SCD is defined as unexpected, non-traumatic cardiac death within one hour of symptom onset in an individual with no known potentially lethal cardiovascular condition. It may be due to various causes, which are conventionally divided into congenital abnormalities (structural or electrical), which are more common in individuals aged under 35, and acquired abnormalities, which are more frequent after the age of 351,3,6,9,10 (Figure 1). The main causes of SCD vary depending on the athlete's age and geographical region, due to genetic and environmental factors; for example, in the USA the most common cause of SCD in individuals aged under 35 is hypertrophic cardiomyopathy (HCM), followed by congenital coronary artery anomalies,1,11,12 while in Italy arrhythmogenic right ventricular dysplasia (ARVD) is the most prevalent cause (Figure 2).13 In athletes aged over 35, the leading cause of SCD is atherosclerotic coronary artery disease.14

Figure 1.

Structural, electrical and acquired abnormalities associated with sudden cardiac death in athletes. Adapted from Chandra et al.1

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ARVD: arrhythmogenic right ventricular dysplasia; AS: aortic stenosis; CAAC: congenital coronary artery anomalies; CAD: coronary artery disease; CSD: conduction system disease; DCM: dilated cardiomyopathy; HCM: hypertrophic cardiomyopathy; LAD: left anterior descending artery; LVH: left ventricular hypertrophy; MVP: mitral valve prolapse; WPW: Wolff-Parkinson-White syndrome.'> ARVD: arrhythmogenic right ventricular dysplasia; AS: aortic stenosis; CAAC: congenital coronary artery anomalies; CAD: coronary artery disease; CSD: conduction system disease; DCM: dilated cardiomyopathy; HCM: hypertrophic cardiomyopathy; LAD: left anterior descending artery; LVH: left ventricular hypertrophy; MVP: mitral valve prolapse; WPW: Wolff-Parkinson-White syndrome.' title='Causes of sudden cardiac death in athletes in the USA and Italy. (A) Distribution of cardiovascular causes of sudden death in 1435 young competitive athletes. From the Minneapolis Heart Institute Foundation Registry, 1980–2005 (adapted from Maron et al.12,20). (B) Causes of sudden death in athletes in the Veneto region, Italy, 1979–1999 (adapted from Corrado et al.13). ARVD: arrhythmogenic right ventricular dysplasia; AS: aortic stenosis; CAAC: congenital coronary artery anomalies; CAD: coronary artery disease; CSD: conduction system disease; DCM: dilated cardiomyopathy; HCM: hypertrophic cardiomyopathy; LAD: left anterior descending artery; LVH: left ventricular hypertrophy; MVP: mitral valve prolapse; WPW: Wolff-Parkinson-White syndrome.'/>

Figure 2.

Causes of sudden cardiac death in athletes in the USA and Italy. (A) Distribution of cardiovascular causes of sudden death in 1435 young competitive athletes. From the Minneapolis Heart Institute Foundation Registry, 1980–2005 (adapted from Maron et al.12,20). (B) Causes of sudden death in athletes in the Veneto region, Italy, 1979–1999 (adapted from Corrado et al.13). ARVD: arrhythmogenic right ventricular dysplasia; AS: aortic stenosis; CAAC: congenital coronary artery anomalies; CAD: coronary artery disease; CSD: conduction system disease; DCM: dilated cardiomyopathy; HCM: hypertrophic cardiomyopathy; LAD: left anterior descending artery; LVH: left ventricular hypertrophy; MVP: mitral valve prolapse; WPW: Wolff-Parkinson-White syndrome.

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There is no consensus on how to combat SCD, mainly because of a lack of evidence of its true incidence either in the general population or in athletes or of the frequency of the different causes; there are also few data on the sensitivity and specificity of the electrocardiogram (ECG) for detecting pathological cases. This lack of data, together with the rarity of the event, makes use of the ECG in preparticipation screening difficult to implement, since the process must be cost-effective.

Studies on the incidence of SCD report varying figures (Table 1), mainly due to different methods for collecting information on deaths; in some cases this is limited to media reports or insurance claims, while in others the source is official government records.3,15 A prospective observational study in Italy, where preparticipation ECG screening and reporting of SCD are obligatory, revealed an incidence of 3.6/100000 athletes, a similar figure to that reported in more recent studies in the USA.3,16–18

On the basis of such studies, Italy began to include an ECG in preparticipation screening as well as physical examination and clinical history, resulting in a decrease of 89% in SCD in athletes between 1979 and 2004.9,18,19 In the USA, the recommendations of the American Heart Association (AHA) for preparticipation cardiovascular screening of competitive athletes include only medical history and physical examination, citing the high number of false positives and low cost-effectiveness of large-scale ECG screening programs. The ESC, on the other hand, while not stipulating that ECG assessment is mandatory, recommends it in all athletes (Table 2).

In 60%–80% of athletes the ECG shows changes from what is considered normal,5,21 due to cardiac remodeling, both mechanical and electrical, known as athlete's heart, which gives rise to the large number of false positives in some studies. This phenomenon results from physiological adaptation of the autonomic nervous system, with increased vagal tone and decreased sympathetic tone, and changes in cardiac dimensions, including increased left ventricular (LV) wall thickness and LV cavity size, which may be reflected on ECG and echocardiography. This remodeling permits enhanced filling of the left ventricle in diastole and augmentation of stroke volume, allowing generation of a large and sustained cardiac output even at rapid heart rates.1,21Table 3 summarizes the ECG alterations considered normal in athletes.10 Various studies have also shown that there is considerable variability in ECG patterns between genders, ages, ethnicities and types of sport.4,21–30

The guidelines take into consideration the bias due to athlete's heart in order to improve the accuracy of screening. Implementation of the 2010 European guidelines on ECGs in athletes, rather than those on athletes with cardiovascular disease of 2005, resulted in a reduction of 43%–59% in the number of ECGs classified as abnormal,32,33 with a parallel reduction in the number of false positives (from 16%–17% to around 10%).34,35 The report on the ‘Seattle Summit’,10 published at the end of 2012, as well as updating the criteria for classifying abnormal ECGs in athletes, highlights the concerns of some that physicians may lack experience in interpreting ECGs in athletes and that this hampers its use for preparticipation screening. Investment in medical training and the use of aids to interpretation, with standardized criteria for athletes, have been proposed as a way to improve this situation. Drezner et al. compared the accuracy of ECG interpretation among different physician specialties: 16 primary care specialists, 22 primary care residents, 12 sports medicine physicians and 10 cardiologists, first without and then with an ECG criteria tool based on the ESC consensus statement for interpretation of the 12-lead ECG in athletes, and observed an improvement in sensitivity from 70% to 91% and in specificity from 89% to 94% across all the different medical specialties.10,36

The ECG changes in those who undertake regular and intense exercise may be the result of physiological cardiac remodeling, and thus do not require further investigation, or may indicate an increased likelihood of SCD and thus require a thorough diagnostic workup that in most cases will result in disqualification from participation in competitive sports and treatment to prevent a fatal event. In the ESC guidelines these alterations are divided into two groups depending on whether they are training-related.31

Figures 3 and 4 and Table 3 show the ECG patterns associated with athlete's heart. Sinus bradycardia, defined as heart rate <60 bpm, is found in up to 80% of trained athletes, and in highly trained athletes, marked bradycardia (down to 30 bpm) is considered normal; sinus arrhythmia is also common (>50% of athletes, particularly young ones).21 Traditional examples of early repolarization referred to ST-segment elevation of >1 mV only, but newer definitions also include J waves or terminal QRS slurring, most commonly seen in the precordial leads (Figure 4) and are present in up to 45% of Caucasian athletes and 63%–91% of Afro-Caribbean athletes; 13%–25% of black athletes present J-point elevation with a domed ST segment in leads V1–V4, followed by T-wave inversion in the same leads and do not require further assessment in the absence of symptoms, positive family history or abnormal physical examination.5,21

Figure 3.

Electrocardiographic patterns associated with athlete's heart. AV: atrioventricular; HR: heart rate; LV: left ventricular; RBBB: right bundle branch block. Adapted from Drezner et al.5

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Figure 4.

(A and B) Classic definition of early repolarization based on ST elevation at QRS end (J-point); examples without (A) and with (B) a J-wave; (C and D) new definitions of early repolarization showing slurred QRS downstroke and new J-point (C) and J-wave (D) without ST elevation. Adapted from Drezner et al.5

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The most commonly used criterion for left ventricular hypertrophy (LVH), that of Sokolow-Lyon (SV1 + [RV5 or V6] >3.5 mV), is found in 45% of male and 10% of female athletes. The isolated presence of this criterion is no longer regarded as abnormal in athletes, since it almost always reflects increases in cardiac chamber size and/or wall thickness that are a physiological response to regular exercise, and its measurement is unreliable.5 However, the physician should ensure that there are no additional non-voltage criteria for LVH such as left atrial enlargement, left axis deviation, ST-segment depression, T-wave inversion or pathological Q waves that could indicate HCM or another condition.37

Table 4 presents the criteria for pathological ECG alterations for various cardiac conditions that may be detected in preparticipation screening, while Figure 5 shows some ECG traces illustrating cardiac abnormalities that have been identified as associated with SCD. Since most of these conditions, such as channelopathies and HCM, are diagnosed by ECG, the physician must be familiar with the typical ECG patterns for each disease in order to improve the diagnostic accuracy of preparticipation screening, particularly in the age-groups most likely to be affected.

Table 4.

Electrocardiographic criteria for pathological alterations in athletes that require further diagnostic investigation.

ECG alterations	Criteria for further assessment	Illustration	ECG alterations	Criteria for further assessment	Illustration
			LBBB, RBBB, and IVCD	QRS >120 ms
Q waves	>3 mm in depth and/or 40 ms duration in any lead except III, aVR, aVL and V1		QRS axis deviation	Further left than –30°, further right than +115°
ST-segment depression	>0.5 mm below the PR isoelectric line between the J-junction and beginning of the T wave in V4, V5, V6, I, aVL >1 mm in any lead		QTc abnormalities	>470 ms in men >480 ms in women <340 in any athlete
T-wave inversion	≥1 mm in leads other than III, aVR, and V1/2 (except V2 and V3 in women aged <25 years)		BrS	BrS type 1: coved-type ST segment in V1 and V2 that gradually descends into an inverted T wave
Atrial abnormalities	Right: P-wave amplitude >2.5 mm Left: (i) a negative component of the P wave in V1 or V2 of 40 ms duration and 1 mm amplitude; (ii) total P-wave duration of >120 ms		Ventricular preexcitation	Delta wave and PR interval <120 ms
Right ventricular hypertrophy	Age >30 years: (i) R >7 mm in V1; or (ii) R/S >1 in V1; or (iii) sum of R in V1 and S in V5 or V6 >10.5 mm Age <30 years: the above plus right atrial abnormalities, T-wave inversion in V2/3, and/or right-axis deviation >115°		VES, cardiac block and supraventricular arrhythmia	Atrial fibrillation/flutter, supraventricular tachycardia, complete heart block, or ≥2 VES on a 12-lead ECG

BrS: Brugada syndrome; ECG: electrocardiographic/electrocardiogram; IVCD: intraventricular conduction delay; LBBB: left bundle branch block; RBBB: right bundle branch block; VES: ventricular extrasystoles.

Adapted from Uberoi et al.39

Figure 5.

Electrocardiograms illustrating some structural and electrical cardiac abnormalities associated with sudden cardiac death.

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Electrical cardiac abnormalities are the most frequent cause of sudden unexplained death (SUD) on autopsy studies, particularly in children and young adults. Postmortem genetic testing indicates that channelopathies caused by mutations in ion channels are responsible for 25%–35% of SUD.16,45 Inherited cardiac arrhythmias and conduction disorders that can cause SCD include the following:

• (1)

  LQTS and short QT syndrome (SQTS) are inherited or acquired channelopathies, often associated with the use of drugs including antihistamines, antibiotics, antifungals, and antipsychotics, in which ventricular repolarization alterations lead to life-threatening polymorphic ventricular arrhythmias such as torsade de pointes, caused by abnormalities in K+, Na+ and Ca2+ ion channels. While SQTS is rare, affecting 1:10000 individuals, the prevalence of LQTS is relatively high (1:2000) and may even be underestimated due to changes in the definition of a ‘normal’ QT interval. Diagnosis is based on a combination of clinical and family history, ECG findings and genetic tests. A total of 13 genes have been identified that are involved in the condition, affecting Na+ or K+ channels in 95% of cases.43,45 LQTS is known to be responsible for 15%–20% cases of autopsy-negative sudden death45,46 (Figure 5B-3 and B-4).

• (2)

  Catecholaminergic polymorphic ventricular tachycardia is a rhythm disorder originating from a ventricular ectopic focus that is triggered by exercise or emotional stress, and generally appears between the ages of 7 and 9. Patients usually have structurally normal hearts; the condition is caused by mutations in the genes coding for ryanodine receptors and calsequestrin, which regulate Ca+ channels, and predisposes to syncope, VF and SCD. The ECG is normal at rest but shows abnormalities during exercise testing, including adrenergic-mediated ventricular tachycardia as well as monomorphic extrasystoles that progress to bidirectional and polymorphic VT.1,45,46 Besides prohibiting sports, treatment consists of arrhythmia control with beta-blockers, verapamil or flecainide and an implantable cardioverter-defibrillator (ICD)47 (Figure 5B-5).

• (3)

  Brugada syndrome (BrS) is a genetic disease with autosomal dominant transmission and incomplete penetrance, of which 20%–25% of cases (and around 40% of cases with prolonged PR interval) are caused by mutations in the SCN5A gene affecting Na+ channels.45,46

  BrS involves an imbalance between the positive currents (Na+ and K+) in phase 1 of the action potential (Figure 7A). This imbalance causes early repolarization, accentuating the notch caused by the transient K+ outflow,48 which leads to a paradoxical prolongation of the action potential dome in epicardial cells due to the delay in its formation.49 This causes the epicardium to repolarize after the endocardium, resulting in T-wave inversion and producing the characteristic coved ECG. However, if the epicardium still repolarizes before the endocardium, the T wave remains positive (saddleback ECG).50

  
  

  Figure 7.

  (A) Schematic representation of right ventricular epicardial action potential changes proposed to underlie the electrocardiographic manifestations of Brugada syndrome (adapted from Antzelevitch et al.49); (B) The three electrocardiographic patterns associated with Brugada syndrome: type 1 – coved ST-segment elevation of ≥2 mm followed by a negative T wave with little or no isoelectric separation in one or more right precordial leads (V1–V3); type 2 – ST-segment elevation followed by a positive or biphasic T wave, resulting in a saddleback configuration; and type 3 – ST-segment elevation in the right precordial leads of <1 mm, coved or saddleback configuration; diagnostic criteria for Brugada syndrome (adapted from Sheikh and Ranjan51).

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  BrS is estimated to cause 5%–20% of autopsy-negative SUD. Death usually occurs at rest due to vagal hyperactivity induced by prolonged training. Diagnosis is by ECG, which most often shows a type 1 pattern (Figure 7B), but can be difficult because the alterations are often intermittent and provocative testing with sodium channel blockers may be necessary to trigger the type 1 pattern. The only treatment to date is an ICD1,49,51–54 (Figure 5B-6).

• (4)

  Wolff-Parkinson-White syndrome (WPW) has a prevalence of 0.1%–0.3% both in the general population and in athletes. It consists of ventricular pre-excitation through an anomalous AV accessory pathway (AP) that bypasses the separation of cardiac conduction between the atria and the ventricles. In sinus rhythm, the electrical impulse can pass through the AV node or through the AP, which is faster and thus gives rise to AV reentrant tachycardia. This is the most common tachyarrhythmia in WPW patients, accounting for 95% of all reentrant tachycardias, but around a third of these individuals have atrial fibrillation, which can degenerate into ventricular fibrillation, causing SCD. Figure 8 shows the pathophysiological mechanism of two variants of reentrant tachycardia that can occur in WPW: orthodromic and antidromic. WPW is diagnosed by ECG, which shows a delta wave, a short PR interval, prolonged QRS and, in some cases, repolarization abnormalities. Most individuals are asymptomatic (WPW pattern), while others (WPW syndrome) may experience palpitations, syncope and/or arrhythmias, with or without hemodynamic compromise, or even SCD. Athletes with WPW should undergo exercise testing to stratify SCD risk and to guide treatment. Intermittent pre-excitation during sinus rhythm, or complete and sudden disappearance of pre-excitation on exercise testing, are considered low risk, while high risk is defined as an RR interval <250 ms (heart rate 240 bpm) following induced fibrillation. The current guidelines state that only high-risk athletes should be treated, by catheter ablation of the AP, and can return to sports after three months1,45,55,56 (Figure 5B-7).

  WPW). (a) Sinus rhythm with preexcitation of the WPW type: antegrade conduction via the atrioventricular (AV) node (green) and the accessory pathway (AP) (red). Rapid conduction over the AP leads to early repolarization, which correlates to the delta wave; (b) orthodromic reentrant tachycardia: antegrade conduction over the AP is blocked due to its longer refractoriness. Conduction to the ventricles occurs only via the AV node (black) and reaches the AP when it is able to conduct back to the atria (blue); (c) antidromic reentrant tachycardia: the AV node reaches refractoriness before the AP, and so antegrade conduction occurs only via the AP (red) and reaches the AV node when it is able to conduct back to the atria (black). Adapted from Estner et al.73'> WPW). (a) Sinus rhythm with preexcitation of the WPW type: antegrade conduction via the atrioventricular (AV) node (green) and the accessory pathway (AP) (red). Rapid conduction over the AP leads to early repolarization, which correlates to the delta wave; (b) orthodromic reentrant tachycardia: antegrade conduction over the AP is blocked due to its longer refractoriness. Conduction to the ventricles occurs only via the AV node (black) and reaches the AP when it is able to conduct back to the atria (blue); (c) antidromic reentrant tachycardia: the AV node reaches refractoriness before the AP, and so antegrade conduction occurs only via the AP (red) and reaches the AV node when it is able to conduct back to the atria (black). Adapted from Estner et al.73' title='Pathophysiological mechanisms of Wolff-Parkinson-White syndrome (WPW). (a) Sinus rhythm with preexcitation of the WPW type: antegrade conduction via the atrioventricular (AV) node (green) and the accessory pathway (AP) (red). Rapid conduction over the AP leads to early repolarization, which correlates to the delta wave; (b) orthodromic reentrant tachycardia: antegrade conduction over the AP is blocked due to its longer refractoriness. Conduction to the ventricles occurs only via the AV node (black) and reaches the AP when it is able to conduct back to the atria (blue); (c) antidromic reentrant tachycardia: the AV node reaches refractoriness before the AP, and so antegrade conduction occurs only via the AP (red) and reaches the AV node when it is able to conduct back to the atria (black). Adapted from Estner et al.73'/>
  

  Figure 8.

  Pathophysiological mechanisms of Wolff-Parkinson-White syndrome (WPW). (a) Sinus rhythm with preexcitation of the WPW type: antegrade conduction via the atrioventricular (AV) node (green) and the accessory pathway (AP) (red). Rapid conduction over the AP leads to early repolarization, which correlates to the delta wave; (b) orthodromic reentrant tachycardia: antegrade conduction over the AP is blocked due to its longer refractoriness. Conduction to the ventricles occurs only via the AV node (black) and reaches the AP when it is able to conduct back to the atria (blue); (c) antidromic reentrant tachycardia: the AV node reaches refractoriness before the AP, and so antegrade conduction occurs only via the AP (red) and reaches the AV node when it is able to conduct back to the atria (black). Adapted from Estner et al.73

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Early studies estimated the incidence of SCD in female athletes at 0–1:1300000. This figure was subsequently challenged by Harmon et al., who put it at 1:77000, although this was still 2.3 times less common than in male athletes.62 This difference has been explained by the fact that male gender is an independent risk factor for SCD, not only due to coronary artery disease.12 Most studies of female athletes focus on gender differences in repolarization alterations, which are considerably less common in women (5.9% vs. 21%), with statistically significant differences in the prevalence of J-point elevation (21.5% vs. 35%) and of ST elevation (0.5% vs. 3.3%).63 Rollin et al. demonstrated that although repolarization abnormalities are less prevalent in women, an early repolarization pattern is a risk factor for all-cause and cardiovascular mortality, with hazard ratios of 4.77 and 7.11, respectively.64

The Seattle criteria were the first guidelines to mention Afro-Caribbean individuals specifically, due to the particularly high incidence of SCD in this group (5.6:10000018) and a series of typical ECG patterns that came to be seen as physiological adaptations to training. Black athletes are more likely to have voltage criteria for LVH (68% vs. 40%), repolarization alterations including J-point elevation with concave or convex ST segment (85% vs. 62%) and deep T-wave inversion (12% vs. 0%) than their white counterparts.1,22 Multivariate analysis showed that black ethnicity was a predictor of ECG abnormalities (relative risk of 2.3 compared to non-blacks).22 HCM, for example, is 10 times more prevalent in blacks than in whites, which makes the ECG particularly valuable in this group.1,65

The Seattle criteria have not been validated for athletes younger than 14. Characteristics associated with younger ages are the absence of gender-related differences on the ECG (probably due to the lack of influence of sex hormones),66 T-wave inversion in the precordial leads,67 and shorter PR, QRS and QT intervals (partly due to higher heart rates in children). These differences will tend to disappear as adulthood approaches, but there is no specific age at which this occurs, which can make it difficult to differentiate between persistent juvenile patterns from patterns associated with underlying heart disease.

The debate concerning the best way to identify athletes at risk for SCD continues, and there is still disagreement between the ESC and the AHA. The Seattle criteria aimed to resolve one of the major problems with preparticipation ECG screening, that of the high proportion of false positives observed using the criteria of previous guidelines.57,58,68 Achieving a false positive rate of 1.7%59 led to a change in focus from false positives to false negatives. There is currently no reason to doubt the safety of the Seattle criteria, but further prospective studies are needed to ascertain the outcome of all the athletes assessed.

Another major concern with the use of the ECG is its financial impact and its poor cost-effectiveness. According to Wheeler et al.,69 addition of electrocardiography to preparticipation screening saves 2.06 life years per 1000 athletes at an incremental cost of $89 per athlete, yielding a cost-effectiveness ratio of $42900 per life year saved, which is much less than other public health initiatives such as dialysis ($20000–$80000) or public access to defibrillators ($55000–$162000).

Asif et al.59 addressed another important question regarding opposition to the inclusion of electrocardiography in preparticipation screening by assessing what psychological impact this would have on athletes, including the effect of false positives. They concluded that there were no statistically significant differences in anxiety levels with and without the ECG, and that those who received an ECG were more satisfied with their screening, felt safer during competition, and stated the ECG positively impacted their training.

Another study demonstrated the benefit of early detection and treatment of LQTS in reducing the risk of SCD. Johnson et al.70 analyzed 353 individuals with LQTS, of whom 130 remained in competitive athletics. These received counseling and were treated with beta-blockers, left cardiac sympathetic denervation, and/or an ICD. In a mean follow-up of 5.1 years, none of the 130 athletes died and only one received appropriate ICD shocks. Although these results cannot be extrapolated to other conditions, they demonstrate the need for further studies to provide a solid basis of scientific evidence to guide treatment decisions and to determine eligibility for participation in sports.

Evidence supporting the inclusion of the ECG in screening continues to mount. Nevertheless, in order to be effective, there is a need for improved medical training and for tools to assist with interpreting the ECG, since the cost-effectiveness of electrocardiography in preparticipation screening will depend on the competence of physicians as well as on their response to abnormal and borderline alterations. The algorithm for evaluating athletes (Figure 9) proposed by Chandra et al.1 to identify possible cardiac causes of sudden death highlights the role of the ECG. Acceptance of this algorithm, as well as improvements in training for primary health physicians, sports medicine specialists and cardiologists, are needed before including an ECG in preparticipation screening protocols, in order to avoid unacceptable levels of false positives.

DCM: dilated cardiomyopathy; HCM: hypertrophic cardiomyopathy; LA: left atrial; LBBB: left bundle branch block; LQTS: long QT syndrome; LVH: left ventricular hypertrophy; MRI: magnetic resonance imaging; RBBB: right bundle branch block; SCD: sudden cardiac death; WPW: Wolff-Parkinson-White syndrome. Adapted from Chandra et al.1'> DCM: dilated cardiomyopathy; HCM: hypertrophic cardiomyopathy; LA: left atrial; LBBB: left bundle branch block; LQTS: long QT syndrome; LVH: left ventricular hypertrophy; MRI: magnetic resonance imaging; RBBB: right bundle branch block; SCD: sudden cardiac death; WPW: Wolff-Parkinson-White syndrome. Adapted from Chandra et al.1' title='Algorithm for evaluating athletes for conditions capable of causing sudden cardiac death. ARVC: arrhythmogenic right ventricular cardiomyopathy; CCAA: congenital coronary artery anomaly; DCM: dilated cardiomyopathy; HCM: hypertrophic cardiomyopathy; LA: left atrial; LBBB: left bundle branch block; LQTS: long QT syndrome; LVH: left ventricular hypertrophy; MRI: magnetic resonance imaging; RBBB: right bundle branch block; SCD: sudden cardiac death; WPW: Wolff-Parkinson-White syndrome. Adapted from Chandra et al.1'/>

Figure 9.

Algorithm for evaluating athletes for conditions capable of causing sudden cardiac death. ARVC: arrhythmogenic right ventricular cardiomyopathy; CCAA: congenital coronary artery anomaly; DCM: dilated cardiomyopathy; HCM: hypertrophic cardiomyopathy; LA: left atrial; LBBB: left bundle branch block; LQTS: long QT syndrome; LVH: left ventricular hypertrophy; MRI: magnetic resonance imaging; RBBB: right bundle branch block; SCD: sudden cardiac death; WPW: Wolff-Parkinson-White syndrome. Adapted from Chandra et al.1

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The authors declare that no experiments were performed on humans or animals for this study.

The authors declare that they have followed the protocols of their work center on the publication of patient data.

The authors declare that no patient data appear in this article.