ATRIAL FIBRILLATION
Parasympathetic-mediated atrial fibrillation during tilt test associated with increased baroreflex sensitivity
1 Laboratory of Autonomic and Cardiovascular Reactivity, Syncope Unit and Emergency Department, Hospital Pró-Cardíaco/PROCEP, Rio de Janeiro, RJ, Brazil; 2 Post-Graduate Program in Cardiovascular Sciences, Universidade Federal Fluminense, Niterói, RJ, Brazil; 3 Department of Physiology and Pharmacology, Universidade Federal Fluminense, Niterói, RJ, Brazil
Manuscript submitted 18 October 2005. Accepted after revision 21 February 2006.
* Corresponding author: Rua Cinco de Julho, 318/1001, Icaraí, Niterói, Rio de Janeiro, Brazil. Tel: +55 21 8201 0008; fax: +55 21 2629 2405. E-mail address: anobrega{at}urbi.com.br
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Abstract |
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The autonomic mechanism that triggered atrial fibrillation in a patient during tilt test was investigated. Neurocardiogenic syncope is often characterized by diminished baroreflex sensitivity during the hypotension period. Increased barorereflex sensitivity preceding the onset of atrial fibrillation in tilt testing may indicate the involvement of a vagally mediated mechanism, as shown in the present case.
Key Words: Syncope, Atrial fibrillation, Tilt table test, Autonomic nervous system, Baroreflex sensitivity
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Introduction |
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It is well known that autonomic influences play an important role in the triggering of atrial fibrillation.1
–7 Both intense parasympathetic and sympathetic stimulation can cause atrial fibrillation by different pathways: vagal stimulation shortens the atrial refractory period2–5 and sympathetic hyperactivity increases automatism and microreentry.6
Direct recording of autonomic fibre activity is an invasive approach, and is not suitable for routine clinical evaluation. Therefore, the identification of vagal or sympathetic-mediated atrial fibrillation is usually based on clinical history and physical examination.8,9 More recently, non-invasive methods have been employed to estimate autonomic modulation of cardiovascular function, such as heart rate variability and baroreflex sensitivity.10,11
It has been suggested that vagally mediated atrial fibrillation is usually triggered in young patients with normal hearts during the night, when the vagal tone is relatively high.8,9 On the other hand, sympathetic-mediated atrial fibrillation is believed to occur during the day, in older patients with structural cardiac disease.6,8 Unfortunately, these are quite weak rules and are not supported by many studies.8 For instance, Amar et al.7 showed that both increased parasympathetic and sympathetic activities trigger post-operative atrial fibrillation. Understanding the mechanism that triggers atrial fibrillation is a critical step for the development of new treatments for this high-incidence arrhythmia.
We present the case of an elderly patient who developed atrial fibrillation during a tilt test in which increased parasympathetic activity has been identified by means of spontaneous baroreflex sensitivity.
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Case presentation |
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The patient signed an informed consent form allowing the publication of this case. This case report was also approved by the Institutional Review Board.
A 72-year-old woman presented to our laboratory complaining of several syncopal episodes that were preceded by pallor and sweating. All episodes were related to standing for a long time in a hot environment. She had not sought diagnostic evaluation previously, but a recent episode, which resulted in cranial trauma, prompted her to seek medical assistance.
There was no history of cardiovascular or any other chronic disease. She was being treated for depression with fluoxetine and diazepam. Physical examination was unremarkable. The resting electrocardiogram showed sinus rhythm. Chest X-ray and echocardiogram were also normal.
As there was no evidence pointing to a cardiac cause of syncope, and medical history suggested neurocardiogenic syncope, the patient was submitted to a tilt table test. During the test, we digitally recorded the 12-lead electrocardiogram (ECG 98®, Heart Ware, Brazil) and continuous arterial pressure by digital photoplethysmography (Finometer®, Finapres, the Netherlands).
After a 10 min supine rest, the patient was passively tilted to 70°. Twenty minutes thereafter, sublingual isosorbide dinitrate (1.25 mg) was administered. After 14 min, the patient presented with high ventricular rate atrial fibrillation and hypotension (Figure 1A). Although the patient did not complain of any symptom, not even palpitations, the test was terminated because of hypotension (fall of 70 mmHg in systolic blood pressure) and atrial arrhythmia. The patient returned to sinus rhythm within 15 min of intravenous administration of amiodarone.
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Atrial fibrillation seemed not to be the underlying mechanism of the syncope episodes, as no other signs or symptoms occurred during the test. The patient had no cardiac disease (not even hypertension), and has never felt palpitations or any other symptom suggestive of cardiac disease. Also, she had a recent normal 24-h Holter recording and clinical history pointed towards neurocardiogenic or postural hypotension related syncope. Therefore, we decided to submit the patient to another tilt test following the same protocol one day later, while the patient was still in sinus rhythm.
During the second tilt test, the patient developed pallor, sweating, and syncope but after isosorbide administration, there was a sudden fall in blood pressure and a small decrease in heart rate, characterizing vasodepressor type of neurocardiogenic syncope (Figure 1B). The patient remained in sinus rhythm and did not present another paroxysm of atrial fibrillation.
As this patient has developed different responses to the same orthostatic stimulus (tilt test), we decided to investigate what mechanism could have triggered atrial fibrillation.
Beat-by-beat blood pressure and heart rate data from both tests were analysed to generate measures of time-domain heart rate variability (standard deviation of pulse intervals)11 and spontaneous baroreflex sensitivity with a commercially available software (PRVBRS.exe®, Finapres, the Netherlands) which estimates the spontaneous baroreflex sensitivity using the regression slope of same-direction changes in blood pressure and pulse interval (minimum of four intervals).
Figure 2 shows the heart rate variability and the spontaneous baroreflex sensitivity during different phases of each tilt test. Although the patient had similar spontaneous baroreflex sensitivity and heart rate variability at rest before tilting, these variables were clearly higher during hypotension in the first test when atrial fibrillation occurred. The occurrence of atrial fibrillation may have influenced the higher heart rate variability during and after the first tilt test.12 Nevertheless, it is interesting to note that baroreflex sensitivity was only clearly higher when hypotension developed in the first tilt test, i.e. when atrial fibrillation occurred.
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Discussion |
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Increased baroreflex sensitivity preceding the onset of atrial fibrilation is the major finding of this study, suggesting the involvement of vagally induced atrial fibrillation. Samniah et al.13
showed that patients with neurocardiogenic syncope present normal baroreflex sensitivity at the beginning of a tilt test. The patient shown in the present report had normal baroreflex sensitivity values that were only changed when atrial fibrillation developed.
Also, Samniah et al.13 stated that when hypotension develops during neurocardiogenic syncope, the baroreflex sensitivity is usually diminished. The higher baroreflex sensitivity in our patient during the hypotension phase when atrial fibrillation was initiated is intriguing. To our knowledge, the only explanation for this was the upright position associated with isosorbide administration inducing a greater vagal response, shown by the higher baroreflex sensitivity (an index of parasympathetic activity) and this also triggered atrial fibrillation by shortening the atrial refractory period.
Our findings are apparently at odds with the classical concept of the autonomic mechanisms underlying atrial fibrillation triggering. Actually, using the classical concept, it would be impossible to determine if the episode was triggered by enhanced vagal activity (at the onset, not at night) or sympathetic drive (elderly person presenting atrial fibrillation during the day). It should be emphasized that identifying the autonomic mechanism triggering atrial fibrillation is an important step in the decision making process that guides preventive measures. For example, some authors advise that patients with vagally mediated atrial fibrillation should avoid vagal predominant situations, such as ingestion of very cold drinks.9 In the case of persistent atrial fibrillation, it is even more important to take into consideration the role of autonomic influences, because beta-blockers, quinidine, and digitalis can be either beneficial or detrimental according to the underlying mechanism.4
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Conclusion |
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Atypical baroreflex response may have precipitated the atrial fibrillation in this case. Whether this observation pertains to spontaneous atrial fibrillation in other situations requires study. Further investigation is needed to confirm the intriguing autonomic influences of heart rate and rhythm during a tilt test. Determination of the autonomic mechanism that triggers paroxysmal atrial fibrillation may be useful to guide preventive and treatment decisions.
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Acknowledgements |
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We appreciate the medical assistance of Dr Alexandro Coimbra and Dr Arnold Preger, the technical assistance of Ms Patricia Pereira da Silva, and Dr André d'Ávila for insights included in the discussion.
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References |
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[1] Go AS, Hylek Em, Phillips KA, et al. Prevalence of diagnosed atrial fibrillation in adults: national implications for rhythm management and stroke prevention: the anticoagulation and risk factors in atrial fibrillation (ATRIA) study. JAMA 2001; 285: 2370–5.
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