, potassium and copper that occur
with weight loss may result in the electrical instability of the myocardium (34). In addition, rapid weight loss
may cause a loss of ATPase and development of insulin resistance (35), which could make the myocardium
more sensitive to norepinephrine. This information may be important for the athletes that are engaging in
weight loss combined with prolonged physical training and consumption of performance-enhancing
supplements.
New research is now underway that is addressing distinct molecular mechanisms of sudden death in HCM,
arrhythmogenic right ventricular cardiomyopathy, CPVT and heart failure with preliminary data showing that in
each distinct pathology there may be a separate mutation or the cluster of cellular abnormalities that may be
responsible for the eventual sudden death (36,37,38).
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