Download Paroxysmal atrial fibrillation in male endurance athletes. A 9

Europace (2004) 6, 222e228
Paroxysmal atrial fibrillation in male endurance
athletes. A 9-year follow up
Jan Hoogsteena,), Goof Schepb, Norbert M. van Hemelc,
Ernst E. van der Walld
a
Department of Cardiology, Maxima Medical Centre, Dommelstraat Zuid 5,
5500 MB Veldhoven, Netherlands
b
Department of Sport Medicine, Maxima Medical Centre, Veldhoven, Netherlands
c
Department of Cardiology, Heart Lung Centre, Utrecht, Netherlands
d
Department of Cardiology, Leiden University Medical Centre, Leiden, Netherlands
Submitted 13 May 2003, and accepted after revision 18 January 2004
KEYWORDS
atrial fibrillation;
endurance athletes
Abstract Aims To study the course and circumstances of atrial fibrillation in
endurance sports.
Background Atrial fibrillation is the main cause of symptoms in athletes and frequently disturbs the performance during the practising of sport. The course of the
arrhythmia is seldom reported in this population.
Methods In 1993 and 2002 symptoms and clinical presentation of atrial fibrillation
were evaluated in 30 well-trained athletes with a specially designed questionnaire.
Results In 1993 paroxysmal atrial fibrillation was present in 30 male athletes at
the mean age of 48:1 G 7:8, 3 (10%) of them also had paroxysmal atrial flutter. Three
(10%) of the athletes died before 2002. In 2002 paroxysmal atrial fibrillation continued in 15 (50%) athletes, permanent atrial fibrillation emerged in 5 (17%) athletes
and 7 (23%) of them showed no further atrial fibrillation. In 1993 paroxysms of atrial
fibrillation started at a relatively low level of training intensity compared with the
mean maximal training intensity of 11 G 7 versus 8 G 4 h=week (p ! 0:05). The first
attack of adrenergically induced paroxysmal atrial fibrillation was more often present in younger athletes (p ! 0:005) and vagally induced paroxysmal atrial fibrillation
was more apparent in older athletes (p ! 0:05). In 10 (38%) of the athletes a familiar
form of paroxysmal atrial fibrillation was present.
Conclusion A small proportion of the athletes (26%) was asymptomatic. Paroxysmal atrial fibrillation remained stable in half of the athletes whereas the arrhythmia
changed into permanent atrial fibrillation in a minority of this population.
ª 2004 The European Society of Cardiology. Published by Elsevier Ltd. All rights reserved.
) Corresponding author. Tel.: D31-40-8888210; fax: D31-40-8888216.
E-mail address: [email protected] (J. Hoogsteen).
1099-5129/$30 ª 2004 The European Society of Cardiology. Published by Elsevier Ltd. All rights reserved.
doi:10.1016/j.eupc.2004.01.004
Atrial fibrillation in male endurance athletes
Introduction
In general practice atrial fibrillation (AF) is a very
common arrhythmia. The incidence is about 0.5%
in young patients (!40 years) and more than 5%
in patients older than 65 years [1e3]. Atrial fibrillation is one of the most frequent causes of symptoms in athletes and often interferes with strong
physical activities. In athletes the arrhythmia
shows a prevalence of 0.2% [1]. Some recent data
suggest that life-long endurance training may
be arrhythmogenic [4], particularly in young male
athletes [5e7]. Because the course of symptomatic paroxysmal AF in athletes who continue
sporting activities is not well established, the management of the endurance athlete with this arrhythmia is unclear. Therefore, we developed a
questionnaire to study the course of AF, the symptoms and relationship of the autonomic nervous
system with this arrhythmia. The same group of
athletes was asked to fill out the questionnaire
both in 1993 and in 2002 disclosing the course of
paroxysmal AF and detect possible mechanisms and
circumstances of induction of AF.
Methods
Data collection
By means of an advertising campaign in Dutch
medical journals, general practitioners and cardiologists were asked to recruit athletes with electrocardiographically documented AF. Athletes
were asked to fill out the questionnaire, which
addressed medical history, course and level of
sporting activities and therapeutic interventions
for AF. Athletes with known causes of atrial fibrillation were excluded from the study. In addition,
cardiac examination (Holter monitoring included)
and results of other medical investigations to
determine the cause of AF were retrieved from
the cardiologist in charge. In 2002 the same group
of athletes was asked again to fill out the same
questionnaire. Height, weight and body surface
area (BSA) of each athlete were determined.
Definitions
Athletic performance was defined as 50 min maximal running time for a 10 km circuit or a 90 min
maximal cycling time for a 40 km distance. The
symptoms caused by AF were categorized ‘‘most
severe’’ when the arrhythmia forced an athlete
223
to discontinue sporting activity or daily duty or
work, and/or led to hospital admission for treatment of AF. The symptoms were classified ‘‘moderate’’ when AF could be tolerated, normal daily
functioning could be continued but sporting activity during atrial fibrillation had to be interrupted.
The symptoms were labelled ‘‘mild’’ when sporting
activity could be continued because AF was well
tolerated. Lone AF was defined as presence of the
arrhythmia without detectable heart disease or
any other cause. Resting heart rate was assessed
in the early morning just before getting up. Paroxysmal AF was defined as self-terminating AF with
a duration varying from 10 min to 7 days, and permanent AF was defined as an ongoing arrhythmia
despite therapeutic measures. Vagally induced AF
was called AF occurring at night, after heavy meals
or in the immediate hours after (intensive) exercise
[7,18]. Adrenergically induced AF was defined as AF
starting during daytime and provoked by exercise,
stress or caffeine [7,18]. Overtraining is a mosaic
pattern with parasympathetic and/or sympathetic
components. Sympathetic overtraining is the condition defined by an elevated resting heart rate,
loss of weight, disturbed sleep, elevated resting
blood pressure, orthostatic hypotension, susceptibility to infection, and reduced performance.
Parasympathetic overtraining is the condition
characterized by a low resting heart rate, a tendency to hypoglycaemia, phlegmatic behaviour
and reduced performance [25,26].
Statistical analysis
Statistical analysis was performed with the 2
sample pooled t test for difference in means and
unknown variances and the Chi-square test [9].
A value of p ! 0:05 was considered statistically
significant.
Results
Athletes’ profile
Thirty athletes responded in 1993 and 27 filled out
the questionnaire in 2002. Seven athletes (23%)
were medical practitioners. Female athletes could
not be included due to lack of response to the
advertising campaign. Between 1993 and 2002
height, weight, BSA and resting heart rate of the
athletes did not change significantly (Table 1).
The mean duration of sporting practice was
16:5 G 9:3 years. The mean age of the athletes at
the first attack of symptomatic atrial fibrillation
224
Table 1
J. Hoogsteen et al.
Anthropometrical characteristics of the athletes in 1993 and 2002 (means G SD)
Number of athletes
Age (years)
Age of first complaint (years)
Height (cm)
Weight (kg)
BSA (m2)
Resting heart rate (bpm)
1993
2002
30
48.1 G 7.8
41.7 G 11.4
182.5 G 6.2
81.1 G 5.4
2.03 G 0.09
49 G 10 (n ¼ 25)
27
57.1 G 7.5
was 41:7 G 11:4; all athletes had more than 10 years
of sporting practice at that time. The running time
increased in 2002 by 15.9 min but the difference
was not significant compared with 1993. The
40-km cycling time significantly increased by
19.4 min (p ! 0:005) (Table 2).
Symptoms: onset and termination of
atrial fibrillation
In 1993 symptomatic paroxysmal AF was present in
29 athletes, of whom 3 (10%) also had paroxysmal
atrial flutter. Only 1 athlete had asymptomatic AF
(Fig. 1). Nine years later, symptomatic paroxysmal
AF continued to occur in 15 (56%) athletes, in 7
(26%) athletes no symptoms of AF were observed,
whereas in 5 (18%) athletes paroxysmal AF had
evolved to become permanent. In 1993 almost all
the athletes were treated medically with a single
antiarrhythmic drug or with a combination of antiarrhythmic drugs: sotalol 37% (n ¼ 11), flecainide
20% (n ¼ 6), amiodarone 10% (n ¼ 3), digoxin 10%
(n ¼ 3), quinidine 3% (n ¼ 1); in 2002, sotalol 30%
(n ¼ 8), flecainide 22% (n ¼ 6), amiodarone 7%
(n ¼ 2), digoxin 11% (n ¼ 3) in combination with
a betablocker or verapamil.
The familiar form of lone AF was apparent in 10
(38%) of the athletes. Training intensity at the time
of the first attack of symptomatic AF in 1993 was
significantly less than the maximal training intensity in hours per week (8 G 4 versus 11 G 7 h,
p ! 0:05) (Fig. 2). During follow up 3 (10%)
athletes underwent pacemaker implantations, 3
(10%) athletes underwent AF catheter ablative
therapy and 3 (10%) athletes underwent Maze
p
182.5 G 6.4
80.9 G 8.4
2.02 G 0.13
53 G 15 (n ¼ 22)
ns
ns
ns
ns
surgery and were without symptoms postoperatively. All continued sport activity.
Three (10%) athletes died between 1993 and
2002: 1 athlete in whom examination prior to
this event had ruled out cardiac disease died suddenly. One athlete on warfarin therapy died from
a cerebral haemorrhage, and 1 athlete, not anticoagulated, died from an ischaemic cerebral
infarction.
In 1993 and 2002 7 (23%) and 2 (7%) athletes,
respectively, had symptomatic attacks of AF during
maximal sporting activity, whereas 10 (33%) and 8
(30%) athletes in 1993 and 2002, respectively, had
attacks of symptomatic AF only at night. A termination manoeuvre such as resting was successful in 2
(7%) and 6 (22%) athletes in 1993 and 2002, respectively, whereas a termination attempt such as
sporting activity succeeded in termination of AF
in 6 (22%) and 3 (11%) athletes in 1993 and 2002,
respectively. A vagal manoeuvre to terminate AF
was only successful in 1 athlete in 1993. It was not
possible to terminate AF in 17 (57%) and 12 (44%)
athletes in 1993 and 2002, respectively. Concerning symptoms due to AF: in 1993 12 (40%) and in
2002 16 (59%) athletes had mild symptoms allowing
continuation of sporting activity, whereas in 1993
18 (60%) and in 2002 11 (41%) athletes had moderate or severe symptoms, requiring termination
of all sporting activities (Table 3).
Vagally induced atrial fibrillation
Vagally induced AF was present in 1993 and 2002
in 10 (33%, n ¼ 30) and 10 (37%, n ¼ 27) athletes,
respectively (Fig. 3; Table 3). The mean age,
height, weight, BSA, weekly training schedule in
Table 2 Athletic performance expressed as cycling time for a 40 km distance and running time for 10 km circuit
(means G SD)
Running
Cycling
Athletic performance
1993
Time (min)
2002
Time (min)
p
10 km
40 km
N ¼ 22
N ¼ 20
40.0 G 5.0
66.0 G 9.0
N ¼ 14
N ¼ 18
55.9 G 13.0
85.4 G 18.6
ns
!0.005
Atrial fibrillation in male endurance athletes
N=30
1993
Death
N=3
225
Adrenergically and vagally induced
atrial fibrillation in 1993 and 2002
2002
Number of
athletes
N=27
14
13
15
10
10
10
adrenergically
7
vagally
3
5
unclassified
0
1993
No symptoms
N=7(26%)
PAF
N=15(55%)
Chronic AF
N=5(19%)
Figure 1 Distribution of athletes with paroxysmal atrial
fibrillation 1993e2002.
hours and sporting activity over the years were
not significantly different from the other athletes.
The resting heart rate in the group with vagally
induced symptomatic AF did not differ from the
rest of the group with symptomatic AF; 48:2 G 9:6
bpm versus 47:1 G 9:0 bpm, respectively. In the
group with vagally induced paroxysmal AF in 1993
(n ¼ 10), chronic AF became apparent in 2 athletes,
1 athlete became asymptomatic, 1 athlete died
suddenly, and in 6 athletes vagally induced
symptomatic AF persisted over the years (Fig. 4).
In this group of 6 athletes there was a tendency
for there to be a longer period of sporting activity
(in years) in comparison with the rest of the
group i.e. 22:7 G 6:6 versus 17:2 G 10:7 years but
the difference was not significant.
Adrenergically induced atrial fibrillation
Hour / week
Adrenergically induced AF occurred in 7 (23%)
athletes in 1993 and in 3 (11%) athletes in 2002
(Fig. 3). These athletes were significantly younger
than those with vagally induced AF and the other
20
18
16
14
12
10
8
6
4
2
0
Maximal intensity
Intensity first
attack of AF
8±4
N=30
n=29
Figure 3 Distribution of vagally, adrenergically and
mixed triggers of atrial fibrillation.
athletes: aged 40:4 G 8:2 versus 50:8 G 6:8 and
50:3 G 5:7, respectively (p ! 0:05 and p ! 0:005).
The mean age of the athletes with the first symptomatic attack of adrenergically induced AF was
significantly lower than that of the other athletes:
aged 31:3 G 13:3 versus 46:6 G 6:6 (p ! 0:005).
However, the age did not differ significantly from
the group with vagally induced AF. Height, weight,
BSA, years of sporting activity and the weekly training schedule (in hours) were not significantly different in the adrenergically induced AF group in
comparison with the rest of the group. Of the 7
athletes with symptomatic adrenergically induced
AF observed in 1993, paroxysmal AF continued in
5 athletes in 2002, in 3 athletes fewer or no symptoms of AF were noticed, and 1 athlete showed
some progression in symptoms of the arrhythmia
(Fig. 4). In only 1 athlete adrenergically induced
AF changed into vagal AF; he became symptomfree after a Maze procedure. One athlete had an ischaemic cerebral vascular accident and died.
One athlete stopped his sporting activity but the
arrhythmia persisted. Adrenergically induced
AF persisted in 3 athletes over a period of 9 years.
Table 3 Symptoms and course of paroxysmal atrial
fibrillation in athletes
P<0.05
11±7
2002
Figure 2 Maximal training intensity in hours per week and
training intensity at the first attack of atrial fibrillation.
Asymptomatic
Tolerable and continue
sporting activity
Stop sporting
activity and normal
function in day to
day life
Sick and not able
to work
Progressive illness
and/or admission
to hospital
1993
(N ¼ 30)
2002
(N ¼ 27)
1
11
10
6
12
9
4
2
2
226
J. Hoogsteen et al.
Vagally induced atrial fibrillation
1993
N=10
PAF
N=6
2002
Chronic.AF
N=2
no AF
N=1
Death
N=1
Adrenergically induced atrial fibrillation
N=7
1993
PAF
N=5
2002
Figure 4
no AF
N=1
Athletes with vagally and adrenergically induced paroxysmal atrial fibrillation 1993e2002.
Atrial fibrillation, mental stress and
relation with sport
In 1993 20 (74%, n ¼ 27) and in 2002 15 (68%,
n ¼ 22) athletes presumed a causal relationship between atrial fibrillation and mental stress (Table 4).
In 1993 18 (67%, n ¼ 27) and in 2002 13 (59%,
n ¼ 25) athletes had experienced a causal relationship of AF and sporting activity. Two athletes in
1993 and 2 athletes in 2002 benefited from sport
for the termination of AF.
Discussion
This study aimed at disclosing the course, symptoms, inducing circumstances and dependency of
the autonomic nervous system in 30 athletes with
paroxysmal AF over a 9-year period. In half of the
athletes paroxysmal AF continued, paroxysmal AF
converted to permanent AF in 5 individuals and 7
athletes had no symptoms of AF. Two of the 3
athletes died from causes not directly related to
AF. The mean age of the athletes with the first
attack of atrial fibrillation was 41:7 G 11:4 and
the training intensity at the time of the AF onset
Table 4
Death
N=1
was significantly lower than the maximal training
intensity in their sporting careers. The majority
of the athletes presumed a causal relationship between paroxysmal AF and both mental stress and
sporting activity.
Atrial fibrillation related to the
autonomic nervous system
Atrial fibrillation in young healthy athletes can be
initiated by vagal or adrenergic predominance or
their combined form [5,6,18] and all types can be
associated with the overtraining syndrome.
Interruption of training for a certain period of
time could eradicate this overtraining syndrome
[5]. It is reported that adrenergically induced atrial
fibrillation is more common in subjects with structural heart disease [18] and therefore this type
might be expected to occur more frequently in
older athletes. Our study showed that vagally
induced paroxysmal AF occurred in 10 (33%) and
adrenergically induced paroxysmal AF occurred in
7 (23%) athletes. In contrast to the literature previously published, we observed that athletes
with adrenergically induced paroxysmal AF were
significantly younger than athletes with vagally
The subjective causal relation of atrial fibrillation and sport activity
Effect of mental stress
1993
2002
Relation to sport (subjective)
1993
2002
Improvement
Indifferent
Light arousal
Strong arousal
Unknown
0
7
11
9
0
0
7
7
8
4
Therapeutic
Indifferent
Light causal
Intermediate causal
Strong causal
2
7
12
3
3
2
10
8
3
2
N ¼ 27
N ¼ 26
N ¼ 27
N ¼ 25
Atrial fibrillation in male endurance athletes
induced AF (p ! 0:05). Moreover, the first attack of
paroxysmal AF emerged in athletes at a significantly
earlier age than in other athletes (p ! 0:005). Mont
[7] demonstrated that in the majority (72%) of the
sporting individuals, he studied, with paroxysmal
AF vagal dependency could be determined. This
could not be confirmed in our study although the
mean age of our athletes with a first attack of vagally induced AF did not differ from that in the
study of Mont [7] (42:7 G 11:2 versus 39:5 G 13:2).
The same holds for the years of sporting practice:
(17:6 G 8:6, Mont [7] versus 23:7 G 10:9, in this
study).
Speculations on the mechanism of vagally induced AF involve cardiac adaptations characterized as the ‘‘athletic heart syndrome’’ [10e17].
Atrial dilatation and remodelling belong to this syndrome and reflect structural changes. One can assume that atrial dilatation progresses and at
a certain level this benign adaptation to intensive
sporting activities creates pathological changes
leading to unfavourable fibrosis/collagen deposits,
and sometimes to right atrial dysplasia [8]. These
structural changes cause abnormal and heterogeneous conduction properties. Eventually, the enhanced vagal tone, promoting shortening of atrial
refractory period, could serve as the trigger for
the induction of AF in this abnormal atrial substrate. Mont [7] could not show any causal relationship between sporting activity and atrial
dimension, but only 6 (19%) of his individuals were
endurance athletes and the remainder performed
other sports such as weight lifting, soccer and
swimming. In addition, the mean left atrial dimension in the small group of endurance athletes with
paroxysmal AF was within normal limits. Unfortunately, echocardiographic data were not sufficiently available for our study to elaborate this point.
Atrial fibrillation and training intensity
Long and intense periods of training could generate
substantial shifts in body fluids due to changes in
volume regulation, and changes in potassium and
sodium levels. In these circumstances with high
body temperature, hourly loss of 1 or 2 l of body fluids is not exceptional [19,20]. Inappropriate fluid
intake can lead to dehydration triggering atrial arrhythmias [21]. In addition, long-lasting training
schedules can induce a significant loss in magnesium and without proper supplementation, chronic
hypomagnesemia can induce arrhythmias [22]. In
our study the majority of the athletes presumed
a causal relationship between paroxysmal AF and
sporting activity. Thirty percent and 11% of the
227
athletes in 1993 and 2002, respectively, experienced reduction of attacks of AF by reducing sporting activity, but 43% and 52% of the athletes in 1933
and 2002, respectively, did not notice any relationship. Moreover, AF started at a relatively low level
of training intensity compared with the mean and
maximal training intensity (p ! 0:05) (Fig. 1), ruling
out dehydration, hypomagnesemia or sympathetic and parasympathetic overtraining as a trigger
for AF.
Atrial fibrillation and heart disease
In particular, adrenergically induced AF could be
the first sign of heart disease. Forty percent of
the athletes with WolffeParkinsoneWhite syndrome or a concealed atrioventricular bypass tract
show periods of AF [23,24], the arrhythmia could
manifest hypertrophic cardiomyopathy or arrhythmogenic right ventricular cardiomyopathy [5].
None of our athletes, including the 3 deceased individuals had overt cardiac disease.
Limitations
The study group had a small sample size and a selection bias due to the fact that only athletes with
more serious symptoms of AF responded, of whom
23% were physicians being intrinsically more aware
of rhythm disturbances. Because characteristics of
AF were derived from the questionnaire, the true
incidence of AF remains unclear, as AF can occur
without symptoms and there could also be some
overlap between the syndromes of vagally and
adrenergically induced AF. In addition, it is possible that rate and irregularity of AF and thus, the
awareness and tolerance of AF might have changed
over the years.
Conclusions
This study showed that in half of the endurance
athletes with paroxysmal AF this arrhythmia continued, whereas in a minority permanent AF became apparent. In only 7 of 30 athletes AF
disappeared. A familiar form of atrial fibrillation
was present in 10 athletes (38%). Vagally and adrenergically induced AF could be determined in 10
athletes (33%) and 7 athletes (23%), respectively.
Sixty percent of vagally induced AF continued over
the years. Adrenergically induced AF was clearly
more often present in younger athletes than in
older athletes. The majority of the athletes presumed a causal relationship between paroxysmal
228
AF and mental stress as well as sporting activity.
Our study revealed that AF causes serious symptoms that disturb sporting activity and reduce exercise tolerance and hence more attention should be
paid to preventing arrhythmia during endurance
training.
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