Year : 2010  |  Volume : 3  |  Issue : 2  |  Page : 107--112

Sudden cardiac death in children and adolescents (excluding Sudden Infant Death Syndrome)

Kelly K Gajewski1, Philip J Saul2,  
1 Department of Pediatrics, Louisiana State University School of Medicine, New Orleans, Louisiana, USA
2 Department of Pediatrics, Medical University of South Carolina, Charleston, South Carolina, USA

Correspondence Address:
Philip J Saul
Department of Pediatrics, Medical University of South Carolina, 165 Ashley Avenue, MSC 915, Charleston, SC 29425


Sudden death in the young is rare. About 25% of cases occur during sports. Most young people with sudden cardiac death (SCD) have underlying heart disease, with hypertrophic cardiomyopathy and coronary artery anomalies being commonest in most series. Arrhythmogenic right ventricular dysplasia and long QT syndrome are the most common primary arrhythmic causes of SCD. It is estimated that early cardiopulmonary resuscitation and widespread availability of automatic external defibrillators could prevent about a quarter of pediatric sudden deaths.

How to cite this article:
Gajewski KK, Saul PJ. Sudden cardiac death in children and adolescents (excluding Sudden Infant Death Syndrome).Ann Pediatr Card 2010;3:107-112

How to cite this URL:
Gajewski KK, Saul PJ. Sudden cardiac death in children and adolescents (excluding Sudden Infant Death Syndrome). Ann Pediatr Card [serial online] 2010 [cited 2020 Nov 25 ];3:107-112
Available from:

Full Text


Excluding the Sudden Infant Death Syndrome (SIDS), which has an incidence around 1-1.5/1000 infants, sudden death in a young person is a rare event. Yet, it has a devastating impact when it occurs precisely because it is so unexpected. Sudden cardiac death (SCD) is defined as death that is abrupt, unexpected, and due to a cardiovascular cause. It is generally recognized as death that occurs within 1 hour from the onset of cardiovascular symptoms. However, in young people, it typically occurs within a few minutes of symptom onset. When resuscitation restores spontaneous circulation, it is referred to as "aborted sudden death." The estimated incidence of pediatric SCD ranges from 0.6 to 6.2 per 100,000 children in the United States. [1],[2],[3],[4],[5] Approximately 20-25% of the deaths occur during sports. [6] In patients with congenital heart disease, the numbers are higher and are estimated at 100 deaths per 100,000 patients. [7] In comparison, adults experience SCD at a rate of 400,000 per year (or 135/100,000 population). Since most sudden deaths have a cardiovascular cause, it is theoretically possible to identify the patients at risk prior to the event and prevent it.

 Etiologies of SCD in the Young

There are several known causes of sudden death in young people [Table 1]. These etiologies can be divided into two categories: arrhythmic and non-arrhythmic. The majority of SCD in young people occurs due to arrhythmic causes. These usually result in an abrupt loss of consciousness, with or without a sensation of palpitations. The arrhythmia may be proven or presumed. Non-arrhythmic etiologies result in circulatory collapse in the setting of an organized rhythm. Examples of the latter include congestive heart failure, embolic phenomena, or aneurysm ruptures. A variety of identifiable conditions have been associated with SCD in the young.{Table 1}

 High Risk Populations

Hypertrophic cardiomyopathy

Hypertrophic cardiomyopathy (HCM) is the most common cause of SCD in the United States in people 30 years old or younger. [8],[9] The disease prevalence has been estimated as high as 1 per 500 in young adults. [10],[11] It is typically non-obstructive and presents in mid to late adolescence. HCM is often clinically silent, but the ECG typically may show left ventricular hypertrophy or T-wave abnormalities. The diagnosis traditionally has been best confirmed by echocardiography. However, carriers of an HCM genetic mutation may have little or no hypertrophy, especially earlier in life. Associated sudden death is often exertional and is usually secondary to malignant ventricular arrhythmias. HCM is an autosomal dominant congenital disorder typically characterized by asymmetric septal hypertrophy and marked disarray of ventricular muscle fibers, which contribute to the risk of arrhythmias even in patients with minimal hypertrophy and no evident left ventricular outflow tract obstruction. HCM has been found to be caused by genetic abnormalities involving primarily sarcomeric contractile proteins (such as b-myosin and troponin T). However, there is marked genetic and phenotypic heterogeneity. To date, over 20 HCM-susceptibility genes have been identified, and penetrance has been estimated at 30-80%, based on the particular mutation. The Heart Failure Society of America's 2009 practice guidelines support genetic testing of the one most clearly affected person in a family to facilitate family screening and management (level of evidence A). Genetic testing even in clinically apparent disease may have prognostic significance. [12],[13],[14] Risk factors for sudden death in patients with HCM include septal thickness ≥30 mm, family history of sudden death, non-sustained VT, syncope, and hypotensive response to exercise. Restriction from most competitive athletics is recommended in patients with HCM. [15],[16]

Dilated cardiomyopathy

Although less common than HCM, dilated cardiomyopathy (DCM) is also a known cardiac risk factor for SCD. DCM is characterized by cardiac dilation and decreased systolic function. It can be acquired from ischemic injury, myocarditis or toxins, or it can be inherited, usually as an autosomal dominant trait, with variable penetrance. There are currently more than 20 different gene mutations identified that cause DCM. The genes responsible encode diverse myocyte proteins including those of the sarcomere, cytoskeleton, nucleus, sarcoplasmic reticulum, and the cell membrane. It is estimated that 20-50% of "idiopathic" DCM has a genetic basis. Although the disease is progressive and often clinically silent in childhood, SCD can occur prior to the development of heart failure and symptoms. Genetic testing may help to identify those at risk for sudden death prior to heart failure. Lamin A/C (LMNA) mutations are a relatively common cause of DCM (6-8% of all idiopathic DCM) and are associated with a high risk for SCD. In fact, a study in the New England Journal of Medicine in 2006 found 8 of 19 (42%) patients who underwent permanent pacing and internal cardioverter and defibrillator (ICD) implantation solely on the basis of LMNA gene mutations associated with cardiac conduction defects and normal ventricular function received an appropriate ICD intervention. [17]

Coronary artery anomalies

In the United States, coronary artery anomalies are the second most common cause of SCD in the young. The most common abnormality associated with SCD is origin of the left main coronary ostia from the right sinus of Valsalva when the coronary artery traverses between the aorta and the pulmonary artery. [18],[19],[20],[21],[22],[23],[24] Ischemia has been proposed to occur during exertion when the great vessels increase in size and compress the left main coronary artery. Although anomalous origin of the right coronary artery from the left sinus of Valsalva traversing between the aorta and pulmonary artery is far more common, [24],[25],[26],[27],[28] it seems to have a much lower association with SCD than the left coronary artery originating from the right sinus. Coronary artery anomalies are unlikely to be identified without imaging studies unless complaints of early fatigue, angina, or exercise-induced syncope lead to a directed evaluation. Further, coronary anomalies may be difficult to screen for with a routine echocardiogram.

Rarely, acquired premature coronary artery disease can appear in an athlete under age 30. Familial predisposition plus other risk factor prevalence can sometimes lead to coronary events resulting from typical atherosclerosis. Attention to risk factors, such as a strong family history, and to the early symptoms of ischemia, angina and other effort-related symptoms should be pursued in younger athletes as in older athletes.

Arrhythmic channelopathies and primary arrhythmias

A variety of relatively rare conditions can cause primary arrhythmias in young people [Table 2]. Although there are cases where SCD is the first symptom with these conditions, recurrent syncope often precedes more malignant symptoms. Fortunately, the surface 12-lead ECG is abnormal in most of these conditions. So a minimal evaluation of an ECG and a careful history are indicated for recurrent syncope, and have been advocated as screening tests for athletes by many investigators [29] and several organizations. [29],[30]{Table 2}

Long QT syndrome

The congenital form of the long QT syndrome (LQTS) is a familial genetic disorder that occurs in about 1 in 2500-3500 individuals. [31] It manifests primarily as ventricular repolarization abnormalities caused by cardiac ion channel mutations. For symptomatic patients, the presenting symptom is usually syncope, which is due to the form of ventricular tachycardia known as "torsades de pointes." The syncope may occur with specific triggers, such as stress, swimming, and loud auditory stimuli, or it may occur when the child is relatively bradycardic, as during rest or sleep. In most cases, the corrected QT interval is prolonged, but there is considerable overlap with the normal distribution of QT intervals in the healthy population. In fact, 15-25% of patients with LQTS may have a QTc that falls within the "normal range." [32] This has made clinical diagnosis difficult. In 1993, Peter Schwartz developed a set of diagnostic criteria that combined ECG and clinical criteria into a point system to aid in the diagnosis of LQTS. [33] Family history of LQTS or sudden unexplained cardiac death are important factors in these criteria. However, points are also given for syncope, which occurs in up to 30% of the healthy population, and for QTc >450, which can be found in 2-5% of the healthy population. Further clinical evaluation of the QT interval during exercise or with epinephrine infusion can aid in the diagnosis, as QTc prolongation may become more exaggerated at increased heart rates as the QT interval fails to shorten in some patients. There are a variety of genetic abnormalities of ion channels which have now been identified, and it is estimated that up to 80% of patients with a high index of suspicion for LQTS have a mutation in one of the known LQTS genes. [34],[35] The specific phenotype may be predicted from the genetic mutation found and may aid in the assessment of risk for sudden death or response to therapy. [36] Currently, the mainstay of therapy remains beta-blockade, which prevents severe symptoms and sudden death in most cases, but may be less effective for LQTS3. If symptoms recur on beta-blocker therapy, implantation of an ICD is generally considered indicated. [37]

Catecholaminergic polymorphic ventricular tachycardia

Catecholaminergic polymorphic ventricular tachycardia (CPVT) is characterized by ventricular ectopy induced by exercise or emotional stress. [38] It is a genetic channelopathy, most commonly caused by mutations of the ryanodine receptor gene (RYR2) which encodes a sarcoplasmic calcium ion channel. [39] The onset of CPVT symptoms typically occurs in childhood and adolescence. Exercise stress testing is important for diagnosis, since CPVT cannot be diagnosed on surface ECG. During exercise stress testing, ectopy is enhanced at greater levels of activity and often a "bidirectional" VT with a beat-to-beat 180΀ rotation of the QRS complex is observed. If left untreated, CPVT is lethal in 30-50% of patients. Although beta-blockers are the recommended therapy, many patients will continue to have arrhythmic symptoms and may need to have an ICD placed.

Brugada's syndrome

Brugada's syndrome is an inherited arrhythmogenic syndrome characterized by specific ECG abnormalities and life-threatening ventricular arrhythmias. [40] It commonly presents in men in the fourth decade as syncope and ventricular arrhythmias. The characteristic ECG findings are coved or saddle-back ST-segment elevation in leads V1-V3 with complete or incomplete right bundle branch block and T-wave inversion. The ECG abnormalities may not be evident until unmasked by an infusion of a sodium channel blocker (flecainide, ajmaline or procainamide). A handful of genetic mutations have been discovered to cause Brugada's syndrome; however, SCN5A is the most commonly occurring defect. Treatment is limited to ICD implantation.

Arrhythmogenic right ventricular dysplasia

Arrhythmogenic right ventricular dysplasia or cardiomyopathy (ARVD/ARVC) is a rare cause of SCD in the United States, but has been reported as the most common cause of SCD in the young athletes in Italy. [41] Clinical presentation typically occurs in early adolescence to young adulthood. It is a heritable, progressive cardiomyopathy characterized by fatty and fibrous replacement of the myocardium, classically causing thinning of the right ventricular (RV) free wall. However, biventricular and left-dominant patterns are now being recognized. [42],[43] It is also characterized by electrical instability, and patients may present with a variety of ventricular arrhythmias, which are often provoked by exercise. The diagnosis is often difficult to make clinically. The RV changes are very hard to detect by echocardiography, but if suspicion is high, it can be detected by RV angiography and magnetic resonance imaging (MRI). [44] The resting ECG may be mildly abnormal with ventricular premature beats with a left bundle morphology, T-wave inversion in leads V2 and V3, a so-called epsilon wave following the QRS in lead V1, and a wide QRS in leads V1-V3. Genetic testing may aid in the diagnosis, particularly if there is a strong family history. Although both drug therapy and catheter ablation are occasionally successful, implantation of an ICD is usually recommended for patients with significant symptoms.

Other causes

Commotio cordis

Commotio cordis, defined as SCD due to a relatively innocent chest wall impact in individuals with a normal heart, is a very rare cause of SCD in young people, although it may be underestimated in its frequency. [45],[46] Victims are typically males less than 18 years of age. Commotio cordis requires a blow directly over the heart, exquisitely timed to within a narrow 10-30 msec window just before the T-wave peak during the vulnerable phase of repolarization. [47] Collapse may occur immediately or after light-headedness for a period of few seconds. When an initial rhythm is documented, it is usually ventricular fibrillation. Only about 25-35% of commotio cordis victims survive, usually associated with timely cardiopulmonary resuscitation (CPR) and defibrillation. Since most reported cases have occurred in sports such as baseball, it had been thought that prevention could be best accomplished by a combination of chest protectors and reduced impact force baseballs. However, these interventions are proving inadequate for prevention of sudden deaths from commotio cordis in recent studies. [48],[49]

Congenital heart disease

The incidence of sudden death in patients with congenital heart disease is about 100/100,000 patient years. [50] It is highest in cyanotic and left heart obstructive lesions and may be due to arrhythmic, embolic, or circulatory phenomenon. The risk of sudden death appears to increase with age and time since surgery. Certain congenital defects have a high associated risk of acquired arrhythmias following repair. Specifically, tetralogy of Fallot is associated with higher incidence rates of known ventricular tachycardia and intra-atrial re-entry tachycardia and a 0.5-6% risk of SCD. Patients with both single-ventricle physiology status-post Fontan, and transposition of the great arteries status-post atrial switch (Senning or Mustard) also have high acquired arrhythmia rates with increased incidence of SCD.

 Screening for SCD Risk in the Young

As reviewed above, sports participation has been associated with an increased risk of SCD in young people. Therefore, cardiovascular screening for conditions that could lead to an increased risk of sudden death has focused mainly on the pre-participation screening of athletes. In the United States, current recommendations are for a focused personal and family history of the athlete with special emphasis on history of exertional chest pain, syncope or a family history of early sudden death, as well as examination for blood pressure, murmurs, and stigmata of Marfan's syndrome. [51] If any abnormalities are found, additional studies are initiated to systematically exclude known causes of sudden death. A relatively intense debate has been ensuing over the effectiveness of universal electrocardiogram (ECG) screening for athletes and/or all infants. [30] For the past 25 years in Italy, all athletes have undergone ECG) screening, with some data indicating fewer deaths during athletic activities associated with institution of the screening program. [29],[52] Although the reduction in SCD has been related to disqualification of young people found to have HCM, ARVC and other rare abnormalities, the current reported rate of SCD (about 0.8/100,000 per year) [52] is not very different from that reported for unscreened athletes in the United States. [53] These data and the relatively large number of estimated eligible athletes in the United States that would require screening (10-12 million) have led to the current recommendations against universal ECG screening in the US. The cost of the ECG and its interpretation, in addition to further testing due to frequent false positive results, has been determined to have an unfavorable cost-benefit ratio. However, new guidelines are currently being vetted and the situation may change as more data are available.

 General Treatment and Prevention of SCD in the Young

Although each of the conditions discussed above have specific therapies, the most effective immediate treatment to change SCD into resuscitated SCD is to increase the prevalence of CPR training in the general population, and the availability of automatic external defibrillators (AEDs). AEDs are best located in places where large groups of people gather, including where young athletes may be competing. Such devices have continued to decrease in cost and have improved ease of use, but financial and other barriers still remain to their widespread deployment.

For survivors of near SCD events, systematic evaluation should be performed to determine the cause of the event and treatment should be focused around the underlying etiology. For many of the underlying cardiac pathologies, an ICD is indicated.


Sudden death in the young is rare. About 25% of cases occur during sports. Most young people with SCD have underlying heart disease, with HCM and coronary artery anomalies being most common in most series. ARVD and LQTS are the most common primary arrhythmic causes of SCD. It is estimated that early CPR and widespread availability of AEDs could prevent about 25% of pediatric sudden deaths.


1Botvinick EH, Dae MW, Krishnan R, Ewing S. Hypertrophic cardiomyopathy in the young: Another form of ischemic cardiomyopathy? J Am Coll Cardiol 1993;22:805-7.
2Garson A Jr. Sudden death in the young. Hosp Pract (Off Ed) 1991;26:51-60.
3Gow RM. Sudden cardiac death in the young. Can J Cardiol 1996;12:1157-60.
4Liberthson RR. Sudden death from cardiac causes in children and young adults. N Engl J Med 1996;334:1039-44.
5Driscoll DJ, Edwards WD. Sudden unexpected death in children and adolescents. J Am Coll Cardiol 1985;5:118B-21.
6O'Connor FG, Kugler JP, Oriscello RG. Sudden death in young athletes: Screening for the needle in a haystack. Am Fam Physician 1998;57:2763-70.
7Silka MJ. Sudden death due to cardiovascular disease during childhood. Pediatr Ann 1991;20:360-7.
8Maron BJ, Shirani J, Poliac LC, Mathenge R, Roberts WC, Mueller FO. Sudden death in young competitive athletes. Clinical, demographic, and pathological profiles. JAMA 1996;276:199-204.
9Keren G. Etiology of sudden death in healthy active subjects. Isr J Med Sci 1989;25:607-9.
10Corrado D, Basso C, Schiavon M, Thiene G. Screening for hypertrophic cardiomyopathy in young athletes. N Engl J Med 1998;339:364-9.
11Maron BJ, Thompson PD, Puffer JC, McGrew CA, Strong WB, Douglas PS, et al. Cardiovascular preparticipation screening of competitive athletes. A statement for health professionals from the Sudden Death Committee (clinical cardiology) and Congenital Cardiac Defects Committee (cardiovascular disease in the young), American Heart Association. Circulation 1996;94:850-6.
12Keren A, Syrris P, McKenna WJ. Hypertrophic cardiomyopathy: The genetic determinants of clinical disease expression. Nat Clin Pract Cardiovasc Med 2008;5:158-68.
13Bahl OP, Massie E. Electrocardiographic and vectorcardiographic patterns in cardiomyopathy. Cardiovasc Clin 1972;4:95-112.
14Ackerman MJ. Genetic testing for risk stratification in hypertrophic cardiomyopathy and long QT syndrome: Fact or fiction? Curr Opin Cardiol 2005;20:175-81.
15Maron BJ, Chaitman BR, Ackerman MJ, Bayιs de Luna A, Corrado D, Crosson JE, et al. Recommendations for physical activity and recreational sports participation for young patients with genetic cardiovascular diseases. Circulation 2004;109:2807-16.
16Mitten MJ, Maron BJ, Zipes DP. Task Force 12: Legal aspects of the 36th Bethesda Conference recommendations. J Am Coll Cardiol 2005;45:1373-5.
17Meune C, Van Berlo JH, Anselme F, Bonne G, Pinto YM, Duboc D. Primary prevention of sudden death in patients with lamin A/C gene mutations. N Engl J Med 2006;354:209-10.
18Liberthson RR, Dinsmore RE, Fallon JT. Aberrant coronary artery origin from the aorta. Report of 18 patients, review of literature and delineation of natural history and management. Circulation 1979;59:748-54.
19Vetter VL. Sudden death in infants, children, and adolescents. Cardiovasc Clin 1985;15:301-13.
20Phillips M, Robinowitz M, Higgins JR, Boran KJ, Reed T, Virmani R. Sudden cardiac death in Air Force recruits. A 20-year review. JAMA 1986;256:2696-9.
21Corrado D, Thiene G, Cocco P, Frescura C. Non-atherosclerotic coronary artery disease and sudden death in the young. Br Heart J 1992;68:601-7.
22Nakamura CT, Canete DR, Lau JM. A review of the anomalous origin of the left coronary artery from the anterior sinus of Valsalva: Is prevention possible? Hawaii Med J 1993;52:294-9.
23Lipsett J, Cohle SD, Berry PJ, Russell G, Byard RW. Anomalous coronary arteries: A multicenter pediatric autopsy study. Pediatr Pathol 1994;14:287-300.
24Taylor AJ, Byers JP, Cheitlin MD, Virmani R. Anomalous right or left coronary artery from the contralateral coronary sinus: <> abnormalities in the initial coronary artery course and heterogeneous clinical outcomes. Am Heart J 1997;133:428-35.
25Maron BJ, Roberts WC, McAllister HA, Rosing DR, Epstein SE. Sudden death in young athletes. Circulation 1980;62:218-29.
26Chadow H, Kwan T, Huber M, Feit A. Anomalous origin of the right coronary artery above the left posterior sinus of Valsalva associated with a normal aortic valve. A case history. Angiology 1994;45:963-6.
27Ghosh PK, Agarwal SK, Kumar R, Chandra N, Puri VK. Anomalous origin of right coronary artery from left aortic sinus. J Cardiovasc Surg 1994;35:65-70.
28Rinaldi RG, Carballido J, Giles R, Del Toro E, Porro R. Right coronary artery with anomalous origin and slit ostium. Ann Thorac Surg 1994;58:829-32.
29Corrado D, Pelliccia A, Bjψrnstad HH, Vanhees L, Biffi A, Borjesson M, et al. Cardiovascular pre-participation screening of young competitive athletes for prevention of sudden death: Proposal for a common European protocol. Consensus Statement of the Study Group of Sport Cardiology of the Working Group of Cardiac Rehabilitation and Exercise Physiology and the Working Group of Myocardial and Pericardial Diseases of the European Society of Cardiology. Eur Heart J 2005;26:516-24.
30Pelliccia A, Zipes DP, Maron BJ. Bethesda Conference #36 and the European Society of Cardiology Consensus Recommendations revisited a comparison of U.S. and European criteria for eligibility and disqualification of competitive athletes with cardiovascular abnormalities. J Am Coll Cardiol 2008;52:1990-6.
31Schwartz PJ, Stramba-Badiale M, Crotti L, Pedrazzini M, Besana A, Bosi G, et al. Prevalence of the congenital long-QT syndrome. Circulation 2009;120:1761-7.
32Vincent GM, Timothy KW, Leppert M, Keating M. The spectrum of symptoms and QT intervals in carriers of the gene for the long-QT syndrome. New Engl J Med 1992;327:846-52.
33Schwartz PJ, Moss AJ, Vincent GM, Crampton RS. Diagnostic criteria for the long QT syndrome. An update. Circulation 1993;88:782-4.
34Tester DJ, Ackerman MJ. Genetic testing for cardiac channelopathies: Ten questions regarding clinical considerations for heart rhythm allied professionals. Heart Rhythm 2005;2:675-7.
35Tester DJ, Will ML, Haglund CM, Ackerman MJ. Compendium of cardiac channel mutations in 541 consecutive unrelated patients referred for long QT syndrome genetic testing. Heart Rhythm 2005;2:507-17.
36Schwartz PJ, Priori SG, Spazzolini C, Moss AJ, Vincent GM, Napolitano C, et al. Genotype-phenotype correlation in the long-QT syndrome: Gene-specific triggers for life-threatening arrhythmias. Circulation 2001;103:89-95.
37Schwartz PJ, Spazzolini C, Priori SG, Crotti L, Vicentini A, Landolina M, et al. Who are the long-QT syndrome patients who receive an implantable cardioverter-defibrillator and what happens to them?: Data from the European Long-QT Syndrome Implantable Cardioverter-Defibrillator (LQTS ICD) Registry. Circulation 2010;122:1272-82.
38Leenhardt A, Lucet V, Denjoy I, Grau F, Ngoc DD, Coumel P. Catecholaminergic polymorphic ventricular tachycardia in children. A 7-year follow-up of 21 patients. Circulation 1995;91:1512-9.
39Tester DJ, Arya P, Will M, Haglund CM, Farley AL, Makielski JC, et al. Genotypic heterogeneity and phenotypic mimicry among unrelated patients referred for catecholaminergic polymorphic ventricular tachycardia genetic testing. Heart Rhythm 2006;3:800-5.
40Vincent GM. The Long QT and Brugada syndromes: Causes of unexpected syncope and sudden cardiac death in children and young adults. Semin Pediatr Neurol 2005;12:15-24.
41Corrado D, Basso C, Thiene G. Arrhythmogenic right ventricular cardiomyopathy: An update. Heart 2009;95:766-73.
42Sen-Chowdhry S, Syrris P, Ward D, Asimaki A, Sevdalis E, McKenna WJ. Clinical and genetic characterization of families with arrhythmogenic right ventricular dysplasia/cardiomyopathy provides novel insights into patterns of disease expression. Circulation 2007;115:1710-20.
43Sen-Chowdhry S, Syrris P, McKenna WJ. Role of genetic analysis in the management of patients with arrhythmogenic right ventricular dysplasia/cardiomyopathy. J Am Coll Cardiol 2007;50:1813-21.
44Sen-Chowdhry S, Prasad SK, Syrris P, Wage R, Ward D, Merrifield R, et al. Cardiovascular magnetic resonance in arrhythmogenic right ventricular cardiomyopathy revisited: Comparison with task force criteria and genotype. J Am Coll Cardiol 2006;48:2132-40.
45Maron BJ, Gohman TE, Kyle SB, Estes NA 3 rd , Link MS. Clinical profile and spectrum of commotio cordis. JAMA 2002;287:1142-6.
46Maron BJ, Link MS, Wang PJ, Estes NA 3 rd . Clinical profile of commotio cordis: An under appreciated cause of sudden death in the young during sports and other activities. J Cardiovasc Electrophysiol 1999;10:114-20.
47Link MS, Wang PJ, Pandian NG, Bharati S, Udelson JE, Lee MY, et al. An experimental model of sudden death due to low-energy chest-wall impact (commotio cordis). N Engl J Med 1998;338:1805-11.
48Weinstock J, Maron BJ, Song C, Mane PP, Estes NA 3 rd , Link MS. Failure of commercially available chest wall protectors to prevent sudden cardiac death induced by chest wall blows in an experimental model of commotio cordis. Pediatrics 2006;117:e656-62.
49Doerer JJ, Haas TS, Estes NA 3 rd, Link MS, Maron BJ. Evaluation of chest barriers for protection against sudden death due to commotio cordis. Am J Cardiol 2007;99:857-9.
50Silka MJ, Hardy BG, Menashe VD, Morris CD. A population-based prospective evaluation of risk of sudden cardiac death after operation for common congenital heart defects. J Am Coll Cardiol 1998;32:245-51.
51Maron BJ, Thompson PD, Puffer JC, McGrew CA, Strong WB, Douglas PS, et al. Cardiovascular preparticipation screening of competitive athletes. A statement for health professionals from the Sudden Death Committee (clinical cardiology) and Congenital Cardiac Defects Committee (cardiovascular disease in the young), American Heart Association. Circulation 1996;94:850-6.
52Corrado D, Basso C, Pavei A, Michieli P, Schiavon M, Thiene G. Trends in sudden cardiovascular death in young competitive athletes after implementation of a preparticipation screening program. JAMA 2006;296:1593-601.
53Maron BJ, Doerer JJ, Haas TS, Tierney DM, Mueller FO. Sudden deaths in young competitive athletes: Analysis of 1866 deaths in the United States, 1980-2006. Circulation 2009;119:1085-92.