a Department of Cardiology, University Hospital Gasthuisberg, University of Leuven, Leuven, Belgium
b Department of Cardiology, Maxima Medical Centrum, Veldhoven, Netherlands
c Department of Cardiology, Hospital Oost-Limburg, Genk, Belgium
d Members of the Cardiological Committee of the Union Cycliste Internationale (U.C.I.), Belgium
* Correspondence to: Hein Heidbüchel, M.D., Ph.D., Department of Cardiology, University Hospital Gasthuisberg, Herestraat 49, B-3000 Leuven, Belgium. Tel: 32-16-34 42 48; fax: 32-16-34 42 40
E-mail address: Hein.Heidbuchel{at}uz.kuleuven.ac.be
Received 27 January 2003; revised 25 March 2003; accepted 18 April 2003 This paper was guest edited by Prof. Martin Schalij, Leiden University Medical Center, The Netherlands
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Abstract |
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Results We report on 46 high-level endurance athletes with ventricular arrhythmias (45 male; median age 31 years) followed-up for a median of 4.7 years. Eighty percent were cyclists. Hypertrophic cardiomyopathy or coronary abnormalities were present in 5%. Eighty percent of the arrhythmias had a left bundle branch morphology. Right ventricular (RV) arrhythmogenic involvement (based on a combination of multiple criteria) was manifest in 59% of the athletes, and suggestive in another 30%. Eighteen athletes developed a major arrhythmic event (sudden death in nine, all cyclists). They were significantly younger than those without event (median 23 years vs 38 years; P=0.01). Outcome could not be predicted by presenting symptoms, non-invasive arrhythmia evaluation or morphological findings at baseline. Only the induction of sustained ventricular tachycardia (VT) or ventricular fibrillation (VF) during invasive electrophysiological testing was significantly related to outcome (RR 3.4; P=0.02). Focal arrhythmias were associated with a better prognosis than those due to reentry (P=0.02) but the mechanism could be determined in only 22 (48%).
Conclusions Complex ventricular arrhythmias do not necessarily represent a benign finding in endurance athletes. An electrophysiological study is indicated for risk evaluation, both by defining inducibility and identifying the arrhythmogenic mechanism. Endurance athletes with arrhythmias have a high prevalence of right ventricular structural and/or arrhythmic involvement. Endurance sports seems to be related to the development and/or progression of the underlying arrhythmogenic substrate.
Key Words: Athlete Sports Arrhythmia Sudden death
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1. Introduction |
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We report on a group of 46 high-level endurance athletes, predominantly cyclists, with complex ventricular arrhythmias (i.e. at least non-sustained ventricular tachycardia). The findings at initial work-up and their followup (with a median of 4.7 years) is described.
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2. Methods |
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2.2. Evaluation
Apart from routine non-invasive testing (ECG, Holter, exercise testing) electrophysiologic studies (EP studies) were performed in 40 of the 46 athletes, always off antiarrhythmic drugs (5xhalf-life) and without sedation. A supraventricular arrhythmia was excluded. The ventricular stimulation protocols were standard, consisting of fixed rate pacing (at cycle lengths down to 240ms) and delivery of up to three extrastimuli at basic cycle lengths of 600 and 400ms, both in the right ventricular apex and outflow tract (down to the ventricular refractory period but never <180ms). In all but three athletes a similar stimulation protocol was applied during isoproterenol infusion (14µg/min) if the baseline study was negative. Only the induction of monomorphic VT was considered specific under these conditions.
Efforts were made to distinguish automatic or triggered foci from reentrant circuits as the mechanism of the arrhythmia. A focal mechanism was suspected in the case of frequent spontaneous monomorphic (or multiple monomorphic) premature ventricular contractions (PVCs) or runs of PVCs (on Holter or induced by exercise testing or administration of isoproterenol), with variable coupling intervals and shortening of the cycle length with increasing adrenergic tone, and/or with a morphology typical for idiopathic right ventricular outflow tract VT. Reentrant arrhythmias were identified by classical criteria during the EP study, like reproducible inducibility by extrastimuli (with a constant or increasing return cycle with decreasing coupling interval), resetting by extrastimuli, entrainment with (concealed) fusion and/or termination by programmed ventricular stimulation.
Signal-averaged ECG measurements were performed on tracings band-pass filtered between 40 and 250Hz, and with a final average noise level of 0.3µV. The following criteria were used: (1) a filtered QRS duration
118ms for women and
120ms for men was considered abnormal; (2) the duration of the high-frequency low-amplitude signals (<40µV) was abnormal if more than 39ms, and (3) the mean voltage of the last 40ms needed to be >20µV for normality. Late potentials (LP) were present if 3/3 criteria were fulfilled, and probable for 2/3 positive criteria.
2.3. Statistical analysis
Summary values are given as mean±SD or median (for not-normally distributed values). The relation between nominal variables was tested using Fischer's exact test or Chi-square analysis. Comparisons between groups were made by non-parametric MannWhitney tests or logistic regression. All tests were two-tailed. KaplanMeier analysis was used to study survival free of sustained ventricular arrhythmias and sudden death, with log-rank testing to compare survival across groups. A P-value <0.05 was considered significant. Relative risk ratios were calculated by a Cox proportional hazard method.
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3. Results |
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Demographic characteristics, presenting symptoms, electrophysiological and morphological findings are summarized in Tables 1 and 2. Most of those referred because of presyncope or syncope had developed symptoms during exertion (26 of 30; 87%). There was very little evidence for underlying coronary or left ventricular disease: most athletes had high-normal or slightly enlarged left ventricular cavities (52mm in 54%) and a high-normal wall thickness, which were considered normal for the endurance athlete's heart.7,8Only one athlete had a septal wall thickness of 17mm, and it was
15mm in four. Coronary angiography revealed bridging over the left anterior descending artery in one (with a stenosis of 20% and without demonstrable ischaemia during exercise).
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There was indication of right ventricular arrhythmogenic involvement in a majority of the athletes. Thirty-seven athletes (80%) had ventricular arrhythmias with a left bundle branch morphology, indicating an origin in the RV or the interventricular septum. Also other electrophysiological observations (negative T-waves from V1 to at least V3 on the resting ECG; epsilon-waves, i.e. a delayed component of the QRS complex in V1 or V2,9late potentials) and morphological findings (angiography; magnetic resonance imaging, myocardial biopsy) pointed more often to RV than LV disease(Tables 1 and 2).
When the diagnostic criteria for ARVD were applied (Table 4),9definite RV arrhythmogenic and/or pathological involvement was present in 27 of the athletes (59%) because of the presence of 2 major or of one major and
2 minor criteria. Moreover, another 14 (30%) had one major and one minor, one major, or two minor criteria. The arrhythmias in these 41 patients had a left bundle branch block morphology in 37 (90%), compatible with a RV origin. From the four patients with an LV septal thickness
15mm, two had definite criteria for RV involvement, and two had very frequent PVCs with left bundle branch block morphology (which also is a major criterion for RV arrhythmogenic involvement). One patient with myocyte fibre disarray on biopsy had no echocardiographic criteria for HCM but instead had two major and two minor criteria for ARVD.
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Eighteen athletes had a major arrhythmic event during follow-up. Half of them (n=9), all cyclists and not treated with an ICD, died suddenly (after a median of 2 years; range 0.59.3 years). Moreover, six of the nine ICD patients received one or more appropriate shocks for VT or VF, while three athletes had recurrences of sustained monomorphic (non-syncopal) VT. All but one episode of sudden death occurred during light or moderate physical activity, none during competitive sports. Eight of those 18 athletes were taking beta-blockers (three in combination with a Class 1 agent and one after a partially successful ablation) and one amiodarone.
Table 3evaluates the predictive value of foregoing findings for major arrhythmias. No symptoms or arrhythmia findings during non-invasive testing (Holter or exercise test) could predict outcome. Major arrhythmias occurred in 15 athletes with no or only mild symptoms (palpitations) at presentation. Also the recognition of overt structural abnormalities (LV or RV) or their degree (as the count of minor and major ARVD criteria) did not discriminate significantly. None of the four patients with LV wall thickness 15mm developed a major event.
Patients with a major event were younger than those without (median 23 years vs 38 years; P=0.01). Theonly diagnostic test identifying patients at risk was an invasive EP study (Fig. 1) with a relative risk of 3.4 in inducible patients (P=0.02). Sensitivity, specificity and total predictive accuracy of EP inducibility was 62%, 74% and 70% respectively. However, even 20% of those with a negative EP study developed major arrhythmias. The cycle length of an induced monomorphic arrhythmia was not related to outcome. Although more athletes with major arrhythmias during follow-up had multiple inducible morphologies (5/9, 56% vs. 6/17, 35%), this did not reach statistical significance. Inducible patients were younger (30±8 years vs 37±11 years; P=0.03). Therefore, after adjusting for age in a Cox proportional hazard model, inducibility lost its statistical significance (P=0.11; RR 2.62 for inducible patients)
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4. Discussion |
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In this series of 46 high-level endurance athletes with complex ventricular arrhythmias both the proportion with evidence for underlying structural abnormalities and the incidence of major ventricular arrhythmic events during follow-up (median 5 years) was significantly higher than previously reported. Moreover, our data point to an unexpectedly high prevalence of RV arrhythmogenic involvement. These observations lead to some intriguing questions like whether the observed RV damage represents typical ARVD, whether there is a (causal) relationship between endurance sports and RV involvement, and whether other findings are helpful in predicting outcome.
Our data, based on a partly retrospective series with all its inherent pitfalls such as the incompleteness of data and inclusion bias, do not allow conclusions about the absolute risk for sudden death in endurance athletes presenting with complex ventricular arrhythmias. However, this risk is definitely higher than expected from data in general athlete populations seen during screening visits.6It is important to note that our data do also not allow calculation of absolute risk comparisons between different sports, even when corrected for the number of athletes participating in a given sport, since more elaborate screening or faster referral in cyclists could have increased their relative proportion.
Our data confirm the difficulty of predicting outcome based on non-invasive investigations. Echocardiographic measurements may be difficult to categorize into adaptive or pathological and depend on the type of sports.10Repolarization abnormalities are more common in endurance athletes, but their predictive value isunclear.4,11,12Arrhythmia findings regarding frequency and complexity may not reliably be extrapolated from larger athlete cohorts as discussed. An extended work-up combining criteria like those for the diagnosis of ARVD may however point to more subtle forms of underlying structural cardiovascular disease, and therefore indicate increased risk.7,13Formal ending of all competitive and semi-competitive sports seems mandatory if there is evidence for underlying structural damage.9,14Also other authors have pointed to the high fatality rate when ARVD is present in a competitive athlete.2The value of an EP study has been suggested before,6,13,15and an EP study was the only test in our series that was statistically related to outcome although its predictive accuracy remained low. This stresses the need for a large, prospective and concerted scientific study with regard to the prognostic power of different investigations. It is clear that this is of paramount importance for all athletes with (semi)-professional sports activity. The association between age and EP inducibility may indicate inclusion bias, i.e. athletes with more progressed disease and/or at higher risk probably present with symptoms at younger age.
RV structural changes can result in reentrant arrhythmias, as expected. Less anticipated was the fact that in others the arrhythmia mechanism was of focal origin. A few athletes had a focal mechanism without detectable structural RV damage, although this may have been too limited to be diagnosed.16Although the numbers are small and preclude definitive statements, it is interesting to note that a focal mechanism seems to be correlated with better outcome than reentry. It strengthens the importance of the underlying structure for prognosis and of an EP study in risk stratification.
4.2. Endurance sports and arrhythmogenic structural RV damage
Our series only included a small minority of athletes with preexisting left ventricular or coronary disease. This contrasts with previously published series of athletes with (aborted) sudden death, that included primarily basketball and American football players (68%) but was virtually free of cyclists.1The low prevalence of HCM may be attributable to prior screening visits with ECG and echocardiography more easily detecting LV than RV disease. Italian series of athletes with arrhythmias have reported a high incidence of ARVD although it only accounted for 627% of competitive athletes with arrhythmic manifestations,2,3while its incidence was even lower in non-Italian series.1A combined analysis of the arrhythmic and morphological findings in our series pointed definitely and probably to a RV origin in 59% plus 30% of the athletes. Exercise may act as the trigger for arrhythmias in athletes with pre-existing ARVD. Given the high prevalence of ARVD in their region, certainly in part genetically determined,1719the Italian authors considered this entity as underlying in these athletes.2
On the other hand, there is some evidence that endurance sports by itself may have contributed to the RV structural and electrical modifications. Arguments for such an hypothesis are: (1) ARVD, and familial ARVD in particular, is a rare condition in our countries, as it is in North-America. Familial ARVD was only evident in one athlete. (2) Immediately after a competitive triathlon event, paradoxical RV dilatation (contrasting with the LV) has been documented echocardiographically.20It was attributed to the greater increase in RV work: endurance sports disproportionately lead to greater strain on the RV. (3) Jordaens et al. reported that cyclists with or without documented arrhythmias had more pronounced late potentials (a major ARVD criterion) than basketball players.21(4) In most Italian patients with ARVD MRI revealed clear fat infiltration of the wall, which was absent in our series (present in only two out of 28 MRI studies). The ARVD described by these authors may be of a different aetiology and nature (familial, genetic)1719than the structural RV damage we observed. (5) The incidence of atrial fibrillation is higher in athletes.22,23Atrial dilatation and remodelling has been suggested as a factor explaining this association.22Therefore, we speculate that endurance sports by itself may also lead to RV structural damage that might not have developed without the activity. Long-lasting volume overload could be the mechanism leading to or contributing to the development of RV structural changes.
Doping agents are known to increase the risk of cardiac death.24Chronic use of performance-enhancing drugs may be more prevalent due to the intense demands during endurance sports. However, its prevalence and the type of drugs can never reliably be assessed. At the other hand, direct cardiac effects of these drugs would be expected to be more obvious in the left ventricle (having the largest mass), contrasting with our observations that the majority of arrhythmias is of right ventricular origin. Indirectly, these drugs may promote volume/pressure overload and arrhythmogenic changes by allowing longer and heavier training and competition. Also, it is well recognized that different types of sports have a different influence on the cardiovascular system.2527Cycling is a particular type of strain, even when compared with other endurance athletes like runners: on top of the isotonic and aerobic work of the leg musculature, it also includes an important part of isometric work, particularly with the upper part of the body.10,26,28Moreover, cyclists regularly engage in anaerobic dashes in between long episodes of aerobic work. Practice and competition are performed during much more time than is the case in many other sports.
The type of sports may therefore be an important factor in the prognosis of athletes with arrhythmias. Our data suggest that intense endurance athletes (and cyclist in particular) may have a clinical evolution different from other athletes. Further research is mandatory to assess the importance of the type of sports in the risk stratification of athletes with arrhythmias, and of the different factors involved. If the hypothesis that long-lasting volume overload promotes arrhythmias would prove to be correct, it raises concern about the ever increasing workload presented to competitive endurance athletes.
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5. Conclusions |
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Acknowledgments |
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References |
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