Europace (2018) 20, 1401–1411 REVIEW

doi:10.1093/europace/eux294

The athlete’s heart is a proarrhythmic heart,

and what that means for clinical decision
making

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Hein Heidbuchel*
Department of Cardiology, Antwerp University and University Hospital Antwerp, Wilrijkstraat 10, 2650 Edegem, Belgium

Received 16 July 2017; editorial decision 20 August 2017; accepted after revision 25 August 2017; online publish-ahead-of-print 13 December 2017

Recurring questions when dealing with arrhythmias in athletes are about the cause of the arrhythmia and, more importantly, about the eli-
gibility of the athlete to continue sports activities. In essence, the relation between sports and arrhythmias can be understood along three
lines: sports as arrhythmia trigger on top of an underlying problem, sports as arrhythmic substrate promotor, or sports as substrate in-
ducer. Often, there is no sharp divider line between these entities. The athlete’s heart, a heart that adapts so magically to cope with the
demands of exercise, harbours many structural and functional changes that by themselves predispose to arrhythmia development, at the
atrial, nodal and ventricular levels. In essence, the athlete’s heart is a proarrhythmic heart. This review describes the changes in the ath-
lete’s heart that are related to arrhythmic expression and focuses on what this concept means for clinical decision making. The concept of
the athlete’s heart as a proarrhythmic heart creates a framework for evaluation and counselling of athletes, yet also highlights the difficulty
in predicting the magnitude of associated risk. The management uncertainties are discussed for specific conditions like extreme bradycar-
dic remodelling, atrioventricular nodal reentrant tachycardia, atrial fibrillation and flutter, and ventricular arrhythmias.
...................................................................................................................................................................................................
Keywords Sports • Athlete’s heart • Arrhythmia • Eligibility

an athlete with an underlying and pre-existing condition (structural

Introduction or electrical, inherited, or acquired) may develop an arrhythmic
We marvel about the athlete’s heart, a heart that adapts so magically event, because physical activity sets the stage for an arrhythmia to
to cope with the pursuits of pushing our physical limits. It hypertro- occur. This concept forms the rationale behind preparticipation
phies and enlarges to be able to perform higher stroke work. It slows evaluation of athletes to detect the underlying problem in time, so
down at rest and increases its heart rate reserve to further optimize that unwanted arrhythmic events can be prevented by adaptation of
cardiac output during exercise.1,2 Athletes encounter extreme the level of exercise.3 The second line of interaction is that physical
physiological conditions, both during physical activty and paradoxically activity may promote the development of the underlying arrhythmic
also at rest, with high adrenergic tone, potential for ischaemia, ionic substrate, accelerating the development of the phenotype and of ar-
disturbances and high wall stress during physical activity, and high vagal rhythmic events. A typical example is the promotion of right ven-
tone, bradycardia, and dispersion of repolarization at rest. Mix in atrial tricular (RV) dilatation and arrhythmias in the presence of an
and ventricular extrasystoles as triggers, and all these wonderful underlying desmosomal mutation, as has been clearly demonstrated
structural and functional changes may predispose the athlete’s heart in both animal and human studies.4,5 The third line is that sports by it-
to develop arrhythmias, at the atrial, nodal and ventricular levels. In self, even in the absence of underlying genetic predisposition, but by
essence, the athlete’s heart is a proarrhythmic heart (Figure 1). nature of the remodelling of the athlete’s heart itself, induces a sub-
Conceptually, the relation between sports and arrhythmias can be strate for arrhythmias, as will be further discussed below. Moreover,
considered along three lines: sports as arrhythmia trigger, as arrhyth- it may well be that the three mechanisms reinforce each other: e.g. al-
mic substrate promotor, or as substrate inducer. The most widely though there is no evidence that sports remodelling increases the
held view on the association between sports and arrhythmias is that QTc interval, bradycardia will lead to longer QT intervals and to

* Corresponding author. Tel: þ32 3 821 46 93; fax: þ32 3 830 23 05. E-mail address: hein.heidbuchel@uantwerpen.be, hein.heidbuchel@uza.be, heinheid@gmail.com
Published on behalf of the European Society of Cardiology. All rights reserved. V
C The Author 2017. For permissions, please email: journals.permissions@oup.com.
1402 H. Heidbuchel

more heterogeneity of repolarization at rest that could contribute to

the development of arrhythmias at rest, while a larger cardiac muscle
mass may further enhance the risk for ongoing fibrillation. Such inter-
actions have been poorly studied so far, given the need for large data-
bases linking predisposing conditions to arrhythmic outcomes.
Over the past decades, we have witnessed an increasing propor-
tion of society engaging in ultra-endurance events, which are well in
excess of the health-promoting exercise recommendations.6 As ar-
rhythmia specialists, we are confronted more and more with the di-
lemma to draw the line between what is still physiological or what
becomes pathological, especially when asked to guide athletes on
whether they can continue safely or have to slow down. These are

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difficult judgments, since exercise is one of our strongest medicines
to prevent and revert cardiovascular disease. Insights in how the
athlete’s heart is a proarrhythmic heart may help us to give more ra-
tional recommendations in a field where evidence-based medicine is
often lacking. Description of the adapatations of the athlete’s heart
does not form the primary focus of this text, since there are good re-
cent reviews on the topic.1,2,7 Rather, this text wants to focus on
how these insights play a role in the management decisions in athletes Figure 1 The concept of how the athlete’s heart is also a proar-
with arrhythmias. This article will also highlight the many unknowns rhythmic heart. Many changes of the athlete’s heart parallel changes
in this field, uncertainty that has an impact on our eligibility recom- that are known to be proarrhythmic in general. There is no clear
mendations and that defines the boundaries of the shared decision boundary on when physiological adaptation, which can be extreme
making with the athletes seeking our advice. in highly trained athletes (especially endurance athletes), starts con-
tributing to arrhythmogenesis, or becomes clearly pathologic.

A quick overview on why the increase in LV mass and dimensions.12 In fact, these changes are pre-
athlete’s heart is a proarrhythmic sent and congruent in all four chambers of the heart, both at the ven-
heart tricular and at the atrial level.13 In some athletes, the eccentric
remodelling can be extreme. Despite still being ‘physiological’ (defined
We all agree that conditions that enlarge the atria (like valvular dis- as ‘in concordance with the VO2max of the athlete, and hence ex-
ease, hypertension, or heart failure) predispose to atrial fibrillation pected’) there is no clear definition on when such profound cardiac re-
(AF). We acknowledge the proarrhythmic role of the autonomic ner- modelling may increase the risk for arrhythmias at the atrial and
vous system by ablating vagal ganglia in the hope to increase our abla- ventricular level. Most likely, there is no real threshold: physiological
tion efficacy. We all understand that enlargement of the RV, like in dilatation may create a progressive propensity for developing arrhyth-
pulmonary valve regurgitation, is the strongest predictor for sudden mias (Figure 1). It explains why decision making becomes so difficult.
death in patients with tetralogy of Fallot.8 We know the epidemiolo- Intriguingly, the association between arrhythmias and female athletes
gical data that associate left ventricular (LV) hypertrophy and dilata- is 5 to 10 times weaker, an explanation which remains unclear (less
tion with sudden cardiac death in different populations.9 Finnish intense condition? hormonal factors?).
investigators have demonstrated that early repolariation, which is a The best evidenced example of gradual conversion from exercise-
very common finding in young trained individuals, is associated with a induced benefit to development of an arrhythmogenic substrate is
higher risk for sudden death.10 Yet, somehow, we remain reluctant the U-shaped incidence of AF or flutter (AFl) with endurance activity.
to accept that exactly the same changes may predispose the athlete’s Atrial enlargement, more atrial ectopy, and autonomic changes are
heart to arrhythmias and even sudden death. part of the cardiac adaptations of athlete’s heart,14 thereby
There is an increasing amount of data on the electrical, structural, modestly increasing the risk for AF at the high end of exercise. In a
and functional cardiac alterations of the athlete’s heart. Although for- meta-analysis of smaller studies mainly looking at endurance athletes,
mer research has focused on different remodelling patterns, especially a 5.3-fold increase of AF was noted.15 Later data from three much
in the LV, due to static or dynamic exercise, most athletes nowadays larger studies investigating the interaction between exercise and AF
combine both forms of training in their daily regimes. Pure power ath- confirmed a U-shaped pattern of the exercise dose–response curve
letes (e.g. weightlifters) develop a predominantly concentric remodel- whereby regular mild-to-moderate exercise provides strong protec-
ling but generally do not reach the same magnitude of LV mass as tion from AF, while long-term intensive endurance exercise consti-
endurance athletes. Cardiac alterations are particularly profound in tutes a risk factor, albeit small.16–19
those athletes engaged in high-intensity activities that are of long dur- As mentioned, most focus of ventricular adaptation in the athlete’s
ation and combine endurance with power (e.g. cycling, triathlon, and heart has historically been on the LV. It is the RV, however, that is
rowing).11 Maximal oxygen consumption during exercise correlates most taxed by strenuous endurance exercise. Since pulmonary pres-
strongly and directly with the eccentric cardiac remodelling and the sures increase almost linearly with increasing cardiac output, RV wall
The athlete’s heart, a proarrhythmic heart 1403

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Figure 2 Particular strain on the right ventricle during endurance sports activity. (A) Pulmonary pressures increase almost linearly with increasing cardiac
output, irrespective whether one is trained or not. In athletes, however, higher cardiac output will translate into higher peak systolic pressures. (B) This leads
to higher increase of RV wall stress than LV wall stress during sports. (C) In turn, this may explain why at the end of an endurance event transient contractile
dysfunction of the RV, but not of the LV, is observed during incremental workloads in an exercise cardiac magnetic resonance imaging setup. Data are pre-
sented as means and 95% confidence intervals. P-values are shown for the interaction between the change in ejection fraction and endurance exercise.
Asterisks denote statistically significant differences between baseline and post-race measures (P < 0.05 by paired samples t-test). Adapated from and repro-
duced with permission from Heidbuchel et al., Br J Sports Med 2012 (A&B),23 and Claessen et al., Med Sci Sports Exerc 2014 (C).20

stress increases more than LV wall stress (the latter being attenuated Current hypothesis is that these scar regions are the sequellae of sub-
as a result of the thicker LV wall and reduction of the systemic vascular clinical myocarditis. Athletes with such incidental finding, however,
resistance during exercise) (Figure 2A and B).20 This explains why tran- seem to have a high likelihood to develop major ventricular arrhyth-
sient contractile dysfunction of the RV (‘RV fatigue’), but not of the LV, mias during follow-up. Since similar incidental fibrotic areas in the LV
is observed at the end of an endurance event (Figure 2C), the size of are very rare findings in non-athletes, the hypothesis has been raised
which correlates with the leak of cardiac enzymes.21–23 Intriguingly, that intense exercise has a promoting effect on the development of
minor rises of tropinins are considered as myocardial damage in the this substrate. Maybe, intense exercise during a viral bout may make
context of ischaemic heart disease, whereas sports cardiologists tend the heart more vulnerable to develop scar, or exercise induces such
to call it ‘physiologic’. Why not accept that extreme wall stress on the scar regions on the background of an as yet unidentified genetic predis-
RV may result in some myocyte rupture, which may well repair in position. Clearly, more data are needed on this recently recognized
most instances? But maybe not in all and not after repetitive insults.24 new entity. However, it is another element in the main theme
This explains why exercising arrhythmogenic RV cardiomyopathy described here that underlying structural or electrical disease in ath-
(ARVC) patients and mice with desmosomal mutations develop an letes is not just a coincidence but that it may have been promoted or
overt phenotype of ARVC more rapidly than when sedentary.4,5 This induced by physical activity itself, i.e. recognition of the concept that
also explains why the observation of the development of a similar the athlete’s heart is a proarrhythmic heart.
phenotype even in the absence of mutations (both in humans and in
rats) is pathophysiologically plausible as the extreme of a spectrum,
dubbed ‘exercise-induced ARVC’ (ExI-ARVC) or ‘gene-elusive General consequences of the
ARVC’.25–27
More recently, there have been reports of large areas of delayed
concept
gadolinium enhancement (DGE) in the wall of the LV, sometimes as an Recognizing that the athlete’s heart is a proarrhythmic heart should
incidental finding in athletes presenting with an increase in ventricular not be interpreted as a reason to avoid physical activity. There is
premature beats (VPB) or new repolarization abnormalities.28,29 overwhelming evidence about the benefits of physical activity. Just as
1404 H. Heidbuchel

a tennis elbow is no reason to argue against people playing tennis, the changes may be part of the remodelling proces. These may explain
potential proarrhythmic potential of the athlete’s heart should not be why there is no full reversibility of sinus bradycardia after cessation of
used to scare people of sports. There is not any data that even high- the active carreer: former Tour de Suisse cyclists at an average of
level athletes have a higher mortality rate than non-athletes, on the 28 years after their active carreer had a higher propensity to pro-
contrary.30,31 But this does not negate the fact that some athletes found sinus bradycardia (<40/min; 10% vs. 2%), sinus pauses of >2.5 s
may be the victim of annoying or even life-threatening arrhythmias. (6% vs. 0%), and pacemaker implantation (3% vs. 0%) than matched
Rather, there are three important consequences of the arrhythmic golfers from the same population.36 In athletes, sinus bradycardia or
athlete’s heart concept: (i) that the public should be informed prop- pauses by itself are no reason for concern when they are asymptom-
erly that physical activity to promote health does not require inten- atic. In symptomatic athletes, deconditioning may resolve symptoms.
sive or strenuous workouts, nor competition, in line with current If that does not occur, and symptoms persist after 2–3 months of de-
public health recommendations for moderate activity6; (ii) that like all training, pacemaker therapy may be needed.
sports injuries, more intense physical activity is related to a higher Two situations are of uncertain relevance: when very long pauses

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propensity to develop heart sports injuries like arrhythmias, by itself (e.g. >4 s) develop during sleep, even when associated with abruptly
and/or by triggering those in patients with preexisting structural or increased vagal tone, there may be concern for a propensity to de-
electrical conditions; and (iii) that health professionals should take velop pause-mediated polymorphic ventricular tachycardia (VT) or
the amount of sports and its potential promoting or inducing proar- ventricular fibrillation (VF). Although never substantiated, it could ex-
rhythmic potential into account while evaluating and guiding athletes plain some unexpected sudden deaths in athletes during sleep. Such
with arrhythmias. long pauses require discussion with the athlete about the potential of
The main issue is not whether there is a relation between (too) extreme remodelling. In some, it is associated with a decline in
sports and arrhythmias but rather how large that effect is in the in- general performance (often interpreted as ‘overtraining syndrome’, a
dividual case and to what extent there is a risk for future life- vaguely defined syndrome), which could hint to the desirability of
threatening situations. The answer will define our management temporary and/or partial detraining with follow-up on the reversibil-
and eligibility recommendation. The effect size depends on the ity of the sinus nodal function.
type and phenotypic severity of the underlying disease but also on Secondly, we see athletes at younger age with more profound
the intensity of sports itself. The absolute magnitude, however, is bradycardia than before. This may have to do with the societal trend
very rarely documented in prospective series, and randomized, to start with intensive endurance sports earlier in life. There are no
long-term, studies are almost non-existent in the field of sports data on whether intensive endurance sports has more profound
cardiology. This leads to many grey zones, where some physicians remodelling effects on the developing heart, nor on the long-term
consider the risk as big enough to recommend refrainment from outcome of such findings. A case is shown in Figure 3. Will such ath-
sports, while others will allow continuation. The corrolary is that letes develop symptoms over the years, or is such extreme bradycar-
rigid eligibility recommendations will often be inappropriate, even dia at rest the expression of the ultimate athlete’s heart, capable of
when formulated by ‘groups of experts’. Athletes exploit such the highest performances? Together with colleagues, we have started
situation with medical shopping until they hear the reassurance a long-term athletic remodelling study, the Pro@Heart programme,
they wish for. In a sense, they may be right to do so, since in the to get more insights into long-term changes in the athlete’s heart
context of unclear additional risk, they consider it their right to be (www.proatheart.org). Today, management in such cases requires at
part of the decision to continue or not. The sports cardiological least very careful and long-term follow-up, sensitizing the athlete to
society will have to come up with a new model, where decisions reporting any potential symptoms.
on whether to continue or not are based on informed consent,
ideally as a partnership between athletes, their family, the team
and sports cardiologists. A mechanistic framework to consider Atrioventricular nodal re-entrant
the individual situation is highly needed. Therefore, the concept of arrhythmias
the athletic heart as proarrhythmic heart comes into play during
the evaluation of specific rhythm disturbances in the individual Atrioventricular (AV) nodal re-entrant tachycardia (AVNRT) is usu-
athlete. Some particular situations will be discussed in the next ally regarded as a coincidence when diagnosed in an athlete. We have
sections. noted, however, that athletes presenting with AVNRT have a signifi-
cantly higher proportion of atypical forms (i.e. Slow/Slow or Fast/
Slow subtype)37 compared to typical Slow/Fast AVNRT: in 53 com-
Sinus bradycardia: when is slow petitive athletes ablated for AVNRT at our institution between 1995
too slow? and 2016, 24 (34%) athletes had an atypical form vs. 302 of 1197
(17.6%) non-athletes (P = 0.001; Heidbuchel, unpublished observa-
The hallmark of the athlete’s heart is sinus bradycardia. Many asymp- tion). AVNRT in athletes also was more difficult to ablate, requiring
tomatic athletes have sinus pauses at rest and during sleep, often more RF applications and/or more higher septal or left-sided applica-
even exceeding 3 seconds.32 Sinus bradycardia is generally con- tions. We noted that in many cases there was a profound ‘bulging’ of
sidered the expression of a high vagal tone, i.e. functional in nature. the posteroseptal right atrial region that forms the anatomical target
However, recent elegant research has shown that there is a more for ablation of the slow AV nodal pathway. This may all be the ex-
fundamental intrinsic change of sinus automaticity through decreased pression of the structural remodelling of the athlete’s heart, with
expression of the pacemaker current If.33–35 Also (micro)structural larger atria and a more stretched posteroseptal region, leading to
The athlete’s heart, a proarrhythmic heart 1405

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Figure 3 Extreme bradycardia in a 16-year-old competitive cyclist. The resting ECG showed a sinus rhythm of 35 beats/min (A), while the Holter
at rest indicated heart rates during the night going as low as 23 beats/min, without any major sinus pauses (B). The athlete was completely asymptom-
atic and performing as one of the best in his age category, both at a national and at an international level. One may wonder in how far his extreme
sinus remodelling is merely a reflection of his high training standards, whether it is a marker of his high-performance cardiac potential, or whether it is
a warning sign of symptomatic sinus node disease in the future.

more unusual arrhythmia substrates due to increased anisotropy. Some may prefer to use cryoenergy in such cases, although it may be
The outcome of ablation was similar in athletes compared to non- associated with more frequent recurrences.
athletes, with no athlete developing AV block (neither permanently
nor transiently) during ablation. Nevertheless, it is fair to discuss the
anticipated more complex ablation approach with athletes, maybe Atrial fibrillation and atrial flutter
even with a higher risk of AV block (which would constitute a
carreer-ending event for the athlete), when an AVNRT is anticipated. Apart from the now widely accepted interaction between sports ac-
There are no reports about the association of accessory pathway- tivity and AF, there also is an association between physical activity
related arrhythmias or special substrates in athletes. The most and atrial flutter. We have described the concept of ‘lone atrial flut-
embarrasing situation in athletes is the finding of a concealed para- ter’ (AFL) after observing that men of<65 years presenting with AFL,
Hisian accessory pathway, which not only is more difficult to ablate but without a history of structural heart disease, hypertension, or AF,
but definitely carries more risk for inadvertent third-degree AV block. were more often engaged in regular sports practice (50% vs. 17% of
1406 H. Heidbuchel

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Figure 4 The danger of atrial flutter in athletes. The tracing shows an ECG of a 53-year-old jogger who developed atrial flutter at the end of one of
his recreational runs. He took flecainide 100 mg BID in combination with 240 mg of verapamil for rare paroxysms of AF. He collapsed and required
urgent cardioversion.

other AFL patients; P < 0.0001) or in endurance sports (31% vs. 8%; to that of non-athletic patients. It is unclear in how far this also applies
P = 0.0003).38 Lone atrial flutter, therefore, seems to be a right-sided to athletes with more persistent forms of AF in whom the atrial
expression of the same proarrhythmic changes that lead to AF in the structural alterations may be more widespread. So far, there are no
left atrium, i.e. dilatation, enhanced vagal tone, possibly microfibrosis, data on non-PV triggers, fibrosis mapping, mapping of fractionated
and induction through atrial ectopic beats. electrograms, or potential rotors specifically in athletes with AF.
Given the fact that most of these athletes are younger than the gen-
eral AF population, it is also unclear what the long-term effects of ab-
Atrial fibrillation lations will be in athletes, both concerning efficacy and safety. This
Athletes presenting with AF put the treating physician for therapeutic relates to the inevitable question as to whether sports can be
dilemmas. Although recommendations state that AF per se is not a resumed at the same level after ablation: assuming that physical activ-
contraindication for competitive sports, the ventricular rate should ity contributed to the pathogenesis of AF, it is unlikely that this would
be controlled when AF occurs during sports. Beta-blockers are the only pertain to the pulmonary veins. It is more likely that the changes
logical choice to counteract the enhanced sympathetic tone, but are widespread, judging from the dilatation of both atria. Hence, con-
these will not be tolerated by athletes wishing to perform during tinuation of the same sports stimulus may continue the disease pro-
sports. Calcium channel blockers and digitalis will usually not be po- cess which may lead to recurrence of non-PV dependent AF later. In
tent enough to slow down the ventricalur rate appropriatetly during the absence of definitive data about the long-term recurrence rate in
athletics. Rate control, therefore, is difficult to achieve. Moreover, al- athletes and the effect of sports on it, certainly no firm recommenda-
though Class 1 antiarrhythmic drugs may be able to prevent AF re- tion can be made towards the athlete about continuation or reduc-
currences in athlete’s heart, they cannot be used in monotherapy, tion of sports activities. However, it may be appropriate to discuss
since they may increase the propensity to develop AFL (even without the pathophysiological insights with the athlete, clarify the goals of
its documentation before; called ‘Class 1 AFL’), with prolonged cycle what the athlete wants to achieve with continuation (is he/she merely
length due to the Class 1 effect, which in the absence of adequate looking for the health benefit of it, or are there other performance-
rate control may lead to one-to-one AV conduction, resulting in high related goals that he/she wishes to achieve?), and come to a shared
ventricular rates and very profound intraventricular conduction slow- decision on the desirability to continue at the pre-ablation level. The
ing and haemodynamic compromise. An example is shown in Figure 4 same applies to patients who wish to hold off from ablation and pre-
of an athlete who despite 240 mg of verapamil once daily developed fer a medical treatment instead.
such proarrhythmic state under flecainide 100 mg twice daily at the
end of his Sunday morning running routine; he collapsed and required
urgent cardioversion. Atrial flutter
These limitations bring up early discussions about ablation in ath- In an athlete presenting with atrial flutter, there should be a very low
letes with AF. Smaller series have shown that the outcome of pul- threshold to ablate the cavotricuspid isthmus, given the efficacy and
monary vein isolation (PVI) in athletes with paroxysmal AF is similar safety of the procedure versus the risks for recurrences during sports
The athlete’s heart, a proarrhythmic heart 1407

as discussed above. European recommendations even advice that the other subforms too.47,48 Therefore, some authors argue for con-
isthmus ablation is mandatory in athletes with prior AFL, given the ab- tinued sports participation or at least shared and informed decision
sence of adequate and safe medical treatment.39 They even recom- making rather than flat diseligibility in these athletes.48,49 Ancillary
mend to ablate the isthmus prophylactically in athletes with AF, measures, such as avoiding QT-prolonging drugs, avoidance of elec-
especially when drug treatment is considered (see earlier) or con- trolyte disturbances, or even the provision of an automatic external
comitantly with PVI. Athletes should be explained that there is a high defibrillator (AED) should be discussed.50
propensity for developing AF, even after succesfull isthmus ablation: In a number of such situations, apart from other evaluation tools
in a series of patients presenting initially with AFL only, about 50% de- like (repeat) exercise tests and Holters during training or competi-
veloped at least one episode of AF during the ensuing 2 years after tion, implantation of an implantable loop recorder (ILR) that is cap-
succesful isthmus ablation. The risk for AF was higher in those with a able of remote transmissions may be used as a sort of intermediate
history of endurance sports activity or continuing it after ablation.40 management path. At least, the athlete can be followed closely during
Hence, the same considerations as discussed above after succesfull ongoing sports participation. Limitations of such approach are that

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PVI apply to athletes with only flutter at initial presentation. Again, the first manifestation of arrhythmia will be VF in many cases and that
there are no long-term studies that have shown a reduced incidence these devices were designed primarily to detect AF, not ventricular
of AF after cessation or drastic reduction in sports activity vs. its con- arrhythmias. Many will transmit only a single recorded episode from
tinuation, for the simple reason that such interventional studies are the prior 24 h interval: in case there are both episodes with real ven-
almost impossible, given the unwillingness of most athletes to be tricular arrhythmias and noise due to motion or muscle artefacts (not
randomized in this respect. uncommon in athletes), a relevant episode may not be transmitted
wirelessly. Therefore, athletes with an ILR will also require frequent
manual transmissions or in-person visits for analysis of the logs, pref-
Ventricular arrhythmias erably before newer episodes overwrite older ones. An example is
given in Figure 5.
There is a wide array of ventricular arrhythmias that may develop in When underlying structural disease is present or suspected (like in
athletes, related to the underlying structural or electrical diseases. the case of ExI-ARVC or overt scarring), an electrophysiological
Pathophysiologically, in most cases, there is no difference from non- study (EPS) may add prognostic information. In a series of 46 athletes
athletes except for the fact that sports may facilitate creation of the presenting with RV arrhythmias, inducibility of sustained mono-
circumstances to develop an arrhythmia, i.e. the ‘sports acts as a trig- morphic VT or VF during EPS was significantly related to outcome, al-
ger’ concept. This, however, raises the question as to how much though non-inducibility did not completely rule out major ventricular
sports adds to the natural background risk in these athletes and arrhythmias during follow-up.51
hence to the desirability to limit physical activity in order to poten-
tially prevent arrhythmias. On the other hand, the insight that sports
may promote or even induce the ventricular substrate itself in certain Physical activity as the promotor or
athletes leads to another line of reasoning on whether to limit sports. inducer of ventricular structural damage
Both aspects will be discussed separately below in respect to man- In cases where a contributing effect of exercise to the underlying
agement decisions. pathophysiological process is expected, advice to limit or stop sports
is not so much based on the concern to prevent arrhythmias being
Physical activity as the trigger for triggered by sports but also by the intent to reduce progression of
ventricular arrhythmias the disease itself.39,46 This is especially the case for RV pathology
The trigger effect of exercise plays a role in multiple underlying condi- (both familial ARVC and ExI-ARVC) and definitely also applies to
tions and may be most profound in ischaemic heart disease (coronary asymptomatic ARVC mutation carriers. The John Hopkins group has
artery disease), coronary anomalies (CA), ARVC, and catecholami- clearly demonstrated that the phenotypic expression and develop-
nergic polymorphic VT (CPVT). There is only scarce data, however, ment of arrhythmias are accelerated through physical activity in such
on its magnitude. Corrado et al.41 reported relative risks for sudden carriers.4 Earlier concern that HCM might progress through training
death in athletes vs. non-athletes of 79 in CA, 5.4 in ARVC, and 2.6 in has not been substantiated, however.52
CAD. On the other hand, while hypertrophic cardiomyopathy is re- Apart from assessing the electical impact of continued sports par-
ported as the most prevalent underlying condition in athletes dying ticipation, also the structural impact needs to be considered. While
suddenly,42,43 and while there is rationale for sports acting as a trig- haemodynamic findings at rest can be normal, evaluation should be
ger for arrhythmias (ischaemia and fibre disarray),44 there is growing performed during exercise by echocardiography or by cardiac mag-
debate on the added risk of sports in such patients. Many hyper- netic resonance imaging (Ex-CMR). Our research group developed
trophic cardiomyopathy (HCM) patients die outside of phyisical ac- over recent years a technique for Ex-CMR allowing uninterrupted ac-
tivity.45 Given the unpredictable electrical instability of the tivity and breathing during imaging.53 Imaging during exercise can un-
myocardial substrate, current recommendations retain the position mask contractile deficiencies which are not present at rest and is
to restrict competitive sports in phenotypically overt HCM, while especially helpful in evaluating athletes with RV arrhythmias (even if
relaxing the position in those with only a known mutation but ab- they present as apparent ‘idiopathic’ RVOT ectopy) and athletes with
sence of overt hypertrophy.46 The same holds true for long QT syn- LV scars (certainly when they exceed 10% of LV mass).21,28,53,54 If
drome, especially for LQT3, which is associated with low rates of contractile dysfunction is present during exercise, one can postulate
exercise-related arrhythmias, but with some arguing to extend this to that further strain through continued intensive exercise may lead to
1408 H. Heidbuchel

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Figure 5 Current implantable loop recorders have their limits in detecting ventricular arrhythmias in athletes. (A) The remote transmissions of an
implantable loop recorder, implanted in a 26-year-old former competitive athlete with suspicion of ventricular arrhythmias provides only details of a
single recorded episode per day. This is mentioned at the top of the list of episodes and can also be deducted from the missing episode numbers at
the left. (B) Since exercising athletes often have noisy tracings, which are automatically annotated as ventricular tachyarrhythmic episodes, most tele-
monitoring episodes will be artefacts. Manual remote transmissions or in-office interrogations will download all the available episodes and hence will
allow exclusion of any real arrhythmia.

further deterioration with consequent arrhythmias or maybe even insights, it may be preferrable to reduce physical activity while main-
heart failure symptoms at rest later in life. An example of an interna- taining intense arrhythmic follow-up, potentially including an ILR.
tional professional cyclist with the incidental finding of LV scar (re-
vealed by CMR after a routine yearly ECG showed new
repolarization abnormalities) and with clear subnormal LV contract- An implantable defibrillator as
ile performance, is shown in Figure 6. He stopped his carreer, not so
much because of the associated nonsustained VT (for which an
bailout to continue sports?
implantable cardioverter defibrillator could be implanted), but be- A large Multinational ICD Sports Safety Registry has shown that after
cause of the haemodynamic findings. a median follow-up of 44 months, there were no ocurrences of death
Athletes with RV arrhythmias due to ExI-ARVC often (but not al- nor of arrhythmia- or shock-related physical injury in 440 athletes
ways) have low voltage areas in the RVOT, with a different distribu- who continued organized competitive or high-risk sports after ICD
tion than in typical ARVC, and can succesfully be ablated in those implantation.57 An additional analysis in 82 recreational athletes con-
areas.55,56 However, just like in the case of PVI for AF, as discussed firmed these reassuring outcomes in non-professional athletes
above, the question arises on the possibility for resumption of vigor- (Heidbuchel, unpublished observation), which is relevant for the
ous endurance sports after succesful ablation. Realizing that the ar- many ICD recipients who want to continue recreational sports activ-
rhythmias where the expression of exercise-induced structural ities, some even intensive, after implantation. Although sports partici-
changes, one can wonder whether resumption of the same activities pation with an ICD seems safer than previously considered (and
may lead to more widespread RV changes and new arrhythmias. No hence may lead to relaxation of the current rather restrictive recom-
prospective data are present, but based on the pathophysiological mendations on sports with an ICD),39,58 based on the concept that
The athlete’s heart, a proarrhythmic heart 1409

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Figure 6 Evaluating contractile performance durings exercise. An athlete with LV scar (presumably as the result of silent myocarditis) was sub-
jected to increasing loads of supine cycling while being scanned by cardiac magnetic resonance imaging without interruption of exercise or breathing.
The ratio of left ventricular end-systolic pressure and volume (LV SP/ESV), a marker of contractility was borderline abnormal at rest, but became
manifestly abnormal during exercise (red line; in comparison with other trained athletes without pathology, black lines).

the athlete’s heart is a proarrhythmic heart, two more considerations Conclusions

come into play.
The first is similar to the one after ablation. If sports is contraindi- There is an overwhelming paucity of firm prospective data that can
cated because it can contribute to the progresssion of the underlying guide us in our decision making in athletes with arrhythmias.
disease, an ICD cannot be considered as a substitute for sports re- Nevertheless, recognizing that the athlete’s heart is a proarrhythmic
duction. Recommendations in such circumstances should have a life- heart provides a framework for the evaluation of athletes and shared
time perspective and be based on the optimal preservation of decision making with them. Our evaluation should take into account
structural cardiac integrity. The ICD, however, may allow for more that physical activity may trigger further arrhythmias and that it may
relaxed light-to-moderate physical activity and will often allow ath- contribute to progression of structural abnormalities. Hence, evalu-
letes to regain autonomy instead of being scared to go out for sports ation should include electrical assessment and follow-up (in some
unattended.39 including diagnostic EPS and implantable loop recorders) and haemo-
The second is that ICD shocks in general, even when appropriate dynamic assessment (which should certainly include evaluation during
and safe, will have a psychological impact on the athlete. Thirty to exercise by echocardiography or cardiac magnetic resonance).
40% of the ahtletes who experienced shocks in the Multinational ICD Discussing the resulting findings with the athlete and other involved
Sports Safety Registry at least temporarily stopped participation out parties within the same framework will contribute to more rational
of fear for repeat shocks.57 Considering that ICD therapy is lifelong shared decision making, instead of emotional opiniated choices by
therapy, where quality of life is not only dependent on the ability to athletes or physicians.
perform (competitive) sports but also on continued trust in the de-
vice, physicians should be aware that their own belief in the effective- Conflict of interest: There are no conflicts of interest related to
ness and safety of ICD therapy during sports does not implicitly put the topic of this manuscript. The ICD Registry was supported with an
pressure on the athlete to continue sports. Again, informed decision unrestricted grant from Boston Scientific through the University of
making needs to re-evaluate all options of the athlete after shocks, Leuven. H.H. was coordinating Clinical Investigator for the Biotronik-
including continuing, reducing, or stopping sports.59,60 sponsored EuroEco study on health-economics of remote device
1410 H. Heidbuchel

monitoring, has been member of the scientific advisory boards and/ 22. La Gerche A, Connelly KA, Mooney DJ, MacIsaac AI, Prior DL. Biochemical and
functional abnormalities of left and right ventricular function after ultra-
or lecturer for Boehringer-Ingelheim, Bayer, Bristol-Myers Squibb,
endurance exercise. Heart 2008;94:860–6.
Pfizer, Daiichi-Sankyo, and Cardiome, received travel support from 23. Stewart GM, Yamada A, Haseler LJ, Kavanagh JJ, Koerbin G, Chan J et al. Altered
St. Jude Medical, and received unconditional research grants through ventricular mechanics after 60 min of high-intensity endurance exercise: insights
from exercise speckle-tracking echocardiography. Am J Physiol Heart Circ Physiol
the University of Hasselt from Bayer and through the University of 2015;308:H875–83.
Antwerp from Medtronic, Boston Scientific, and Bracco Imaging 24. Heidbuchel H, Prior DL, La Gerche A. Ventricular arrhythmias associated with
Europe. long-term endurance sports: what is the evidence? Br J Sports Med 2012;46:
i44–50.
25. La Gerche A, Robberecht C, Kuiperi C, Nuyens D, Willems R, de Ravel T et al.
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