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''Roland D. Thijs, Robert H.A. Reijntjes, J. Gert van Dijk''<br/>
''Department of Neurology and Clinical Neurophysiology, Leiden, The Netherlands''<br><br/>


{{case_present|
== Background ==
Exercise-related syncope without organic heart disease
has frequently been reported in young athletes [2, 5,
9–11, 14]. The exact incidence of idiopathic exercise-related syncope among young athletes is not known.
Calkins et al. and Colivicchi et al. found that after a thorough cardiac evaluation athletes with an exertional-related syncope could safely continue to participate in athletics [2, 3]. Tilt-table testing may be a useful diagnostic
tool provoking syncope in 41 % of 24 athletes and up to
79 % after isoproterenol infusion [5]. Idiopathic exercise-related syncope has been reported to result from
hypotension together with a normal HR, tachycardia,
bradycardia or asystole [2, 9]. The pathophysiology of
this condition is poorly understood [9]. Atenolol, hydrofludrocortisone, disopyramide, transdermal scopolamine and increased salt intake have been recommended as treatment for exercise-related syncope [2, 5,
10, 11, 13]. To our knowledge this is the first report of a
beneficial effect of water drinking for this condition.
== Case ==
A 20-year-old male pupil of a sporting school had
had attacks of lightheadedness over several months. The
first time he felt unsteady and fell to the ground when he
dismounted his bicycle after 1-hour of moderate exercise. In addition, he had chest pain and was short of
breath. He was not certain whether or not he had passed
out. Nobody had witnessed the event. For two hours afterwards he complained of unclear vision as if “looking
through salad oil”. He had not been incontinent, had
sustained no bruises and no tongue bite. Later, similar
attacks occurred during light cycling, after competition
skating, after skiing and during miction after exercise. He has a medical history of asthma and migraine. Both
a cardiologist and a pulmonologist had analyzed the
presenting complaints previously but could not find an
explanation. Previous examinations had consisted of an
ECG, echocardiography, bicycle stress testing, laboratory screen, chest X-ray and a lung perfusion scintigraphy. His medications were formoterol inhalations 12
mcg bid, budesonide inhalations 200 mcg bid and pantazol 20 mg od. The patient did not use coffee, nicotine
or drugs. On physical examination no abnormalities
were noted. The patient’s supine blood pressure (BP)
was 110/65 mmHg with a resting heart rate (HR) of 70
beats per minute (bpm). Neurological examination
showed slightly impaired fine motor skills and frequent
eye blinks either left or right sided.}}
== Test results ==
A magnetic resonance imaging study of the brain was
normal. Test of HR and BP during rest (70 bpm;
108/65 mmHg), deep breathing, standing up (85 bpm;
121/91 mmHg),a Valsalva maneuver and sustained hand
grip were all normal. A tilt-table test (without medication) showed no abnormalities. Cathecholamine concentrations in plasma were obtained by venapuncture in
both supine and after 30 minutes upright position (norepinephrine(NE): 1.22 nmol/l vs. 3.67 nmol/l, epinephrine(E): 0.13 vs. 0.16 nmol/l, dopamine(DA): 0.04
vs. 0.07 nmol/l, respectively) and in 24-hour urine (NE:
0.43 µmol, E: 0.06 µmol, DA: 2.46 µmol).
In view of the relation to exercise, the patient was
asked to mimic a typical bicycle tour on an ergometer,
while EEG, ECG and BP (Finapres, finger photoplethysmography) were continuously monitored. Cycling at
maximal effort increased HR up to 185 bpm (mean ±
standard deviation: 176 ± 7 bpm) without significant BP
changes (systolic BP (SBP) 119 ±14mmHg; diastolic BP
(DBP) 72 ±9 mmHg). Immediately after cessation of exercise BP fell to 75/45 mmHg, during which the patient
felt unsteady and complained of blurred vision; there
was no loss of consciousness. During the BP drop, electrocardiography revealed sinus tachycardia of 180 bpm.
The patient recognized the sensations as similar to those
of spontaneous attacks.
== Treatment ==
A second exercise test was performed two weeks later, 15 minutes after rapid consumption of 1000 mL water. Symptoms did not recur at
the second test. Compared to the first cycling test the
maximal rise of HR during exercise was reduced to 155
bpm and the BP raised during exercise (SBP
149 ± 21 mmHg; DBP 94 ± 14 mmHg). No significant BP
drop occurred after cycling. Fig. 1 displays the changes of heart rate and blood pressure during both tests. Furthermore exercise-related symptoms were succesfully
prevented by water ingestion. However, after 2 months
our patient complained of attacks during ordinary daily
activity. As these attacks could not be anticipated and
occurred frequently, we advised to stop the extra water
ingestion and precribed sodium tablets (7.2 g/day) instead. After 2 months he had had no complaints.
== References ==
<biblio>
#Bjornstad pmid=1782647
#Calkins pmid=7754948
#Colivicchi pmid=12090751
#Fleg pmid=3717041
#Grub pmid=1670907
#Holtzhausen pmid=8614313
#Jacob pmid=11018167
#Jordan pmid=10662747
#Kosinski2000 pmid=11225599
#Kosinski1996 pmid=8701911
#Sakaguchi pmid=7863992
#Shannon pmid=11904109
#Sneddon pmid=8043337
#Takase pmid=11195600
#Wolthuis pmid=830206
</biblio>

Revision as of 12:00, 15 October 2015

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