Europace Advance Access originally published online on March 13, 2007
Europace 2007 9(4):225-227; doi:10.1093/europace/eum027
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SYNCOPE
The pattern of activation of the sympathetic nervous system during tilt-induced syncope
ko1,*
ciborski3
ci
ski1
1 Teaching Department for Emergency Medical Service, Medical University of Wroclaw, Bartla Street 5, 51-618 Wroc
aw, Poland;
2 Department of Cardiology, Medical University of Wroclaw, Poland;
3 Internal Ward Hospital Olawa, Olawa, Poland
Manuscript submitted 3 May 2006. Accepted after revision 14 January 2007.
* Corresponding author. Tel: +0048717840961; fax: +0048717840961. E-mail address: dzysko{at}wp.pl
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Abstract |
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A 49-year-old patient with a history of situational syncope and minimal electrocardiographic signs of accessory pathway is described. The evidence for pre-excitation was present only during the sympathetic activation caused by exercise testing and isoprenaline infusion. This phenomenon served as an indicator of significant adrenergic drive to the heart after the tilt-induced syncope.
The meaning of the observed electrocardiographic changes in the course of neurocardiogenic reaction and its contribution to the understanding of the sympatho-vagal balance during vasovagal syncope is discussed. The lack of preexcitation signs during syncope and its appearance several seconds after the syncope-related sinus pause indicates sympathetic withdrawal before and shortly after the asystole. The possible pathophysiological mechanisms are discussed.
Key Words: Autonomic nervous system, Tilt testing, Vasovagal syncope
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Introduction |
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The exact pathophysiological mechanisms responsible for postural neurally-mediated syncope have not been fully elucidated. The activity of the sympathetic nervous system during syncope was the subject of numerous studies. Increased sympathetic tone is the cornerstone of the theory which relies on the presence of increased cardiac sympathetic stimulation in a setting of ventricular ‘underfilling’, leading to activation of the Bezold–Jarisc
s reflex which in turn results in hypotension and bradycardia.1
Another theory proposed for explanation of haemodynamic events in this syndrome is unopposed vasodilatation produced by the adrenaline released in excessive amount due to dissociation between the adrenomedulary and the noradrenergic response. The total activity of the sympathetic tone is difficult to assess exactly, especially when rapid changes occur.
The report of neurally-mediated syncope in heart transplant patients allowed the questioning of this theory.2 We believe that our case report of neurally-mediated syncope in a patient with an accessory atrio-ventricular pathway, which was revealed electrocardiographically only during significant sympathetic stimulation, will permit a better understanding of the sequence of events related to the sympathetic nervous system activity during and after syncope.
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Case description |
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A 49-year-old man, a blood donor, with no history of previous disease was admitted to the Department of Cardiology after syncope which occurred following micturition at night. The patient fell down and experienced face trauma, the fresh abrasions of the skin on the forehead were seen on admission. He was frightened, had tachycardia of 100 bpm, and raised blood pressure, 180/100 mmHg. His BMI was 31 kg/m2 and there was no orthostatic hypotension. The electrocardiogram revealed sinus rhythm at 100 bpm, otherwise normal.
There were no signs of impairment of the central nervous system or internal bleeding. In spite of time relation between micturition and syncope, a cardiac cause of syncope was evaluated. Exercise testing performed on the treadmill according to Bruce protocol revealed ST-segment depression without any clinical symptoms. At peak exercise, the QRS morphology changed indicating discrete signs of abnormal ventricular depolarization. During 24-hour ECG monitoring, one episode of asymptomatic ST segment depression was found with a change in QRS morphology, suggesting presence of pre-excitation syndrome. Transoesophageal electrophysiological examination revealed Wenckebach periodicity during atrial stimulation 110 ppm, atrioventricular node refractory period 240 ms, atrial refractory period 220 ms. Stimulation with single extrastimulus did not prompt any pre-excitation. After isoprenaline infusion at a rate of 5 µg/min had been started, the cycle length shortened to 600 ms.3 Atrial stimulation revealed a Wenckebach periodicity at 180 ppm. Stimulation with a single extrastimulus revealed discrete signs of pre-excitation. Constant stimulation with cycle length 400 ms (150/min) revealed pre-excitation morphology of alternate QRS complexes. Twelve milligrams of adenosine was administered intravenously during the infusion of isoprenaline, but there was no further change in QRS morphology.4 During the hyperadrenergic state after adenosine administration, the heart rate was 110 bpm and discrete features of pre-excitation were present. Unfortunately, the patient refused any invasive electrophysiological evaluation.
In the 26th minute of head-up tilt testing performed according to the Italian protocol with nitroglycerine provocation, vasovagal syncope occurred with asystole lasting 25 s. The maximal heart rate during tilt testing was 91 bpm. A careful examination of the two ECG tracings revealed that pre-excitation signs appeared not at the peak of the test but shortly after the end of the induced pause (Figure 1).
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Because of a close relation between hyperadrenergic state and the presentation of a delta wave in this particular patient, we concluded that the most prominent sympathetic activation (probably adrenaline-dependent) occurred only after syncope and could, therefore, be pause-related. There were no pre-excitation signs on electrocardiographic monitoring during and immediately after tilt testing, but they appeared about 20 s after asystole had ended. Their presence was also shown during voluntary exercise performed when the heart rate was 80 bpm. However, a supraventricular extrasystole occurred immediately after syncope, which was conducted with a prolonged PQ interval and no sign of pre-excitation.
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Discussion |
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The starting point for evaluation of syncope includes a careful history, physical examination including orthostatic blood pressure measurements and the standard 12-lead electrocardiogram.1
The presented case is rather typical and would not deserve detailed examination, but for the pre-excitation signs being a marker of regional autonomic activity, allowing us a unique opportunity to evaluate this in the immediate post-syncope phase. In our patient syncope occurred after micturition, suggesting a neurally-mediated type but other aetiologies were considered. Increased blood pressure on admission raised the possibility of structural heart disease, prompting us to perform Holter monitoring, exercise testing, and later tilt table testing. Asymptomatic depression of ST segments were observed during exercise testing and Holter monitoring, possibly indicating silent ischaemia but the findings were false positive due to pre-excitation.5 Tilt table testing may be positive in patients with situational syncope but not strongly so if only passive tilt was undertaken6: our patient required nitroglycerine provocation. Vasovagal syncope occurred with a VASIS 2B collapse pattern.7
This case might offer an improved understanding of the pathophysiology of vasovagal syncope. The results of the tests indicated that sympathetic activation revealed pre-excitation signs, such that when present the degree of sympathetic stimulation may be presumed to be strong. The alternative possibility that pre-excitation signs could be revealed by parasympathetic stimulation and decrease conduction through the atrio-ventricular node was, we believe, excluded by Holter monitoring at night when pre-excitation was not observed. The existing data on sympathetic activation during vasovagal syncope are not consistent. Although some authors have shown an increase in plasma adrenaline before the syncope,8 the microneurographic studies suggest rather sympathetic withdrawal (noradrenaline) and parasympathetic predominance.9 Neither method is suitable for direct assessment of cardiac sympathetic activity, because an increase in the activity of one part of the autonomic nervous system in one organ or part of it and decrease in another part. Plasma catecholamines measured in venous blood are poor markers of local sympathetic activity. Heart rate variability (HRV) in patients during syncope can also provide misleading results probably perhaps due to changes in heart rate and respiration rates and their influence on HRV parameters.10,11 Measurements of adrenaline and noradrenaline during syncope suggest discrepant levels of the two hormones.8,12,13 Conduction via an atrioventricular accessory pathway depends on autonomic influence. During exercise parasympathetic activity decreases and sympathetic drive increases. Adrenaline and noradrenaline act similarly increasing accessory pathway conduction. In the phase immediately before vasovagal syncope sympathetic activity disappears and vagal stimulation increases. In numerous studies, plasma adrenaline rose before syncope but no measurements were made in the coronary vascular bed. The concentration of noradrenaline diminishes as indicated by direct recordings of sympathetic nerves and this hormone rises only slightly in the plasma. Analysing the ECG on tilt during the vasovagal reaction in our patient some phases of autonomic activity can be described: constant increase in heart rate before syncope, sympathetic withdrawal shortly before the asystole, sympathetic activation after a certain period of asystole with first junctional, and then sinus beats with discrete signs of pre-excitation. This presumed increase in catecholamines seems to be the result of asystole together with a decrease in the inhibitory action of the reflex. Strong sympathetic stimulation is believed to produce a strong parasympathetic response during vasovagal syncope but our data do not support this concept. Our observation suggests that significantly increased sympathetic activity (tone) did not precede or accompany tilt-induced vasovagal syncope in our patient until asystole occurred. One case cannot lead to conclusions but—in our opinion—the phenomenon observed may pertain at least to some cases of nervous-mediated syncope.
Neurally-mediated syncope still requires a full understanding of its mechanisms. More detailed study of autonomic activity on the heart is needed. This may show that more than one mechanism is present among these patients.
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References |
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[1] Brignole M, Alboni P, Benditt D, Bergfeldt L, Blanc JJ, Bloch Thomsen PE, et al. Guidelines on management (diagnosis and treatment) of syncope—update 2004. Europace 2004; 6: 467–537.
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