Keywords

FormalPara Learning Objectives
  1. 1.

    Understand the most recent International Criteria for ECG interpretation in athletes.

  2. 2.

    Outline normal ECG findings in athletes related to physiologic cardiac adaptations from regular exercise training.

  3. 3.

    Recognize that two or more borderline ECG findings require further testing.

  4. 4.

    Define abnormal ECG findings in athletes which require further evaluation to exclude a pathologic cardiac disorder before participation in competitive sport.

  5. 5.

    Describe the minimum recommended evaluation for athletes with specific ECG abnormalities.

1 Introduction

While the American Heart Association and American College of Cardiology recommend that athletes undergo a preparticipation evaluation before competitive sports with a history and physical examination [1], many sporting organizations and the European Society of Cardiology (ESC) [2] recommend use of a screening electrocardiogram (ECG). The Canadian Cardiovascular Society recommends an ECG only if there is an abnormal history or physical examination [3], while the American Medical Society for Sports Medicine suggests an ECG should be considered in high risk athlete groups when adequate cardiology resources are available [3, 4]. Whether used for screening or diagnostic purposes, ECG interpretation is a fundamental skill for physicians responsible for the cardiovascular care of athletes.

An ECG increases the detection of disorders at increased risk of sudden cardiac death [5, 6], as most athletes who have a cardiac arrest are asymptomatic prior to their event [3] and the sensitivity and specificity of a screening history and physical examination are poor [6]. However, the ECG is not a perfect screening tool, and some disorders such as coronary artery anomalies or aortic dilatation do not demonstrate ECG abnormalities.

The distinction of ECG findings related to physiologic cardiac adaptations in trained athletes from ECG abnormalities suggesting the possibility of an underlying cardiac disorder is critical in the interpretation of an athlete’s ECG. Certain ECG findings are considered normal in athletes that might be considered abnormal in non-athletes. For this reason, it is important to use athlete-specific ECG interpretation criteria. The first criteria from the ESC defined training-related and training-unrelated ECG findings [7] but there was a high rate of false positive ECG tests, especially in black athletes [8]. Other interpretation standards emerged, including the Seattle Criteria [9], that improved the specificity and reduced the false positive rate without compromising sensitivity [10,11,12,13]. Most recently, the International Criteria for ECG Interpretation in athletes were developed by an international panel of experts in sports medicine and cardiology which defines normal, borderline, and abnormal ECG findings and the secondary tests recommended for each ECG abnormality [14]. The International Criteria should be used for asymptomatic athletes with no concerning family history, and thus may need to be modified in the presence of clinical markers of concern. If there are symptoms suggestive of cardiac disease or a family history of sudden cardiac arrest, Marfan syndrome, cardiomyopathy, or channelopathy, then the athlete should be evaluated by a physician knowledgeable in these disorders.

Importantly, a normal ECG does not confirm a lifetime free of cardiac disease. ECG changes and phenotypic expression of a genetic disorder can occur over time, especially in pubertal age adolescents and young adults, where repeated screening is necessary to exclude the interval development of cardiomyopathies [15]. In addition, if an ECG is abnormal but the secondary testing is normal, serial evaluation is recommended to monitor for the later manifestation of phenotypic disease [16].

2 Normal ECG Findings

These findings do not require any further evaluation (Table 7.1; Fig. 7.1):

Chamber Hypertrophy

  • Right and left ventricular hypertrophy are physiologic adaptations to regular exercise and can be manifested on the ECG as increased QRS voltage.

  • Left ventricular hypertrophy (LVH) by Sokolow-Lyon criteria is seen in up to 45% of athletes in one study [17].

  • While LVH may be present in those with hypertrophic cardiomyopathy (HCM), there are typically other ECG abnormalities such as ST depression, T wave inversions, or pathologic Q waves [16, 17].

  • Right ventricular hypertrophy by voltage criteria is a normal finding seen in up to 12% of athletes [18, 19].

  • Incomplete right bundle branch block usually with an rSR′ pattern and QRS duration <120 ms in lead V1 is also a common finding in trained athletes.

Early Repolarization

  • Early repolarization consists of J point elevation ≥0.1 mV, frequently with a notch called a J wave, and usually followed by ST segment elevation in a convex pattern [20].

  • Early repolarization is often present in normal athletes [21], especially those who are young, male, or of African-Caribbean descent. It has been described in up to 45% of Caucasian [17] and 63% of Black athletes [18].

  • This pattern is not associated with sudden death in young athletes and is considered normal.

Bradycardia, First Degree Atrioventricular (AV) Block, and Second Degree Mobitz Type I AV Block (Wenckebach)

  • Sinus bradycardia is commonly seen in elite athletes. This can also be manifested as an ectopic atrial rhythm or accelerated junctional rhythm.

    • Sinus bradycardia is due to both enhanced vagal tone [22, 23] as well as changes in expression of the HCN4 and If cardiac ion channels [24].

  • First degree AV block between 200 and 400 ms and AV Wenckebach block are also considered normal.

  • If there is any concern whether the findings are pathologic, a short burst of aerobic exercise should cause an increase in heart rate and normalization of AV conduction.

Normal Patterns of T Wave Inversion

  • There are several different normal T wave inversion patterns:

    • An isolated negative T wave in V3.

    • Persistent juvenile T wave pattern with T wave inversions in leads V1–V3 in athletes <16 years of age. T wave inversion extending beyond V2 is an uncommon finding in Caucasian athletes > age 16 [17, 25].

    • Athletes of African-Caribbean descent have a normal T wave repolarization pattern consisting of J point elevation, convex ST segment elevation, and T wave inversion confined to leads V1–V4 (Fig. 7.2) [26]. Typically, the T waves are biphasic positive and then negative. These must be differentiated from T wave inversion associated with HCM and arrhythmogenic right ventricular cardiomyopathy (ARVC), as described below. T wave inversion extending to the lateral leads V5 and/or V6 is always considered abnormal and requires more evaluation. There is variation in T wave inversion based on the athlete’s geographic origin even in normal individuals [27]. Those from Middle and West Africa have a higher rate of T wave inversions, including in the inferior and lateral leads, compared to those from East or North Africa. These findings are correlated with greater left ventricular wall thickness (see also Chap. 26).

Table 7.1 Definitions from the International Criteria for Electrocardiogram Interpretation in Athletes[14]
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Fig. 7.1
figure 1

The International Criteria for ECG Interpretation in Athletes. AV atrioventricular, LVH left ventricular hypertrophy, NSVT non-sustained ventricular tachycardia, PVCs premature ventricular contractions, RVH right ventricular hypertrophy, RBBB right bundle branch block, TWI T wave inversion

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Fig. 7.2
figure 2

19-year-old black male track athlete with ST-segment and J-point elevation followed by T wave inversion in leads V2–V3. This repolarization pattern represents a normal variant in black athletes

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3 Borderline ECG Findings

Some ECG findings previously characterized as abnormal have since been reclassified as a borderline or possibly normal finding in an athlete (Table 7.1; Fig. 7.1). Specifically, the ECG findings below are considered normal if present in isolation, but if two or more borderline findings are present then further evaluation with an echocardiogram to exclude cardiomyopathy is recommended [8].

Right Bundle Branch Block (RBBB)

  • While incomplete RBBB is common in athletes, complete RBBB (QRS duration ≥120 ms) is a less frequent finding in approximately 0.5–2.5% of athletes [28,29,30].

  • Some highly trained athletes have physiologic right ventricular cardiac remodeling manifested as right ventricular dilatation, reduction in right ventricular systolic function at rest, and slight increase in the rate of right bundle branch block [31].

  • While one study showed a slight increase in right ventricular size in those with RBBB, there were no pathologic abnormalities identified and no cardiac events occurred [30]. Other imaging studies have shown normal right ventricular size and function in those with RBBB [31].

  • Complete RBBB when found in isolation without other borderline or abnormal ECG findings does not require additional investigation unless there are clinical markers of concern.

Atrial Enlargement and Axis Deviation

  • Athletes are more likely to have left axis deviation or left atrial enlargement compared to non-athletes [32].

  • There is no correlation, however, between axis deviation or atrial enlargement on ECG with abnormalities found on cardiac imaging.

  • In patients with HCM, left axis deviation or left atrial enlargement in the absence of any other abnormality was not found to be more prevalent compared to normal athletes [25, 33, 34].

  • Therefore, isolated right or left atrial enlargement or right or left axis deviation is considered a normal finding in the absence of any other ECG abnormality.

4 Abnormal ECG Findings

Abnormal ECG findings require further evaluation to exclude a pathologic cardiac disorder. The ECG abnormality alone does not necessarily imply a disease process, but rather indicates that more evaluation is needed. Temporary restriction from sport should be considered while the secondary evaluation is completed. Some ECG abnormalities may be the first manifestation of a cardiomyopathy before morphologic changes are present. Thus, serial evaluation is recommended on an annual basis for athletes with abnormal T wave inversion, ST segment depression, and/or pathologic Q waves.

Pathologic T Wave Inversion

  • T wave inversions ≥1 mm in two or more contiguous leads are considered abnormal. T wave inversion in V5 or V6 alone satisfies the criteria (Fig. 7.3). Leads III, aVR, and V1 should be excluded from measurement.

  • If a T wave is biphasic and the negative portion of the T wave is ≥1 mm in depth, then it is considered abnormal.

  • T wave inversions should be described as anterior (V2–4), lateral (I, aVL, V5–V6), inferolateral (I, II, aVL, aVF, V5–6), or inferior (II, aVF) based on the leads involved. T wave inversions in the lateral leads are most concerning for cardiomyopathy.

Fig. 7.3
figure 3

19-year-old black baseball player with T wave inversion in V4–V6 and borderline in II and aVF. Lateral and inferolateral T wave inversion is an abnormal finding requiring investigation for cardiomyopathy. This athlete was later found to have hypertrophic cardiomyopathy

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T wave inversions may be an early finding for cardiomyopathy, often seen before the development of structural changes [8, 16, 35]. For instance, one study of 81 athletes with pathologic T wave inversions demonstrated that 6% later went on to manifest a cardiomyopathy, including two athletes who had a sudden cardiac arrest [16]. Another study demonstrated that 12.3% of athletes with lateral T wave inversions were found to be gene positive for a cardiac disease, most commonly for a mutation associated with HCM [36]. However, the specificity of this criterion is still imperfect, especially in black athletes with more prevalent T wave inversions [8, 18].

  • There may be associated abnormalities to suggest a cardiomyopathy, including ST segment depression, pathologic Q waves, left bundle branch block, ventricular pre-excitation, or borderline ECG findings.

  • The main disorders associated with T wave inversions include HCM, ARVC, dilated cardiomyopathy, left ventricular non-compaction cardiomyopathy, and myocarditis.

If T wave inversions are found in the lateral leads, an echocardiogram should be completed. In addition, a cardiac magnetic resonance imaging (MRI), which has better resolution for apical HCM, should be performed. Late gadolinium enhancement suggestive of myocardial fibrosis can be seen on MRI even when there is no significant hypertrophy. An exercise ECG test and ambulatory ECG monitoring should be considered if there is left ventricular hypertrophy which falls in the grey zone (13–15 mm wall thickness), where it is difficult to tell if the increased left ventricular hypertrophy is due to HCM or secondary to physiologic changes. If exercise-induced arrhythmias or non-sustained ventricular tachycardia are seen, it is more likely a cardiomyopathy is present.

T wave inversions in the inferior leads can also be seen in HCM though in a much smaller proportion and are usually associated with lateral T wave inversions if pathologic disease is present [18]. If T wave inversions are only present in the inferior leads, further evaluation with an echocardiogram should suffice [8].

Anterior T wave inversion may be related to ARVC, especially if there is an epsilon wave, premature ventricular contractions with a left bundle branch block morphology, prolonged S wave upstroke in leads V1–3, or low amplitude limb lead voltages. Evaluation should include an echocardiogram, cardiac MRI, Holter monitoring, exercise ECG test, and signal averaged ECG depending on clinical suspicion. Examination of the J point and T wave inversions can help distinguish between normal patterns and pathologic findings. If there is J point elevation ≥1 mm and T wave inversions in leads V1–V4, one study demonstrated 100% negative predictive value for cardiomyopathy [37]. However if there is no J point elevation, a flat or depressed ST segment, or additional T wave inversions in the inferior or lateral leads, then cardiomyopathy is more likely to be present.

ST-Segment Depression

  • ST-segment depression is defined as ≥0.05 mV, or 0.5 mm in standard gain, in two or more contiguous leads.

  • ST-segment depression is more commonly associated with cardiomyopathy. Approximately 50% of patients with HCM will have ST-segment depression though it is usually associated with other ECG abnormalities such as pathologic Q waves or T wave inversions [8, 18].

  • Evaluation should include an echocardiogram if seen in isolation. However, if there are other ECG abnormalities, a cardiac MRI should be considered.

Pathologic Q Waves

  • The current definition for a pathologic Q wave is a Q/R ratio ≥ 0.25 or a Q wave duration ≥40 ms in two or more contiguous leads, excluding leads III and aVR [14]. This was one of the significant changes from the Seattle Criteria [9], which used an absolute depth of >3 mm or > 40 ms in duration. The absolute depth was removed from the International Criteria as there was a greater rate of false-positive results in thinner people and those with physiologic left ventricular hypertrophy, who have high precordial voltage but no pathologic abnormalities. This problem is corrected by using the Q/R ratio.

    • It is important to note that placement of ECG leads in the improper position can also cause abnormal Q waves, such as with limb lead reversal or placement of leads V1 and V2 into higher intercostal spaces [38].

    • Recent data suggest that a Q + S wave amplitude in lead III > 1.0 mV may offer additive value to suggest HCM [39].

    • The Q/R ratio ≥ 0.25 or a Q wave duration ≥40 ms is still not perfect as 1–2% of athletes may still have pathologic Q waves but no abnormalities seen [8, 40]. False positives are higher in black and male athletes.

    • Pathologic Q waves are seen in various cardiomyopathies, including HCM, ARVC, dilated cardiomyopathy, and prior myocardial infarction. In addition, the Wolff-Parkinson-White (WPW) pattern can demonstrate pathologic Q waves.

    • If pathologic Q waves are seen, the QRS should be examined for evidence of pre-excitation to suggest WPW. If this is not found, the specific leads where the Q waves are present will dictate the next step. If it is in V1 and V2, the ECG should be repeated with careful attention to correct lead placement in the fourth intercostal space.

    • If the Q waves are still present after repeat ECG, or the pathologic Q waves are found in two or more other leads, an echocardiogram should be completed to exclude cardiomyopathy, especially if there are ST-segment or T wave abnormalities. If there is a high suspicion of cardiomyopathy, a cardiac MRI should be considered.

    • If the athlete is over 30 years old or there is a clinical suspicion or risk factors of ischemic heart disease, especially if there is a wall motion abnormality on echocardiogram, a stress test is indicated [14].

Left Bundle Branch Block (LBBB)

  • LBBB is a rare finding in screening studies of athletes and deserves a comprehensive evaluation to exclude myocardial disease if found [5, 41,42,43].

  • A LBBB usually has other significant ST-segment and T wave changes which would be flagged by the screening criteria [29, 44, 45].

  • There is a high rate of cardiomyopathy in patients with LBBB. One study comparing athletes and patients with HCM showed that 5.9% of patients with HCM had LBBB, but no athlete with normal cardiac imaging had LBBB [46].

  • Athletes with LBBB require an echocardiogram and cardiac MRI with consideration for a stress perfusion study. Alternatively, a CT coronary angiogram or stress testing with imaging may be considered when ischemic heart disease is suspected.

Widened QRS ≥ 140 ms

  • It is unclear whether a QRS duration ≥140 ms in a non-LBBB pattern represents pathologic disease in an athlete population [47].

  • Increased myocardial mass and left ventricular hypertrophy in athletes, or alternatively, neurally-mediated conduction system slowing [48], can increase the QRS duration.

  • Various cardiomyopathies can also have QRS widening.

  • Until there is more data, however, it is prudent to perform further evaluation on those with a widened QRS complex ≥140 ms.

  • An echocardiogram should be completed, and depending on these findings and clinical suspicion, further testing may be indicated.

Wolff-Parkinson-White (WPW) Pattern

  • WPW (ventricular pre-excitation ) is present in about 0.1–0.3% of people [49]. More than half of adolescents with WPW pattern are asymptomatic [49].

  • The WPW pattern consists of a short PR interval <120 ms, widened QRS duration, and delta wave (slurred QRS upstroke).

  • It is important to differentiate WPW from Lown-Ganong-Levine pattern or enhanced AV nodal conduction, which also have a PR interval <120 ms but no delta wave and a normal QRS duration, as these findings are not associated with sudden cardiac arrest (SCA).

  • The most worrisome aspect of WPW is the associated risk of syncope or SCA. Syncope may be due to rapid supraventricular tachycardia from AV reciprocating tachycardia, rapid atrial fibrillation or flutter, or ventricular fibrillation.

  • An echocardiogram should be completed on all patients with WPW as there is an association with Ebstein anomaly, L-transposition of the great arteries, and left ventricular hypertrophy due to LAMP2 or PRKAG2 mutations.

There is debate regarding the best method for risk stratification of patients with asymptomatic WPW to determine the risk of SCA. The most important feature is determining the refractory period of the bypass pathway, where faster pathway conduction is associated with an increased risk of SCA [50]. Intermittent pre-excitation on the resting ECG suggests a lower risk pathway. An exercise test should be performed looking for abrupt loss of bypass pathway conduction (Fig. 7.4). If present, this suggests a low risk pathway and in the absence of symptoms, no treatment is necessary. If there are symptoms, if the bypass pathway does not abruptly stop at higher heart rates, or if the patient does not desire an exercise test, an electrophysiology (EP) study should be performed. The best predictor of SCA is a shortest pre-excited RR interval (SPERRI) in atrial fibrillation of ≤250 ms. In these patients, ablation is then performed if the pathway location is felt to be low risk for heart block or other complication. While this has a high sensitivity, this cutoff has a low specificity, meaning most patients with a low SPERRI will never have SCA [51].

Fig. 7.4
figure 4

18-year-old female basketball player with abrupt loss of pre-excitation (arrow) at 176 beats/minute on a treadmill test which suggests a bypass pathway at lower risk for causing sudden death

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A recent systematic review of 9 studies assessed the risk of SCA and method of risk stratification [52]. There was only one randomized controlled trial, however, on how to manage asymptomatic WPW. In addition, the age range of studies was from 19 to 50 years old so results may not be applicable to adolescents. Overall, malignant atrial fibrillation with an accessory pathway SPERRI ≤250 ms or ventricular fibrillation occurred in 9% and 1.5%, respectively. It is notable that there was no correlation of these outcomes with prior symptoms. Complication rates of EP study with ablation are low at 0.09% to 1% [53].

An autopsy study of 19 persons who died of SCA with an antemortem diagnosis of WPW showed that most events occurred at rest [54]. Four of these had a prior successful ablation. About half of these had other cardiac disease, including HCM, cardiac sarcoid, or idiopathic left ventricular hypertrophy. This argues that WPW can be implicated in SCA and that evaluation with echocardiography should be performed in all patients with WPW, with consideration for MRI if there is a suspicion for a cardiomyopathy.

Prolonged QT Interval

  • Long QT syndrome (LQTS), a genetic disorder due to mutations in cardiac ion channels, is associated with torsade de pointes and SCA.

  • The most common forms are LQT1, LQT2, and LQT3 due to mutations in KCNQ1, KCNH2, and SCN5A, respectively, which make up about 80% of cases.

  • While a QT interval corrected for heart rate (QTc) ≥ 500 ms is highly suggestive of LQTS, there is a gray zone below this with significant overlap in QT intervals between those with genetically confirmed LQTS and normal individuals.

  • A QTc ≥ 480 ms in females and ≥ 470 ms in males are cutoff values classified as abnormal needing further evaluation (Fig. 7.5).

  • It is recognized that there will be some people with lower QT values who have genetic LQTS but their risk of torsades de pointes is lower.

Fig. 7.5
figure 5

18-year-old female soccer player with a prolonged QT interval measuring 508 ms, and a QTc using the Bazett formula of 494 ms. Genetic testing confirmed LQT1

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Measurement of the QT interval can be difficult. The best method is to examine lead II or V5. A straight line should be then drawn as a tangent on the downslope of the T wave. Where this line intersects the baseline is the end of the QT interval. The beginning is the onset of the QRS complex.

Various correction formulas have been used as the QT interval changes with heart rate. In general, Bazett’s QT correction [QTc = QT/√(RR in seconds)] should be used, noting that the accuracy is limited at heart rates below 50 or greater than 90. In these individuals, the athlete should be encouraged to do a small amount of exercise to increase the heart rate if the heart rate is low, or to give additional time for relaxation for the heart rate to decrease. If there is an irregular heart rate due to sinus arrhythmia, an average of multiple beats of both the QT and RR should be used.

  • There is variability in QT measurements even amongst experienced ECG readers [55]. The computer interpretation of the QT interval is about 90 to 95% accurate [14].

  • T wave morphology may also suggest LQTS. Notching of the T wave in the lateral precordial leads, especially if the second part of the notch is greater than the first part of the notch, may suggest LQT2 even if the QT interval is normal [56].

Importantly, a single abnormal ECG with a prolonged QTc does not give a definitive diagnosis of LQTS. If a prolonged QT interval is found, a repeat ECG on a different day should be completed. ECGs of family members and a thorough family history of SCA, seizures, or unexplained deaths can be instructive. QT prolonging medications should be assessed (http://www.crediblemeds.org). In addition, an exercise stress test to assess for exercise-induced arrhythmias and whether the QTc is ≥ 470 ms at 2–5 min of recovery can be used [57]. Genetic testing and the Schwartz score also may be helpful (see also Chap. 21) [58].

Brugada Pattern

  • The Type 1 Brugada pattern is defined as a coved rsR’, ST elevation ≥ 2 mm with downsloping ST-segment, and symmetric T wave inversions in leads V1–V3.

  • The Brugada Type 1 pattern is associated with syncope or SCA usually during rest or sleep.

  • The Corrado index examines the height at the start of the ST-segment/J-point versus 80 ms later [59]. If this ratio is greater than one, the ST-segment is downsloping and is concerning for the Brugada pattern. If the ratio is less than one, then there is upsloping ST elevation and is normal.

  • The Type 2 Brugada pattern has a high takeoff of the r′ ≥ 2 mm, convex ST segment elevation ≥ 0.5 mm, and a positive T wave in V2 [60]. The T wave morphology can be variable in V1. The event rate of SCA or syncope is very low in Brugada Type 2 and for the purposes of screening would not warrant more evaluation (see also Chap. 21) [61].

Profound Sinus Bradycardia

  • Sinus bradycardia is a typical finding in endurance athletes.

  • However, a resting heart rate ≤ 30 beats/min should trigger an evaluation.

  • This may include either having the patient do simple aerobic exercise with a repeat ECG at higher heart rates or performing a structured exercise test to assess chronotropic competence.

  • If these are normal, no further evaluation is necessary.

Profound First-Degree AV Block

  • First degree AV block is common in well-conditioned athletes.

  • However, a PR interval ≥ 400 ms may represent conduction system disease.

  • Limited aerobic exercise or a formalized stress test can be completed to assess for shortening of the PR interval with activity.

  • If there is higher degree AV block with exercise, then further evaluation should be completed which may include an echocardiogram and/or ambulatory ECG monitor.

Mobitz II and Complete AV Block

  • Mobitz II, second degree heart block and complete AV block are rare findings on screening ECG but would suggest significant conduction system disease. Rarely, congenital complete heart block will be found.

  • It is important to differentiate Mobitz Type I versus Type II second degree AV block as Type I is a normal finding and much more common. Similarly, AV dissociation may be due to complete AV block or to sinus bradycardia with accelerated junctional or ventricular rhythms. More P waves than QRS complexes is consistent with complete AV block whereas more QRS complexes than P waves is consistent with accelerated rhythms.

Frequent Premature Ventricular Contractions (PVCs) and Nonsustained Ventricular Tachycardia (NSVT)

  • PVCs have been associated with cardiomyopathy though they may also be seen in normal individuals. Specifically, ARVC, dilated cardiomyopathy, HCM, or myocarditis may have PVCs.

  • On a standard ECG, two or more PVCs would suggest a high burden over a 24-h period and is considered abnormal. It is recognized that there is variability throughout the day or day-to-day in PVC burden and a single ECG may not necessarily pick up frequent PVCs.

An Italian study of 120 competitive athletes with no personal or family history of cardiomyopathy with a median of 3760 premature ventricular beats in 24 h showed that even in those who continued playing sport in the absence of treatment, the number of PVCs significantly decreased to 1240 beats per 24 h [62]. Another study with 5011 athletes undergoing exercise testing showed that 367 athletes had exercise-induced PVCs and demonstrated a reduction on repeat exercise testing even if allowed to continue playing sports [63]. While some have suggested that detraining may be necessary to show a reduction in PVC burden [64], it may simply be regression to the mean with or without detraining to explain why PVC burden decreases.

  • NSVT is rarely seen and requires further evaluation.

  • PVC morphology may have a role in identifying individuals with cardiac disease.

    • In normal individuals, PVCs with a LBBB morphology and an inferiorly directed axis with a variable precordial transition come from the right or left ventricular outflow tracts. PVCs with a RBBB morphology and superior axis frequently may be originating from one of the left bundle fascicles or the left ventricular papillary muscles.

    • If a PVC has a LBBB morphology with a superiorly directed axis, this might be indicative of ARVC as it suggests it is coming from the non-outflow tract portion of the right ventricle.

There has been concern for a form of ARVC induced by extreme endurance exercise [65,66,67]. Studies of some high-level endurance athletes with SCA showed findings of ARVC but a lower than expected rate of positive genetic testing and no family history of ARVC. This proposed type of exercise-induced ARVC may be manifest on ECG by frequent PVCs and in those with a history of intense endurance exercise.

Two or more PVCs on a 10 s ECG requires further evaluation including an echocardiogram, 24-h ambulatory monitor to assess the PVC burden, and additional investigation with exercise stress testing or cardiac MRI as indicated.

Epsilon Wave

  • An epsilon wave is seen in the setting of ARVC (Fig. 7.6).

  • It is a low amplitude, high frequency signal (small deflections and/or notches) between the end of the QRS complex and onset of the T wave in leads V1–V3 [68].

  • It is rarely present on a screening ECG in the absence of other abnormalities such as T wave inversions in the anterior precordial leads.

Atrial Tachyarrhythmias

  • The most common tachycardia on screening ECG is sinus tachycardia, especially if the athlete is anxious. A repeat ECG should be done a few minutes later if the heart rate is >120 bpm after the athlete has been given time to relax.

  • Supraventricular tachycardia, atrial fibrillation and atrial flutter are rarely seen in athletes. If these are present, it may suggest the possibility of a cardiomyopathy or channelopathy.

Fig. 7.6
figure 6

A 32-year-old male cyclist with an epsilon wave (arrows), defined as a low-amplitude high frequency signal between the QRS complex and T wave, present in leads V1–3. T wave inversions in V1–6, II, and aVF are also present

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5 Accuracy of Current Testing

Several studies have shown relatively good inter-observer agreement with ECG screening [69,70,71]. Even limited training can increase reader accuracy [72]. Open access to ECG training modules based on the International Criteria are available at: https://uwsportscardiology.org/e-academy/.

While ECG screening by experienced clinicians using athlete-specific standards typically produces false-positive rates <3–5%, some athlete groups may have a higher rate of ECG abnormalities. A study in athletes from the National Basketball Association showed that the new International Criteria were better than the Seattle Criteria, but 15.8% of African-American players and 11.5% of Caucasian players still had an abnormal ECG, with no disease based on echocardiogram findings [73]. However, cardiac MRI was not routinely performed in athletes with lateral or inferolateral T wave inversions.

Other studies demonstrate lower false-positive rates when applying the International Criteria [11, 12]. A study of 5000 athletes showed a 50% reduction in false positive results and all cases of true disease identified by the International Criteria [74].

Clinical Pearls

  • ECG interpretation in athletes should be completed using athlete-specific standards, the most up-to-date of which is the International Criteria for ECG interpretation in athletes [14].

  • Normal findings or one borderline finding do not require further testing, while two or more borderline findings and any abnormal finding requires further testing.

  • The most frequent abnormal findings include T wave inversions, ST-segment depression, pathologic Q waves, and ventricular pre-excitation/WPW pattern.

  • ECG abnormalities alone do not represent a disease in most cases, but should trigger additional evaluation to exclude pathologic cardiac disease.