KEY TEACHING POINTS
Key Teaching Points
The autonomic nerve system, especially the parasympathetic nerve system, is strongly
involved in the cause of swallowing-induced atrial tachyarrhythmia (SIAT).
Direct contact from the esophagus seems not to have an association with SIAT.
SIAT can be radically cured by catheter ablation.
Swallowing-induced tachyarrhythmia is a rare clinical entity, and is defined as supraventricular
tachyarrhythmia, such as atrial premature contractions (APCs), paroxysmal atrial tachycardia
(AT), and paroxysmal atrial fibrillation, that is reproducibly and consistently induced
during a wet or dry swallow. Although the first case of a swallowing-induced tachyarrhythmia
was reported as far back as 1926 by Sakai et al,
no more than 50 cases have been described in the worldwide literature, as Tada et
organized in a report.
In this present report, we describe a case of swallowing-induced AT arising from the
superior vena cava (SVC), which is assumed to have considerable association with parasympathetic
A 36-year-old man suffered from recurrent episodes of palpitation, which occurred
several seconds after swallowing solid foods or drinking hot water. APCs and AT during
swallowing were documented on electrocardiography and 24-hour Holter monitor. P wave
morphology was positive in inferior leads and positive in V1 lead. Since beta-blockers
and other antiarrhythmic drugs could not reduce episodes of this tachycardia, he was
admitted to our hospital for an electrophysiological study and a catheter ablation.
No structural heart disease was recognized in the echocardiogram.
An esophagogram by swallowing contrast media revealed that the esophagus was located
relatively leftward and was not adjacent to the right atrium. A decapolar catheter
was placed into the SVC, and 2 decapolar circular catheters (Lasso; Biosense-Webster,
Baldwin Park, CA) were placed into the left superior pulmonary vein and the right
superior pulmonary vein. Figure 1 shows the location of these catheters and the intracardiac
electrocardiogram of APCs after swallowing hot water. The earliest activation site
of sinus rhythm was near SVC4, and this level was at the SVC–right atrium junction.
The earliest activation site of APCs after swallowing was SVC1–2, which was above
the SVC–right atrium junction.
In this patient, heart rate variability (HRV) during the procedure was evaluated using
a real-time HRV analyzing system (MemCalc; GMS Co, Ltd, Tokyo, Japan). This system
can eliminate extrasystoles automatically and calculate HRV every 2 seconds. Low-frequency
(LF) and high-frequency (HF) components of the patient’s heart rate were measured
in order to evaluate changes in autonomic tone during the procedure. The HF component,
which indicates parasympathetic nerve activity, increased immediately after swallowing,
followed by APC induction. On the other hand, the LF/HF ratio, which indicates sympathetic
nerve activity, decreased after swallowing (Figure 2A-1).
APCs were mapped in the SVC using a 4-mm-tip ablation catheter. The earliest activation
site of APCs was the posteroseptal aspect of the SVC and the local activation at the
site preceded the onset of the P wave of APCs by 38 ms. APCs recorded from the unipolar
lead of the ablation catheter showed a QS pattern at the site (Figure 3). Radiofrequency
energy was applied at the site during sinus rhythm and the sinus interval was decreased
from 760 to 700 ms. After ablation at this site, APCs or AT did not occur even after
After successful ablation, LF and HF components of the patient’s heart rate were measured
again. The HF component was strongly suppressed and did not increase even after swallowing,
while the LF/HF ratio was suppressed as before (Figure 2A-2).
The HF component in 24-hour Holter monitoring was consistently suppressed significantly
at 1 day after ablation compared to preablation 24-hour Holter monitor (Figure 2B-1
and B-2), which means a suppression of parasympathetic nerve activity continued even
at 1 day after ablation.
APCs did not occur for 15 months after this procedure.
The true mechanism of swallowing-induced AT is still unclear. Direct mechanical interaction
between the distended esophagus and the adjacent left atrium was previously suggested.3,
4 Burton et al
reported a case in which the patient needed intrapleural repositioning of the esophagus
for curing swallowing arrhythmia. This suggested the direct mechanical stimulation
from the esophagus to the left atrium.
On the other hand, Lindsay
proposed a vagal nerve–mediated neural reflex as the initiating mechanism. In a case
report by Morady et al,
an esophageal manometric study demonstrated that the swallowing tachycardia was coincident
with relaxation of the upper esophageal sphincter and preceded the peristaltic activity
in the esophageal body. They also described that the most possible mechanism was a
vagally mediated neural reflex involving a neurotransmitter other than acetylcholine
because atropine and bethanechol did not affect the swallowing-induced AT. Recently,
many other reports suggested a neural reflex as the cause of swallowing-induced AT.8,
9, 10, 11
In this case report frequent atrial extrasystoles arising from the SVC were provoked
by swallowing. The fact that the SVC was far away from the esophagus suggested that
extrasystoles were provoked by neural reflex, not by direct contact from the esophagus.
We also found a significant involvement of the autonomic nerve system in this AT from
an HRV evaluation during the catheter ablation. The increase of parasympathetic nerve
activity with suppression of sympathetic nerve activity were recognized when swallowing-induced
AT occurred. The HF component was solely suppressed after ablation with suppression
of APCs, suggesting that parasympathetic nerve activity was strongly involved in the
cause of this arrhythmia rather than the sympathetic nerve system. Since AT was suppressed
by ablation at a single site, not by SVC isolation, the success site might be the
end of axons from ganglionated plexi (possibly the SVC–aorta ganglionated plexi),
which contained mainly the parasympathetic nerve system, as previously reported.10,
We experienced a case of swallowing-induced AT arising from the SVC that was cured
by catheter ablation. HRV measurement revealed that this AT had a strong involvement
of the parasympathetic nerve system as the cause of arrhythmia.