Download Parasympathetic-mediated atrial fibrillation during tilt test

Europace (2006) 8, 349–351
doi:10.1093/europace/eul024
CASE REPORT
Parasympathetic-mediated atrial fibrillation during tilt
test associated with increased baroreflex sensitivity
Renata Rodrigues Teixeira de Castro1, Evandro Tinoco Mesquita1,2,
and Antonio Claudio Lucas da Nobrega1,2,3*
1
Laboratory of Autonomic and Cardiovascular Reactivity, Syncope Unit and Emergency Department, Hospital
Pró-Cardı́aco/PROCEP, Rio de Janeiro, RJ, Brazil; 2 Post-Graduate Program in Cardiovascular Sciences, Universidade Federal
Fluminense, Niterói, RJ, Brazil; and 3 Department of Physiology and Pharmacology, Universidade Federal Fluminense,
Niterói, RJ, Brazil
Received 18 October 2005; accepted after revision 21 February 2006
KEYWORDS
Syncope;
Atrial fibrillation;
Tilt table test;
Autonomic nervous system;
Baroreflex sensitivity
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.
Introduction
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
* Corresponding author: Rua Cinco de Julho, 318/1001, Icaraı́, Niterói,
Rio de Janeiro, Brazil. Tel: þ55 21 8201 0008; fax: þ55 21 2629 2405.
E-mail address: [email protected]
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.
Case presentation
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.
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350
During the test, we digitally recorded the 12-lead electrocardiogram (ECG 98w, Heart Ware, Brazil) and continuous arterial pressure by digital photoplethysmography
(Finometerw, Finapres, the Netherlands).
Figure 1 Haemodynamic changes during both tilt tests. Heart rate
(thick black lines), systolic (thin black lines), and diastolic blood
pressure (grey lines) curves, during the first (A) and second (B) tilt
tests. Phases: Resting, supine position (10 min); Tilt, 708 upright
position (20 min); Tilt þ isosorbide, 708 upright plus isosorbide
administration until hypotension development; Hypo, hypotension
period; Supine 1, supine position until restoration of normal arterial
blood pressure; Supine 2, supine position with normal blood
pressure.
R.R.T. de Castro et al.
After a 10 min supine rest, the patient was passively tilted
to 708. 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.
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 timedomain heart rate variability (standard deviation of pulse
intervals)11 and spontaneous baroreflex sensitivity with a
commercially available software (PRVBRS.exew, Finapres,
the Netherlands) which estimates the spontaneous baroreflex sensitivity using the regression slope of same-direction
Figure 2 Baroreflex sensitivity and heart rate variability recorded at different phases of the two tilt tests. Bars: baroreflex sensitivity (BRS);
lines: standard deviation of pulse (SDPI) (1st tilt test, grey lines and bars; 2nd tilt test, black lines and bars). Phases: Resting, supine position
(10 min); Tilt, 708 upright position (20 min); Tilt þ isosorbide, 708 upright plus isosorbide administration until hypotension development;
Hypo, hypotension period; Supine 1, supine position until restoration of normal arterial blood pressure; Supine 2, supine position with
normal blood pressure.
Parasympathetic-mediated atrial fibrillation
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.
351
beneficial or detrimental according to the underlying
mechanism.4
Conclusion
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.
Discussion
Acknowledgements
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
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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