© 2004 by European Society of Cardiology
CASE REPORT
A patient with recurrent syncope and ST-elevation on the electrocardiogram
aDepartment of Cardiology, Academic Medical Centre Amsterdam, The Netherlands; bDepartment of Internal Medicine, Academic Medical Centre Amsterdam, The Netherlands
Manuscript submitted 21 October 2003. Accepted after revision 14 March 2004.
*Corresponding author. Academic Medical Centre, Meibergdreef 9, F4-222 1105 AZ Amsterdam, The Netherlands. Tel.: +31-20-5669111. E-mail address: n.colman{at}amc.uva.nl (N. Colman).
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Abstract |
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A 56-year old woman had over 100 episodes of syncope since the age of 8. Because the patient's description of the episodes suggested vasovagal syncope she was studied by a head up tilt test (HUT). Seconds after the uncomplicated HUT the patient experienced a typical syncope with bradycardia, marked ST-elevation and chest pain. After treatment with nifedipine she has had one syncopal spell in a follow up period of 31 months. We conclude that the syncopal events in this patient were caused by a combination of vasovagal syncope and coronary spasm.
Key Words: syncope, ST-elevation, coronary spasm, hyperventilation
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Introduction |
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Syncope can have several causes. The most important are neurally mediated syncope, cardiac syncope and orthostatic hypotension. Of these causes vasovagal syncope is the most common type. Usually it has a prodrome, and is provoked by triggering events, although both characteristics may be absent. The diagnosis can be made based on the history and a positive tilt table test. Cardiac syncope is usually characterised by a sudden loss of consciousness, and quick recovery. The diagnosis is made through rhythm registration at the time of the episode or by findings of structural heart disease.
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Case report |
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A 56-year old woman had over 100 episodes of loss of consciousness since the age of 8, of which there had been 10 episodes in the last 12 months. A feeling of discomfort in the epigastric region, light-headedness, profuse sweating and chest pain usually preceded the episodes. Sometimes it was accompanied by shoulder pain, palpitations, forced breathing and muscular cramps around the mouth. There was often loss of urinary sphincter control. The episodes occurred both in the standing and sitting positions, but had also occurred in supine position on a few occasions. Sometimes they were provoked by emotion. On regaining consciousness the patient was immediately oriented.
The patient had no history of cardiac disease. The family-history revealed a sister of 57 years old in whom Brugada syndrome was diagnosed after she was successfully resuscitated from an out of hospital cardiac arrest. An ICD was implanted and a sodium channel mutation was identified [1]
. The patient's mother was also a frequent fainter. Both the mother and father had their first myocardial infarction during their fifties. The patient had no children.
The medication she used at the time of presentation was temazepam 10 mg nightly, omeprazole 10 mg daily and dexchlorofeniramine 6 mg twice daily.
Prior EEG, CT-brain and chest X-ray had not revealed any abnormalities.
On physical examination of the heart there were no abnormalities.
The electrocardiogram showed sinus rhythm, intermediate axis, PQ interval of 160 ms, QRS duration of 90 ms, and no ST-segment displacement and especially no features of Brugada syndrome (Fig. 1).
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Based on the history, physical examination and ECG the most probable diagnosis was vasovagal syncope.
During 24 h Holter monitoring the patient experienced two episodes of near syncope. The first episode showed second degree AV block, probably Wenkebach, with a minimum ventricular frequency of 41 beats/min (Fig. 2). During the second episode there was sinus bradycardia of 48–60 beats/min.
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Flecainide challenge test (10 mg/kg in 10 min) showed marked conduction disturbance at a dose of 50 mg. The PQ interval increased to 200 ms, and the QRS complex to 160 ms. This test can reveal Brugada-type electrocardiographic features but no ST-elevation was observed in the right precordial leads.
Genetic testing in the patients' family revealed a mutation (R367C) in SCN5A, the gene encoding the fast cardiac sodium channel. This mutation was also found in the patient.
On cardiovascular reflex testing using the Finapres for continuous blood pressure monitoring we found a supine blood pressure of 152/73 mmHg with a heart rate of 100 beats/min. On standing there was a normal orthostatic adjustment. The blood pressure after 3 min of standing was 167/86 mmHg.
Carotid sinus massage in the supine and standing positions revealed no abnormalities.
During 20 min of passive 60° HUT we found no significant changes in blood pressure or heart rate. After the additional administration of 400 µg nitroglycerine sublingually she developed a tachycardia of 125 beats/min. The blood pressure varied greatly, which suggested strong sympathetic activation. The patient had some spinning and shaky sensations. Fifteen minutes after administration of nitroglycerine the patient was tilted back. At that moment the patient was experiencing a slight headache. After approximately 2 min in the supine position the patient was tilted back to the standing position to be able to step off the table and end the session. The Finapres was taken off. The patient felt suddenly unwell, with increase in headache, pain in the neck and nausea. She recognised these symptoms from many syncopal episodes at home. The patient was pale, sweating profusely and had difficulty in breathing with muscular cramps of the fingers. She also complained of chest pain. The patient was put in supine position. On examination there was a bradycardia of 40 beats/min and a blood pressure of 103/60 mmHg. The electrocardiogram showed marked ST-elevation in leads II, III and AVF of at least 3 mm with reciprocal ST-segment depression in the left lateral and anterior leads, compatible with RCA occlusion (Fig. 3). Nitroglycerine sublingually was administered. The complaints resolved, the ST-elevation decreased instantly and the blood pressure recovered to 128/70 mmHg 10 min after symptom onset.
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The patient was admitted to the coronary care unit for evaluation of ischaemia. Coronary angiography showed no stenoses or other abnormalities, in particular the right coronary artery was free of abnormalities. A provocation test for coronary spasm was not performed. The patient had no complaints on further observation for 3 days. On the suspicion of coronary spasm the patient was put on nifedipine 60 mg slow release. It might be reasoned that a calcium blocker should be avoided in Brugada syndrome (only based on theoretical considerations, however, and its vasodilatory effect may adversely affect vasovagal syncope). Yet careful monitoring of the ECG while establishing nifedipine therapy did not reveal any significant ST changes or other problems.
An electrophysiological study was not performed because the tilt table test elicited a very recognizable episode without ventricular arrhythmias. Furthermore, the patient experienced over hundred similar episodes during her life, which makes it highly unlikely that ventricular arrhythmias had played a role. Finally flecainide provocation test did not elicit ECG abnormalities which are typical of Brugada syndrome.
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Follow up |
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In 3.5 years follow up the patient experienced one episode of syncope 3 months after the HUT in a period of grief over the death of a family-member. Although there were a few episodes of slight pre-syncopal dizziness, she had no more episodes of chest pain.
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Discussion |
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We evaluated a 56-year old patient with recurrent syncope: 24 h Holter monitoring revealed no abnormalities besides sinus bradycardia and AV block, which could either be related to a vasovagal reaction or ischaemia of the inferior wall. Minutes after the HUT the patient developed typical symptoms with marked ST-elevation on the electrocardiogram. Further cardiac testing revealed no coronary disease. The patient was put on nifedipine and has been almost free of complaints since then.
The mechanism of syncope in this patient is difficult to understand. There are four major options.
Firstly, vasovagal syncope that is accompanied by hyperventilation which is known to be able to provoke coronary spasm [2]. The sensation of forced breathing and Trousseau's sign in this patient are typical symptoms of hyperventilation. Secondly, coronary spasm causing chest pain might have evoked vasovagal syncope with pain or anxiety as a trigger. Thirdly, coronary spasm might itself evoke brady- or tachyarrhythmias. Our patient, indeed, had bradycardia on the 24 h Holter and at the time of HUT. Finally, a sodium channel mutation associated with Brugada syndrome might have caused Brugada related rhythm disturbances [3]. It has been described that vagal reactions can induce episodes of VF in patients with Brugada-type ECG abnormalities [4].
There are several reports of patients with coronary spasm and syncope. One report describes a patient with Brugada-type ECG abnormalities and proven coronary spasm, who was relieved from syncopal spells after being put on a calcium antagonist [5]. Another case report deals with a patient with recurrent episodes of dyspnoea and syncope. This patient was treated with diltiazem, educated to control her respiratory rate, and, as a result, became free of syncopal spells [6]. Wang et al. describe three patients with unexplained syncope, who underwent HUT with isoprenaline and had marked ST-elevation caused by coronary spasm. All three patients were successfully treated with calcium-antagonists [7]. The same author described a few years later a patient with proven coronary spasm, who had persistent ST-elevation after HUT which did not respond to nitroglycerine and verapamil and had to be resuscitated [8,9].
The mechanism of coronary spasm is still not clearly understood. It is suggested that conflicting parasympathetic and sympathetic tone, as occurs in a tilt table test, can induce coronary spasm. [10] Yasue et al. on the other hand studied the effect of injection of acetylcholine, the neurotransmitter of the parasympathetic nervous system, in the coronary artery and found that it could induce coronary spasm, which suggests increased activity of the parasympathetic nervous system [11]. In spite of different results it is generally agreed that the parasympathetic and sympathetic nervous system indeed play a role in coronary spasm.
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Conclusion |
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In our patient both changes in vagal activity and hyperventilation might have caused the susceptibility to coronary spasm. As the pre-syncope was provoked by HUT, it is more likely that changes in sympathetic and parasympathetic tone are responsible for the syncopal spells and that hyperventilation was a secondary phenomenon. Brugada syndrome as the cause of the attacks is highly unlikely, as the patient has had numerous syncopal episodes since the age of 8 and no ventricular arrhythmias were documented during typical symptoms. The fact that nifedipine efficiently prevented further syncopal episodes and chest pain supports the theory that most episodes of syncope were indeed caused by a combination of vasovagal syncope and coronary spasm.
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Acknowledgements |
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Supported by a grant (NHS 99.181) from the Netherlands Heart Foundation, the Hague, the Netherlands.
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References |
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[1] Boersma L, Jaarsma W, Jessurun ER, van Hemel NHM, Wever EFD. Brugada syndrome: a case report of monomorphic ventricular tachycardia. Pacing Clin Electrophysiol 2001; 24: 112–115.[CrossRef][Medline]
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[5] Chinushi M, Kuroe Y, Ito E, Tagawa M, Aizawa Y. Vasospastic angina accompanied by Brugada-type electrocardiograms. J Cardiovasc Electrophysiol 2001; 12: 108–111.[CrossRef][Web of Science][Medline]
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[8] Wang CH, Hung MJ, Kuo LT, Cherng WJ. Cardiopulmonary resuscitation during coronary vasospasm induced by tilt table testing. Pacing Clin Electrophysiol 2000; 23: 2138–2140.[CrossRef][Medline]
[9] Miyata S, Inoue H, Horimoto M, et al. Head-up tilt test combined with isoproterenol infusion provokes coronary vasospastic angina. Jpn Circ J 1998; 62: 670–674.[Medline]
[10] Lanza GA, Pedrotti P, Pasceri V, Lucente M, Crea F, Maseri A. Autonomic changes associated with spontaneous coronary spasm in patients with variant angina. J Am Coll Cardiol 1996; 28: 1249–1256.[Abstract]
[11] Yasue H, Horio Y, Nakamura N, et al. Induction of coronary artery spasm by acetylcholine in patients with variant angina: possible role of the parasympathetic nervous system in the pathogenesis of coronary artery spasm. Circulation 1986; 74: 955–963.
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