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  1. 1. Word count: 4367 Electrocardiography In Elite Athletes F. CARRE and J.C. CHIGNON* Department of Physiology, Pontchaillou Hospital 35003 Rennes, France *National Institute of Sports, 11 Avenue du Tremblay, 75012 Paris, France. Electrocardiographic (ECG) features commonly observed in top rankingsportsmen were first described in 1929 by Hoogerwerf. The development ofnew non-invasive exploration methods (i.e. cardiac echocardiography andmagnetic resonance imaging) in the early 1970s offered physiologists themeans of investigating the so-called "Athletes Heart Syndrome" recognized byits specific ECG features. Standard ECG tracings have the advantage of low cost, readyavailability and ease of use and remain an essential investigation tool. Intrained subjects, ambulatory ECG monitoring and stress testing ECG areparticularly important as they provide supplementary information to theclassical 12-ECG which records only a brief period of cardiac electrical activity. The features of the athletes ECG basically reflect the hearts normalphysiological adaptation to repetitive physical training. However severalunusual patterns appear to be quite similar to pathological aspects occurring indifferent heart diseases. It is thus essential to acquire a full understanding ofthe ECG patterns in the elite athlete.Interpretation of the athletes ECG
  2. 2. 2 A highly trained athlete is usually defined as a subject who practices atleast ten hours a week at a level of intensity reaching at least 60 percent of hismaximal oxygen consumption ( O2max). Consequently, and athletes ECGmust always be interpreted in light of his individual level of training, bothqualitatively and quantitatively, and in accordance with the physicalexamination, functional signs and his personal and familial cardiovascular riskfactors, including age. The most common ECG features described in elite athletes can beobserved in all age groups and in both men and women, however they are notalways found in every elite athlete. They result from physiological adaptationsto physical conditioning and should not be immediately interpreted as markersof heart disease. The mechanisms underlying the disturbances observed onthe athletes ECG are not yet fully understood although modifications inautonomic nervous system tone and cardiac hypertrophy are often proposedas significant explanations. Modifications in autonomous nervous system tone have been describedin the athletes heart syndrome on the basis of biochemical andpharmacological tests. Another way of evaluating the effect of changes inparasympathetic and sympathetic tone is to study heart rate variability.Characteristically, there is an increase in parasympathetic tone and a decreasein sympathetic tone (perhaps through the effect of lower baroreceptorsensitivity). At rest, vagotonia appears to predominate whereas during exercisethe deceased sympathetic drive results in the slower heart rate observed inathletes compared with untrained subjects performing the same work load. Cardiac hypertrophy in the athlete was first suspected by Henschen in1899 on the basis of chest percussion and has been confirmed by non-invasivemorphology investigations including radiology, echocardiography and more
  3. 3. 3recently magnetic resonance imaging. It is described as a four-chamberharmonious wall hypertrophy-chamber dilation which can be observed at allages and appears to be totally reversible after deconditioning. There is some controversy in the literature as to the real incidence ofECG disturbances. For example, in two studies based on a large samplepopulation (Venerando published a series of 12,000 subjects and in our ownpersonal unpublished work we investigated 6,487 subjects) the globalprevalence of ECG disturbances was found to be 13 and 44 percentrespectively. This difference could be explained by differences in methodologyin the training level since the ECG criteria for diagnosis of cardiac hypertrophyhave not been standardized. The mean ± SD values of classical ECG criteria as observed in our studyare given in Table I in comparison with the ranges classically described in astandard population. In general, the ECGs of athletes lie within standard limits.A few trends which increase with training level can however be seen. Thedurations of the PR interval, the QRS complex and the corrected QT intervalincrease with the Sokolow-Lyon Index and frontal QRS axis turns to the left.Even though the ECGs of elite athletes lie within normal limits, differentpatterns of ECG disturbances have been described. For the purposes of this review, we have divided these changes intorhythm disorders, atrio-ventricular conduction impairment, cardiac hypertrophyrelated ECG criteria and disturbed repolarization. Finally, we shall try to specifythe potential differences observed in endurance versus resistance in thetrained athlete.Changes in cardiac rhythm Hypokinetic Arrhythmias
  4. 4. 4 The respective incidences of changes in cardiac rhythm and hypokineticarrhythmias are summarized in Table II. Resting sinus bradycardia is the most common finding among trainedathletes. It is difficult to determine the real incidence of athletes bradycardiadue to the lack of a common definition of bradycardia. The incidence variesfrom 8 to 85% in studies using the cut-off of 60 beats per minute, and in ourstudy, we found only 9% of our athletes with a resting heart rate below 50beats per minute. Controlled Holter recordings have shown a significantly lowermean hourly heart rate. Training undoubtedly affects the incidence ofbradycardia but the role of individual sensitivity and the mechanisms oftraining-induced bradycardia have yet to be established. Classically, thealterations in the autonomous nervous system described above would have aneffect, but some studies have shown that lower intrinsic heart rate is alsorelated to athletes bradycardia. In most cases, the bradycardia is benign asconfirmed by normal rhythms recorded during stress testing and also by thepersistence of physiological circadian variations (lower nocturnal heart rate) onHolter recordings. Rarely, the bradycardia is associated with dizziness,syncope or hyperkinetic arrhythmias due to vagal tone. In general, thesesymptoms disappear with deconditioning. Electrical stimulation is rarely neededand usually concerns older athletes in whom a latent sinus node disease isunmasked by the increased vagal tone. The resting heart rate in individualswith athletes bradycardia correlates with their individual level of peak training,and is used as a criteria for evaluating their level of training although it is notwell correlated with performance or O2max. A better index of training levelwould be the heart rate recovery curve. The rapidity at which the heart ratereturns to the basal level (or near basal level) would be an indication of a goodlevel of training. An unusual disturbance of the resting sinus rate which cannot
  5. 5. 5be explained by a change in the training regimen, is commonly considered tobe a feature of overtraining. Other hypokinetic dysrhythmias also concern the sinus rhythm and arerelated to altered autonomous tone. They disappear during stress training.These modifications are frequently observed on ambulatory ECG recordings,particularly at night. They are of no prognostic significance. The prevalence of sinus dysrhythmia , the so-called "respiratoryarrhythmia", would appear to be significantly higher in athletes than in thestandard population, but in fact the apparent sinus dysrhythmia disappearswhen the variability of R-R interval as a function of basal heart rate is taken intoaccount (R-R interval variation increases with decreasing heart rate). This is awell-recognized ECG pattern on ambulatory ECGs where the sinus pausesduring both awake and (especially) sleeping hours are significantly longer onathletes recordings than on control recordings. Ectopic atrial rhythm including the wandering atrial pacemaker orcoronary sinus rhythm have also been described.Nodal rhythm is more frequent in elite athletes. The escape threshold variesfrom 45 to 65 beats per minute and in some cases (in 15% of the subjects inour study) escape rhythm totally disappears only above 100-120 beats perminute. Idioventricular rhythm (Figure 1) is the event of a low sinus rate and/orof sinus pauses. This cardiac rhythm originates in pacemaker cells at a rate of40 to 100 beats per minute. Hyperkinetic Arrhythmia Hyperkinetic arrhythmia involves premature supraventricular andventricular beats. These disorders can be detected on the resting ECG butmost of the studies have used Holter monitoring to best quantify these
  6. 6. 6episodes of arrhythmia. A training session during the monitoring period isuseful because ECG stress training does not always produce significantepisodes. It is important to study arrhythmia during exercise and duringrecovery to clarify the links with autonomous tone and the epinephrine effect. Supraventricular Arrhythmias The incidence of premature supraventricular beats observed in trainedathletes (37.1 to 100%) is similar to, or higher than, that seen in the standardpopulation (20-80%). Some authors relate premature supraventriculararrhythmias to training level and suggest athletes bradycardia could be anexplanation. Most often, these premature beats are isolated and infrequent(less than 15 to 20 per 24 hours). They are asymptomatic and may disappearduring exercise. Complex supraventricular tachyarrhythmias which provokepalpitations are rarely described (0.5 to 5%) and suggest an underlying heartdisease such as the Wolff-Parkinson-White syndrome or prolapsus of themitral valve. The role of vegetative imbalance has been suggested in cases ofparoxysmal atrial fibrillation. Ventricular arrhythmias On resting ECG recordings, the incidence of ventricular arrhythmias intrained athletes is similar to or much higher (0.5 to 4%) than in the standardpopulation (0.6 to 0.7%). On the basis of Holter studies, most authors concludethat the incidence in athletes (30 to 45%) is the same as in untrained subjects(16-55%) but in one controlled study, the incidence was higher in athletes(70%). Generally, premature ventricular beats are unifocal, isolated, infrequent(less than 50 per 24 hours), asymptomatic and disappear at the onset ofexercise.
  7. 7. 7 In our clinical experience with regularly screened athletes, wedistinguished (Figure 2) between old asymptomatic arrhythmia, whichdisappears during exercise and reappears during the slow phase of recoverand which we consider to be benign, and a newly occurring, often symptomatic(unexplained decline in performance) ventricular arrhythmia which usuallypersists or becomes worse during stress testing. This situation, which suggestscatecholamine sensitive focal arrhythmia, always requires a complete cardiacexamination to eliminate a latent heart disease. Overtraining, which sometimesprovokes hyperkinetic arrhythmias through changes in biological mechanisms,must be suspected only if the cardiac examination is normal. Other complex ventricular arrhythmias such as multifocal or repetitivepremature ventricular beats, ventricular tachycardia and R on T phenomenaappear to have the same incidence in trained and untrained individuals. Someauthors have observed paroxysmal ventricular tachycardia in 0 to 7.5% ofathletes (ventricular tachycardia is classically nocturnal but sometimes appearsin daytime) and in 0 to 5.7% in untrained subjects. Here again some authorsdescribe a higher incidence of complex arrhythmias in trained subjects andexplain their controversial results by the training level in the general population.For these authors regular moderate physical training could protect againstventricular arrhythmias while very intensive training could favor them, perhapsthrough a prolonged QT interval. In contrast with cases of pathological cardiachypertrophy, no study has been able to demonstrate a correlation betweenECG or echocardiographic cardiac hypertrophy and hyperkinetic arrhythmia inathletes. In concluding this chapter, it can be stated that hypokinetic arrhythmiasin athletes are common and benign. The discovery of an episode ofhyperkinetic arrhythmia, particularly ventricular hyperkinetic arrhythmia, in anathlete often raises the question as to how many single extra beats should be
  8. 8. 8tolerated. This is especially true in high level trained subjects who undertakemaximal exercise regularly and often encounter the well-known adrenergicstress. It would appear that the prevalence of hyperkinetic arrhythmia is nearlythe same in trained and untrained people and that cardiac adaptation tointensive training itself is not a determinant cause of malignant arrhythmia.Therefore the discovery of a recent or serious episode of hyperkineticarrhythmia in an elite athlete would require a full cardiac examination withHolter monitoring, stress testing, echocardiography, and if necessary anelectrophysiologic study.Impaired atrio-ventricular conduction First or second (with a Luciani-Wendkeback period, see Figure 3)degree atrio-ventricular block is relatively common in athletes (Table III).Inversely, third degree functional block is rarely described and until now theMobitz type II and higher degree atrio-ventricular blocks must be considered aspathological and require cardiologic screening. These disorders result mainlyfrom changes in autonomous tone and disappear during stress testing and orpharmacological tests. Their higher, although intermittent (nocturnal predominance), incidencein Holter studies (Table III) would confirm their functional character. Acorrelation with training intensity has been reported. Although the samephysiological explanations have been proposed as for hypokinetic arrhythmiaand conduction disorders in athletes, it must be noted that no real correlationhas yet been described linking the two phenomena. The prevalence of the pre-excitation syndrome (i.e. the Wolff-Parkinson-White syndrome and the short PR syndrome) in athletes is nearlythe same as in the standard population (0.16 to 1%) even though changes in
  9. 9. 9autonomous tone could unmask accessory pathways. The discovery of a pre-excitation syndrome in trained subjects always requires a full cardiacexploration.Ecg Disturbances Partly Related To Cardiac HypertrophyAs noted above, cardiac hypertrophy in the athlete is described as a classical"physiological" example of adaptative increase in heart volume. Many differentECG criteria have been proposed for the diagnosis of athletes cardiachypertrophy based on isolated voltage criteria (i.e. the Sokolow-Lyon Index) orvoltage and non-voltage criteria (i.e. the Romhilt-Estes Point Score System)such as intraventricular conduction delays and/or repolarization disturbances.Unfortunately, the different ECG parameters of cardiac hypertrophy observedin athletes are poorly correlated with the results of non-invasive investigationssuch as echocardiography or with those of invasive or anatomic studies. Thiscan be explained, at least partially, by the fact that these populations arecomprised of young and physically fit individuals. Thus the ECG does notappear to be an extremely useful tool for the assessment of cardiachypertrophy in the athlete. Nevertheless, it is essential to recognize the features of elite athletesECGs. Increased P wave amplitude, with or without notching, can be observedalthough several studies failed to demonstrate any significant differencecompared with matched controls. Right ventricular hypertrophy, based on theclassical Sokolow-Lyon Index (RV1 + SV5), has been reported in 4.5 to 6.9% ofathletes. In heterogeneous and small samples of athletes, the incidence of leftventricular hypertrophy based on a Sokolow-Lyon Index (SV1 + RV5 or RV6) >35 mm has been reported to vary from 8 to 85% compared with 5% in the
  10. 10. 10general population. Inversely, in our study of a large population of trainedsubjects (Table I), and in the study by Venerando et al. (12,000 subjects), therewas no real enhancement of the Sokolow-Lyon Index. The use of new cardiac hypertrophy ECG criteria, including total QRSamplitude in 12-lead ECGs, appears to be helpful and in our own study (TableIV) we found that this sum (mean: 192 ± 40 mm) was higher than the classicalsedentary sum (< 128 mm) but clearly less than the sums described in heartdiseases (aortic stenosis > 244 mm; aortic regurgitation > 246 mm). Based onvectocardiographic criteria, the prevalence of left ventricular hypertrophy isabout 40% (37-46%). Electrical wave delays have also been studied in athletes. The incidenceof right and left atrial hypertrophy is low. The duration of QRS complexes iscorrelated with the size of the heart chambers and many authors suggest thatthe best criteria for right ventricular hypertrophy in the athlete is the presenceof intraventricular conduction delay. This delay, which appears on the ECGtracing as a notching or slurring of the QRS complex on D3, aVF and on theright precordial leads, is often observed (3.2 to 70%). These features suggest,as does the well-known incomplete right bundle branch block (prevalence 1.7to 51%), an asymmetrical cardiac hypertrophy with right ventricularpredominance. Though vectrocardiographic studies have also noted a highfrequency of right ventricular hypertrophy (18 to 30%) this explanation isquestionable since echocardiographic data do not offer a confirmation.Incomplete right bundle branch block does not appear to be linked to changesin autonomous tone since it persists during stress testing. Ventricular apicalthickness may be involved. Complete right bundle branch block is much rarer(0.08 to 0.31%) and left bundle branch block is normally not observed in theelite athlete.
  11. 11. 11 Unlike cardiac patients, and in spite of these cardiac hypertrophy ECGcriteria, the QRS axis is often normal. A vertical QRS axis may be observed (10to 27%) and left deviation is seldom reported (10 to 12%). Similarly, associatedpathological repolarization is not common. In summary, trained athletes show a high incidence of cardiachypertrophy based on ECG criteria. These phenomena, including right bundlebranch block, are related to physical training since the incidence decreasessignificantly with deconditioning. Nevertheless, these features cannot be fullyexplained by cardiac hypertrophy alone. Besides anatomic heart adaptation,other factors including age, body weight, body surface area, fat-free weight anddepth of the heart in the chest may also play a role. ECG criteria of cardiachypertrophy are however, as are echocardiographic features, quite different inelite athletes as compared with those described in the patients with heartdiseases.Repolarization disturbances Repolarization disturbances are a striking feature observed in "athletesheart syndrome". These phenomena lie between a physiologic and pathologicstate (i.e. pericarditis, ischemia, metabolic disturbances.…). It is difficult to givea precise assessment of their prevalence partly because of seasonal andcareer variations. Holter monitoring is less useful than stress testing in thissituation. No single explanation has been proposed for these disturbances,although changes in autonomous tone and/or cardiac hypertrophy and/orelectrolyte abnormalities have been proposed. These repolarizationdisturbances are generally asymptomatic.Several classifications have been proposed. We think the most useful is thedescriptive classification developed by Zeppilli and Caselli. These authors
  12. 12. 12propose four criteria. Criteria (a) and (b) are classically described asminorrepolarization abnormalities. Criteria (a), the so-called "early repolarization syndrome" is the most frequent (10-100%). The top of the ST-T segment elevation often has a dip in the initial portion. It has been speculated that changes in autonomous tone could be the cause. Sympathetic tone decrease reveals inherent a non-homogeneity phase of the ventricular repolarization, the epicardium repolarizing first. The ECG pattern, well-correlated with duration and training level is age-dependent and benign. This is supported by the fact that it disappears either at the onset or early during stress testing. Criteria (b) is classically characterized as negative T waves in inferior (D2, D3 or aVF) or right precordial (V1-V3) leads; low amplitude or flat T waves can also be observed. Described in 3-31% of the trained population, they regress as a general rule during exercise. They must be related to vagotonic-induced heterogeneity of the myocardial action potential. They are sometimes associated with echocardiographic criteria for cardiac hypertrophy. Criteria (c) and (d) are described as marked repolarization disturbances.In our experience as in that of Venerando, the prevalence is relatively low(0.6-2.8%). A complete cardiac work-up is always needed. Criteria (c) is defined as JT segment depression with positive low- voltage isoelectric or diphasic T waves. This feature which evokes subepicardial ischemia is a questionable physiological adaptation and must be assessed carefully because it disappears inconsistently during stress testing or after a long period of deconditioning.
  13. 13. 13 Criteria (d) is defined as T wave inversion in the left precordial leads (V4 - V6) which also disappears inconsistently during stress testing (Figure 4). In a study involving 98 athletes who presented features (b), (c) and (d),Zeppilli et al. reported no demonstrable heart disease in 53%, prolapsus of themitral valve in 37%, hyperkinetic heart syndrome in 3% and hypertrophiccardiomyopathy in 4%. More recently certain authors have stressed thatnegative T waves on the right precordial leads in athletes, especially whenassociated with incomplete right bundle branch block or premature ventricularbeats with a left bundle branch block configuration, may reveal right ventriculardysplasia. Other repolarization disturbances have been described in the eliteathlete including the common and benign evident U wave (especially inprecordial leads) and a prolonged corrected QT interval (prevalence 10 to15%) which could be explained by changes in autonomous tone and for which,in trained subjects, no real relationship with ventricular arrhythmias has beenobserved. Thus the prevalence of ECG and vectocardiography patterns ofrepolarization disturbances, especially minor abnormalities, is higher in trainedindividuals than in the untrained population. No unequivical explanation hasbeen proposed. These features vary spontaneously and are not correlated withphysical fitness. Their interpretation must take into account different factorsincluding age, ethnic origin, training level and symptoms. Venerando hasstressed the criteria of benign disturbances: healthy and totally asymptomaticathletes with good physical capacity (VO2max), normal duration of QRScomplex and lack of (or constantly reversible) spontaneous (exercise) orinduced (pharmacodynamic tests) ECG abnormalities.
  14. 14. 14 In the present state of the art, the recent discovery of markedrepolarization abnormalities requires a compete cardiac work-up, including atleast stress testing and echocardiography.Comparison Of "Endurance" And "Power" Physiological adaptation is generally divided into two categoriesresulting from the effects of two types of training methods: aerobic andanaerobic. Actually, the results of both ECG and echocardiographic studies arerather controversial. This can be explained, at least in part, by the fact thatmost athletes undertake both types of training simultaneously. In our personal study (Figure 5) we found that the prevalence ofbradycardia and incomplete right bundle branch block was higher in endurancethan in power athletes. Inversely, premature ventricular beats occurred morefrequently in power athletes. Some authors stress the fact that sinus pauseslonger than 2,000 ms, ECG criteria of left ventricular hypertrophy andprolongation of the corrected QT interval are more frequent in enduranceathletes. On the other hand, some authors suggest that marked repolarizationdisturbances tend to be associated more readily with isometric training.
  15. 15. 15Suggested readings:1- Carré F. and J.C. Chignon. Advantages of electrocardiographic monitoring intop level athletes. Int. J. Sports Med. 12: 236-240, 19912- Ferst J.A. and B.R. Chaitman. The electrocardiogram of the athlete. SportsMed. 1: 390-403, 19843- George K.P., L.A. Wolfe, G.W. Burgraff. The "Athletic Heart Syndrome".Sports Med. 11: 300-331, 19914- Huston T.P., J.C. Puffer, W.M. Mc Millan-Rodney. The athletic heartsyndrome. New Eng. J. Med. 313: 24-32, 19855- Lichtman J., R.A. ORourke, A. Klein et al. E.C.G of the athlete. Arch. Intern.Med. 1323: 763-770, 19736- Rost R.and W Hollmann. Athletes heart- a review of its historicalassessment and new aspects. Int. J. Sports Med. 4: 147-165, 19837- Venerando A. Electrocardiography in sports medicine. J. Sports Med andPhys. Fitness. 19: 107-128, 19798- Zeppilli P., A. Pelllicia, M.M Pirrami et al. Ethiopathogenetic and clinicalspectrum of ventricular repolarization disturbances in athletes. J. SportsCardiol. 1: 41-51, 1984
  16. 16. 16Figure LegendsFigure 1. Intermittent idioventricular rhythm in a long distance runner.Precordial lead V3, amplitude divided by two.Figure 2. Two typical cases of isolated premature ventricular beats observedon 24-hour Holter recordings in athletes.Subject 1 was a soccer player with old, asymptomatic, isolated prematureventricular beats. Hourly frequency of premature beats does not vary.Subject 2 was a weight lifter with recent, symptomatic, isolated prematureventricular beats. A peak frequency occurred during two training sessions (T)h = hours of monitoring, nb•h-1 = number of premature ventricular beats perhour.Figure 3. Asymptomatic second degree atrio-ventricular block with a Luciani-Wenckeback period observed in a cyclist during the competition period. Pwaves are noted with an arrow (∇).Figure 4. An asymptomatic, 35-year-old, well-trained long distance runner.Resting ECG shows incomplete right bundle branch block and a negative Twave in the V5 lead.Maximal exercise ECG shows a significant (2 mm) JT depression (V5).Recovery ECG (5 min) showing a normalization of the T wave on V5.Exercise thallium myocardial scintigraphy was normal and echocardiographyshowed an asymmetrical septal hypertrophy (12 mm).Figure 5. Respective prevalence of resting ECG features observed inendurance athletes (n = 5,700) and power athletes ( n = 526) in our own study.
  17. 17. 17BRA = sinus bradycardia, AVB = atrio-ventricular block, RBBI = incompleteright bundle branch block, SVPB = premature supraventricular beats, VPB =premature ventricular beats.
  18. 18. 18Table LegendsTable I. Classical ECG criteria: comparison between trained individuals andgeneral population.These data were obtained in men and women 15 to 40 years of age.Data concerning trained individuals were observed in athletes examined at theFrench National Institute of Sports. Three training level groups were described:I (three to five hours per week), II (five to ten hours per week), III (more thanten hours per week, national team level).Data concerning the general population were described by Blondeau andHiltgen, 1980 (15-19 years of age, n = 200; 20-29 years, n = 200; 29-39 years,n = 200).* T wave amplitude measured on the precordial lead V5** QT corrected for a heart rate of 60 beats per minute*** QT corrected using the Bayes formula.Table II. Incidence (%) of athletes hypokinetic arrhythmiaRanges are based on the highest and lowest values reported in the literatureand were observed in controlled and uncontrolled studies.bpm = beats per minute(--) = no data available.Table III. Incidence of athletes atrio-ventricular conduction impairmentRanges are based on the highest and lowest values reported in the literatureand were observed in controlled and uncontrolled studies.* One study (Viitasalo et al., 1982) reported an incidence of 8.6% for Mobitz IIatrio-ventricular blocks which were, very probably, in fact Luciani-Wenckebach
  19. 19. 19type II atrio-ventricular blocks with a very small increment in the PR intervalduration (personal communication of the authors).Table IV. Comparison of two ECG criteria (mean ± SD) for cardiac hypertrophyin trained subjects, (n = 730).Three training level groups were described (see Table I).O2max = maximal oxygen consumption.S-L Index = Sokolow-Lyon Index (SV1 + RV5 or RV6).Total QRS = sum of the QRS complex amplitudes in the twelve ECG leads.