J Arrhythmia Vol 25 No 1 2009

Case Report

Alcohol-induced Ventricular Fibrillation

in Brugada Syndrome

Takekuni Hayashi MD1 , Haruo Mitani MD2 , Kosaku Goto MD2 ,

Rieko Ishimura MD2 , Susumu Tao MD2 , Sachiko Ito MD2 ,
Jun Masuda MD2 , Hajime Fujimoto MD2 , Yo Fujimoto MD2 ,
Sugao Ishiwata MD2 , Tetsu Yamaguchi MD2 , Minoru Ohno MD2
1
Department of Cardiology, Saitama Medical Center Jichi Medical University
2
Department of Cardiology, Toranomon Hospital

A 37-year-old man lost consciousness suddenly due to ventricular fibrillation (VF). After
cardioversion, twelve-lead ECG showed a pattern characteristic of type 1 Brugada. An
implantable cardioverter defibrillator (ICD) was implanted for Brugada syndrome. In the
following three years, VF occurred eight times after consumption of alcohol. Association
between the Brugada syndrome and alcohol consumption has rarely been reported. Recently,
it was reported that alcohol has inhibitory effect on single cardiac sodium channel gating and
it may be that alcohol acted as a sodium channel blocker in this patient. Here we report a case
of alcohol-induced VF in Brugada syndrome.
(J Arrhythmia 2009; 25: 32–35)

Key words: Alcohol, Ventricular Fibrillation, Sodium channel blocker, Diagnostic criteria

Introduction Case report

The Brugada syndrome is associated with a high
risk for sudden cardiac death in healthy adults. The
ECG manifestations of Brugada syndrome are often
changed and may be modulated by sodium channel
blockers, body temperature, autonomic nervous
activity, antidepressants, and blood electrolyte con-
centration. Sometimes these conditions and agents
induce VF in Brugada syndrome.
Alcohol has been reported to affect the heart in
certain ways, especially the proarrythmic effects of
acute alcohol consumption.1) But, to our knowledge,
a clear relationship between Brugada syndrome and
alcohol has not been reported.
The patient was a 37-year-old man with no family
history of sudden death and no previous abnormal
ECG findings on routine medical examination. He
suddenly lost consciousness for 10 minutes, and was
transported to a hospital. He lost consciousness again
in the emergency room of the hospital. The ECG
monitor showed VF. After electric defibrillation was
performed, his cardiac rhythm returned to sinus
rhythm. Twelve-lead ECG showed ST-segment
elevation of =2 mm followed by a negative T wave
in the V1 lead (Figure 1). This is called Type 1
Brugada ECG. Brugada syndrome is definitively
diagnosed when a type 1 ST-segment elevation is

Received 13, June, 2008: accepted 6, January, 2009.

Address for correspondence: Takekuni Hayashi MD, Department of Cardiology, Saitama Medical Center Jichi Medical University, 1-847,
Amanuma, Omiya, Saitama 330-8503, Japan. Phone 81-48-647-2111 FAX 81-48-644-8617

32
Hayashi T
I aVR V1
aVL V2
II
III aVF V3
observed in more than 1 right precordial lead (V1
to V3), in conjunction with one of the following:
documented VF, polymorphic ventricular tachycar-
dia (VT), a family history of sudden cardiac death
before reaching age 45, coved-type ECGs in family
members, inducibility of VT with programmed
electrical stimulation, syncope, or nocturnal agonal
respiration (2). Therefore, he was diagnosed as
Brugada syndrome. In patients with Brugada syn-
drome who have spontaneous Type 1 ECG and
history of VF, an ICD prevents cardiac sudden death
(class I evidence level).2) The patient was referred to
our hospital since he met the indications for ICD
implantation. Echocardiography, treadmill test, and
enhanced cardiac MRI were normal. We then
performed an electrophysiological study (EPS).
Triple extra stimuli from the right ventricular out-
flow tract induced polymorphic VT developing to
VF (Figure 2). ECG did not change after the admin-
istration of pilsicainide (50 mg). After administration
of propranolol (2 mg), triple extra stimuli from right
ventricular apex induced polymorphic VT develop-
ing to VF. An ICD is necessary to prevent cardiac
sudden death; therefore, he underwent implantation
of an ICD. After he was discharged, he did not
drink alcohol for 6 months. However, he began
drinking after 6 months and VF occurred after
drinking. He has had 8 episodes of VF in the last
three years (Figure 3). All events occurred when he
drank more than 50 g of ethanol, and VF occurred
after at least two hours had passed after his drinking.
We have counseled him to stop drinking, but he is
unable to stop his drinking habit. Thus, we are
considering other treatments such as drugs and
ablation.
Alcohol-induced VF in Brugada Syndrome
V4
V5
Figure 1 Twelve-lead ECG after
transthoracic cardioversion.
V6 ST-segment elevation of =2 mm fol-
1 mV lowed by a negative T wave is observed
in V1.
400 ms This ECG is called type 1 Brugada
ECG.
Discussion
In Brugada syndrome most arrhythmic events
occur at rest and at night.3) Thus, the Brugada
syndrome is inseparably connected with autonomic
nervous activity, especially of the parasympathetic
nervous system. In this respect Brugada syndrome
differs greatly from other cardiac diseases, such as
ischemic heart disease and cardiomyopathy. In these
diseases enhanced activity of the sympathetic nerv-
ous system induce arrhythmic events, but in the
reported case VF occurred at night after drinking,
hence alcohol-induced enhanced activity of the
parasympathetic nervous system may be related to
triggering of VF. Hypokalemia and insulin secretion
cause ST segment changes in patients with Brugada
syndrome.2,4) Humoral regulation from alcohol in-
take may be related to the induction of VF in this
case. In addition, it was recently reported that
alcohol has an inhibitory effect on single cardiac
sodium channel gating.5) Because sodium channel
blockers induce VF in patients with Brugada
syndrome, alcohol may act as a sodium channel
blocker in this patient. However, his ECG was
unchanged when pilsicainide was administered.
A variety of drugs have been reported to produce a
Brugada-like ST-segment elevation including anti-
arrhythmic,6) antianginal,7) psychotropic,8) and other
drugs.9) The diagnosis of Brugada syndrome is also
made when a type 2 (saddleback pattern) or type 3
ST-segment elevation is observed in more than 1
right precordial lead under baseline conditions and
conversion to the diagnostic type 1 pattern occurs
after sodium channel blocker administration. This
patient usually showed normal ECG, and only once
33
J Arrhythmia Vol 25 No 1 2009

II
aVF
V1
V6
CARTO 1–2
CARTO 3–4
HIS 1–3
HIS 1–2
HIS 2–3
HIS 3–4
CS 1–2
CS 3–4
CS 5–6
CS 7–8
CS 9–10
RV 1–2
RV 3–4

CARTO pace

Figure 2 Intracardiac electrograms

Triple extra stimuli from the right ventricular outflow tract induced polymorphic VT.

showed type 1 ECG after electric defibrillation for

VF. Pilsicainide administration could not change his
ECG. Treadmill testing also did not elevate the ST
segment. This case does not show characteristic
findings of the Brugada syndrome. A Brugada-like
ECG can occasionally appear for a brief period or
several hours after direct current cardioversion.10,11)
However, this patient did fulfill the diagnostic
criteria. It is an open question whether the diagnostic
criteria are sufficient to make a definite diagnosis of
Brugada syndrome. However, QT interval, enhanced
cardiac MRI, echocardiography, coronary angiogra-
phy, right ventriculography and cardiac biopsy
findings were normal. There were no findings to
suggest arrhythmogenic right ventricular cardiomy-
opathy (ARVC), long QT syndrome, and other
structural heart disease. We therefore think that this
case shows an atypical Brugada syndrome. It is of
utmost importance for the prevention of VF that he
abstains from drinking; however he is unable to stop
his drinking habit. Therefore, we are considering
other treatments such as drugs or ablation.12) A
number of reports have shown the effectiveness of
quinidine in treatment of Brugada syndrome.13–19)
Because the typical features of Brugada syndrome
were not observed in this case, it is unclear whether
quinidine would have been effective. If VF storms
occur despite the administration of quinidine, we are
Figure 3 ICD record
VF have been documented 8 times, all events occurred after
drinking alcohol.
considering EPS and ablation under alcohol admin-
istration.
Conclusion
Here we reported a rare case of alcohol-induced
VF in Brugada syndrome. Alcohol has a marked
influence on the autonomic nervous system and
functions as a sodium channel blocker. However the
relation between alcohol and Brugada syndrome is
unclear. Future study is necessary in order to manage
Brugada syndrome patients. This case fulfilled the
diagnostic criteria, but it did not show findings
characteristic of Brugada syndrome. It is an open
question whether this case was correctly diagnosed
as Brugada syndrome. Depending on the diagnosis,
the method for the treatment of VF is different.
Therefore, the diagnostic criteria of Brugada syn-
drome should be reconsidered.

34
Hayashi T
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