383
Vol. 34, pp. 383ΐ393, 2006
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Fig. 1. Measurement of electrocardiogram.
J point: O#set of QRS wave determined by limb
leads. J40: Forty milliseconds after J point. J80:
Eighty milliseconds after J point.
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173
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V2 V5 ECG Fig. 3 ῌ V2
123
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type 2 ῍ P P ῌSNRT῍ '>?@ABCD Wenckebach EF
ῌ
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Fig. 2. Actual ECG from PLC test ῌV1 to V3 lead῍.
Left: Positive case ῌGroup P-positive῍ Right: Negative case ῌGroup P-negative῍
Fig. 3. Baseline ECG on PLC test.
Baseline ECG from case 1 to 3 were in Group P-positive and case 4 to 6 were in
Group P-negative, showing no significant di#erence between the groups.
174
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῍ ῌFig. 4῍ῌ
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@AQ0 J FRS560῍ DT Yῑ
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P type 1 C῍ VX#2ῌ
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:YZ[\]^_`a8 Table 2 9.ῌ
Fig. 4. Comparison of Sinus Node Recovery Time ῌSNRT῍ and Wenckebach Rate
ῌWBR῍ between group P-positive and group P-negative.
There were no significant di#erences between the groups.
Table 1. The Index of Intraventricular Conduction Delay
in PLC Test
175
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388
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Fig. 5. Comparison of the indices of intraventricular conduction delay in PLC test.
There were no significant di#erences between the groups.
P P ῍ EPS Vf
P ῌPῒ0.01῍ ῍ ῍ ῍ ῍ !"#$
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ΐ῎ῒῐ῍ῌ
-./0123- P ῎20 ῏456
7 37 89ΐ69 89῍ :; 52 89ῑ9.8 89
<ῌ = P ῎78 ῏4567 36 89
Fig. 6. Comparison of delta J amplitude between V1ῐ3
leads in Group P-positive.
Positive change was largest in V2.
ΐ68 89῍ :; 51 89ῑ10.4 89<ῌ >
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176
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Fig. 7. Patient distribution of Group P-positive by J point elevation in PLC test.
Table 2. Characteristics of Patients
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1:῍ Brugada R type 2῍3 STUV<WX῍
W῍ P D/
Jrx:῍ FG+JHI
PLC YZ[\0 type 1 J]U1::
;Eῌ ¡¢῍ !pd῍ 1:0ῌ ^_3῍ P C/
J `abcd
pd῍ SAECG 3$£ LP C/s῍ $%(¤
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390
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opῌ ni῍ Na " 0 L
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J End "!῍ Epi ῍ End ".
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9rsῌ
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Kῌ 7\῍ EPS LM[efJ
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Ci¯ Vf jJsῌ Type 2῍3 LM
EPS ῍ ^U3op Na (?@
;<>^iK
J῍ 3op
ABk Epi End
Epi K® ῌ
Na (?@ABl Na (?@AB῍ I")῍
AP q=rsYῌ
%[aR῍ 3h:
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CaJ῍ Vf ;
v^YwA,
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Ito C)*J῍ Brugada |BCC}~S
phase 2 reentry 2%['Cnw!w
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`2Coxῌ Type 1 p Vf Kx῍ GHI
HJ"
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#῍
HI Ito C}J῍ K5
type 2῍3 EPS 3oph:" Na (?
Brugada |BCC}! ῌ Vf L
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V[9῍ EEE9M6
rsYKῌ
19῏
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HopN῍ OP) Vf
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178
Brugada f/3»#y¼
391
11῏13ῌ21ῌῌ Brugada 8 2῍3 f>M῍ EPS >. Vf l῍
4 HV } Vf EPS b Vf .
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1ῌ
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filtered QRS ῍ ()*+,-῍ ῌ T'5῍ ; PLC E#>῍
./01
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EPS Vf "V. ICD G
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1ῌ Brugada P and Brugada J. Right bundle
ῌ & PEQ, ῍ QRS ῍ HV branch block, persistent ST segment elevation
R J STUPQ.!.VWῌ /
and sudden cardiac death. A distinct clinical
X89
῍ /0YZ82
and electrocardiographic syndrome. J Am Coll
:;G[2῍ \].
Z^
_%῍ J STU
Cardiol 1992; 20: 1391῏1396.
2ῌ Viskin S, and Belhassen B. Idiopathic ventricu-
!`2V.[>aῌ
lar fibrillation: Am Heart J 1990; 120: 661῏671.
SAECG b LP .῍ type 1 type 1 3ῌ Gussak I, Antzelevitch C, Bjerregaard P, Tow-
R#R
18ῌῌ cd῍ /
bin JA and Chaitman BR. The Brugada syn-
X89
GH῍ <= P #
drome. Clinical, electrophysiologic, and ge-
L P N#L>. LP #QeVWῌ
netic aspects. J Am Coll Cardiol 1999; 33: 5῏15.
῍ P #L>
WM type 2῍3 4ῌ Wilde AM, Antzelevitch C, Borggrefe M. Bru-
Brugada fb
.ghV9
gada J, Brugada R, Brugada P, Corrado D,
./6ij2
Je#rey A. Mini-review: Current perspective.
>.VJKῌ
/689
Hauer R, Kass R, Nademanee K, Priori S and
k>
῍ PLC EF EPS b Vf
Proposed diagnostic criteria for the Brugada
P #L>lW.῍ Na ?@,A
syndrome. Consensus report. Circulation 2002;
Bmnop#G
pV
q2῍ rstu'5o
106: 2514῏2519.
vsjwJKῌ
ῌ
5ῌ Brugada J and Brugada P. Further characterization of the syndrome of right bundle branch
῍
block, ST segment elevation, and sudden car-
Brugada f!"x type 2῍3 f
#yh
diac death. J Cardiovasc Electrophysiol 1997;
qGz{2ῌ Type 2῍3 f|
8: 325῏331.
Brugada }~LG$%b>.V
6ῌ ¤¥῍ ¦(῍ §¨-©῍ ª«.p῎ /}~
>῍ PLC E. Vf jL
%p
# Brugada }~L0z{῍3 1
2
ῌ PLC EF῍ P #L῍
z¬®'¯2E°
P N#LOPQ
y²!῍῎ 3 15 1Q³j´µ¶·
5῍
.
ST TUPQ!MV῍ type 1 4<=¸¹5'<=º῍ p11.
2.!VWῌ EPS b Vf P #L>lW῍ #yh
±²G#
7ῌ Brugada J, Brugada R, Antzelevitch C, Tow-
q.j
bin J, Nademanee K and Brugada P. Long-
&'F().V῍ 'F("#l
term follow-up of individuals with the electro-
ῌ 2῍ type 1 ECG Gw>M
cardiographic pattern of right bundle branch
10῎ Vf jx57ῌ῍ S
block and ST segment elevation in right precor-
Gwxz{G*_%ῌ type
dial leads V1 to V3. Circulation 2002; 105: 73῏
179
ῐῑ῍ΐ
392
῎
78.
ῒ῏
ῌ
15῎ Kurita T, Shimizu W, Inagaki M, Suyama K,
8῎ Priori SG, Napolitano C, Gasparini M, Pap-
Taguci A, Satomi K, Aihara N, Kamakura S,
pone C, Della Bella P, Brignole M, Giordano
Kobayashi J and Kosakai Y. The electro-
U, Giovannini T, Menozzi C, Bloise R, Crotti
physiologic mechanism of ST-segment eleva-
L, Terreni L and Schwartz PJ. Clinical and
tion in Brugada syndrome. J Am Coll Cardiol
genetic heterogeneiety of right bundle branch
2002; 40: 330ῐ334.
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16῎ Yan GX and Antzelevitch C. Cellular basis for
prospective evaluation of 53 families. Circula-
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tion 2000; 102: 2509ῐ2515.
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9῎ Nanke T, Nakazawa K, Arai M, Ryu S, Osada
17῎ Chen Q, Kirsch GE, Zhang D, Brugada R,
K, Sakurai T and Miyake F. Clinical sig-
Brugada J, Brugada P, Potenza D, Moya A,
nificance of the dispersion of the activation-
Borggrefe M, Breithardt G, Ortiz-Lopez R,
recovery interval and recovery time as markers
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Brugada ῍῏ῒῐῌΐ῎ῑ
393
Abstract
Clinical Feature of Saddle-back Type Brugada-type
Electrocardiogram
Hisao Matsuda, Ryoji Kishi, Kiyoshi Nakazawa, and Fumihiko Miyake
Purpose: Brugada type electrocardiogram ῌECG῍ is inconsistent with its morphology, showing frequently Saddle-back type. We aimed to clarify the clinical feature of those who show such ECG type.
Method: The subjects consisted of 98 patients who were found to have the saddle-back type ECG. They
were classified into two groups by Na channel blockade challenge test using Pilsicainide ῌPLC῍; positive for
group P-positive ῌn῎20῍ and negative for group P-negative ῌn῎78῍. Clinical features were compared
between these groups. Result: ῌ1῍ After PLC administration, QRS interval, PEQ interval, and HV interval
were prolonged in both groups with the same degree. ῌ2῍ There were no significant background di#erence
between the groups as sex, obvious structural heart disease, syncopal episode of unknown origin, family
history of sudden death, and the result of LP, except the high incidence of ventricular fibrillation ῌVf῍
induction during electrophysiological study ῌEPS῍ in group P-positive ῌpῐ0.05῍. ῌ3῍ Cardiac event, syncopal attack, death did not occur in both groups for mean follow-up period of 51῏10.3 months. Conclusion:
Under PLC, not all the patients with the saddle-back type ECG showed typical Brugada type ECG, while
these two groups have shown the same degree of intraventricular conduction delay. This means that the
formation of typical Brugada type ECG will not be attributed to conduction delay. Moreover, although Vf
inducibility in the EPS was high in the group P-positive, however, both groups had favorable prognosis.
This will also suggest that defibrillator implantation for Group P-positive will be unnecessary, even with the
successful Vf induction in the EPS.
Key words
Brugada syndrome, Pilsicainide, Na channel blockade challenge test
Department of Internal Medicine, Divisions of Cardiology, St. Marianna University School of Medicine
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