From the Arrhythmia Unit (J.B.), Cardiovascular Institute, Hospital
Clínic, University of Barcelona, Spain; Cardiology Department (R.B.),
Baylor College of Medicine, Houston, Tex; and Cardiovascular Research and
Teaching Institute (P.B.), OLV Hospital, Aalst, Belgium.
Correspondence to Josep Brugada, MD, Arrhythmia Unit, Cardiovascular Institute, Hospital Clínic, University of Barcelona, Villarroel 170, 08036, Barcelona, Spain. E-mail jepbrugada{at}grn.es
Methods and Results—Data on 63 patients (57 men; mean age,
38±17 years) with the described ECG pattern were analyzed in
terms of arrhythmic events and sudden death. Events were
analyzed for patients with at least one episode of aborted
sudden death or syncope of unknown origin before recognition of the
syndrome (symptomatic patients, n=41) and for patients in
whom the ECG pattern was recognized by chance or because of screening
related to sudden death of a relative (asymptomatic
patients, n=22). During a mean follow-up of 34±32 months, an
arrhythmic event occurred in 14 symptomatic patients (34%)
and 6 asymptomatic patients (27%). An automatic
defibrillator was implanted in 35 patients, 15 received pharmacological
therapy with ß-blockers and/or amiodarone, and 13 did not
receive treatment The incidence of arrhythmic events was similar in all
therapy groups (log-rank 0.86); however, total mortality was 0% in the
implantable defibrillator group, 26% in the pharmacological group, and
31% in the no therapy group (log-rank 0.0005). All mortality was due
to sudden death.
Conclusions—Patients without demonstrable structural heart
disease and an ECG pattern of right bundle-branch block and ST-segment
elevation in leads V1 through V3 are at risk
for sudden death. Amiodarone and/or ß-blockers do not protect
them against sudden death, and an implantable defibrillator seems to be
the present treatment of choice.
A patient was considered to have an arrhythmic event if he or she had a
documented episode of syncopal ventricular
arrhythmia or sudden death or received an appropriate shock
from an implantable defibrillator. Shocks were considered appropriate
shocks when ventricular tachycardia or
ventricular fibrillation was documented using the stored
electrograms of the device or when syncope or dizziness preceded the
shock if electrograms were not available.
The probability of survival and event-free analysis was
estimated with the Kaplan-Meier method. The statistical significance of
each comparison was calculated with the log-rank test.
Cross-comparisons were done using
In 46 of the 63 patients, programmed ventricular
stimulation while off drugs was performed. Because patients were seen
at different centers, the stimulation protocol that was used was not
uniform. However, in all cases, up to three ventricular
extrastimuli were used in at least one right ventricular
site. In 37 of the 46 patients (80%), ventricular
fibrillation (n=30) or long runs (>10 seconds) of nonsustained
polymorphic ventricular tachycardia (n=7)
were repeatedly induced with one (n=2), two (n=19), or three (n=16)
premature ventricular stimuli. Inducibility was similar in
symptomatic (25 of 32) and asymptomatic (12 of
14) patients (P=NS).
Treatment was decided by the primary physician and could be not
randomized at that time. Thirty-five patients received an implantable
defibrillator, 15 patients received pharmacological treatment
(ß-blockers and/or amiodarone), and 13 patients had no
therapy. Patients who received a defibrillator were more often
symptomatic and inducible at the
electrophysiological study (Table 1
In Fig 5
The present data show that patients with no demonstrable structural
heart disease and an abnormal ECG pattern consisting of right
bundle-branch block and ST-segment elevation in leads
V1 through V3 are at risk
of sudden death. Most patients were first identified after an episode
of aborted sudden death. In this group, incidence of recurrent
arrhythmic events during follow-up was 34%, similar to the incidence
described in survivors of idiopathic ventricular
fibrillation.8 However, asymptomatic
patients in whom the abnormal ECG was identified during routine ECG
test or family screening had also an incidence of arrhythmic events
during follow-up of 27%. These results strongly stress the need for
careful evaluation of asymptomatic patients with this ECG
pattern and the need for family ECG screening in survivors of cardiac
arrest. With the present data, an abnormal ECG like the one
described should be considered a marker of high risk of sudden death
during follow-up and careful evaluation of the need for therapy should
be done. Mortality rate is very high in patients treated with
pharmacological agents such as amiodarone and ß-blockers, but
no mortality occurred in patients with an implantable defibrillator.
Follow-up of patients with an implantable defibrillator has shown a
high incidence of recurrent arrhythmic events appropriately treated by
the device; this justifies the implantation of such a device in all
patients with the ECG described despite the uncertainties associated
with the pathophysiology of the syndrome.
In conclusion, patients with the abnormal ECG consisting on right
bundle-branch block and ST-segment elevation in leads
V1 to V3 and without
demonstrable structural heart disease are at high risk for sudden
death. Asymptomatic patients with the ECG anomaly have the
same risk of arrhythmic events as do patients who have had an episode
of aborted sudden death. Pharmacological treatment with
amiodarone and/or ß-blockers does not protect patients
against sudden arrhythmic death, and an implantable defibrillator is at
present the treatment of choice.
Received September 18, 1997;
accepted October 13, 1997.
2.
Miyazaki T, Mitamura H, Miyoshi S, Soejima K, Aizawa
Y, Ogawa S. Autonomic and antiarrhythmic drug modulation of ST segment
elevation in patients with Brugada syndrome. J Am Coll
Cardiol. 1996;27:1061–1070.[Abstract]
3.
Proclemer A, Facchin D, Feruglio GA, Nucifora R.
Fibrillazione ventricolare recidivante, blocco di branca destra,
persistente sopraslivellamento del tratto ST in V1–V3: una nuova
sindrome aritmica? G Ital Cardiol. 1993;23:1211–1218.[Medline]
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4.
Bjerregaard P, Gussak I, Kotar SL, Gessler JE, Janosik
D. Recurrent syncope in a patient with a prominent J wave. Am
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5.
Atarashi H, Ogawa S, Harumi K, hayakawa H, Sugimoto T,
Okada R, Murayama M, Toyama J, for the Idiopathic
Ventricular Fibrillation Investigators. Characteristics of
patients with right bundle branch block and ST segment elevation in
right precordial leads. Am J Cardiol. 1996;78:581–583.[Medline]
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6.
Brugada J, Brugada P. Further characterization of the
syndrome of right bundle branch block, ST segment elevation and sudden
cardiac death. J Cardiovasc Electrophysiol. 1997;8:325–331.[Medline]
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7.
Brugada J, Brugada R, Brugada P. Ajmaline unmasks
right bundle branch block-like and ST segment elevation in V1–V3 in
patients with idiopathic ventricular fibrillation.
PACE. 1996;19:599. Abstract.
8.
Wever EFD, Hauer RNW, Oomen A, Peters RHJ, Bakker PFA,
Robles de Medina EO. Unfavorable outcome in patients with primary
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© 1998 American Heart Association, Inc.
Clinical Investigation and Reports
Right Bundle-Branch Block and ST-Segment Elevation in Leads V1 Through V3
A Marker for Sudden Death in Patients Without Demonstrable Structural Heart Disease
Abstract
Top
Abstract
Introduction
Methods
Results
Discussion
Appendix 1
References
Background—Five years ago, we
described a specific ECG pattern of right bundle-branch block and
ST-segment elevation in leads V1 through V3
associated with sudden death in patients without demonstrable
structural heart disease. Information on long-term outcome has become
available due to pooled data on a large cohort of patients with this
syndrome who are followed at 33 centers worldwide.
Key Words: death, sudden • electrocardiography • fibrillation
Introduction
Top
Abstract
Introduction
Methods
Results
Discussion
Appendix 1
References
In 1992,
we1 described eight cases of aborted sudden death
in patients without demonstrable structural heart disease and a
peculiar ECG pattern consisting of right bundle-branch block and
ST-segment elevation in leads V1 to
V3 (Fig 1
). Since
then, new reports have appeared in the worldwide literature suggesting
a more common than previously suspected
disorder.2 3 4 5 In this article, we present the
data and follow-up for a large cohort of patients with this ECG
abnormality.
View larger version (65K):
[in a new window]
Figure 1. Twelve-lead ECG of a 32 year-old man who had an
episode of cardiac arrest requiring cardiopulmonary
resuscitation. Note the typical pattern of right bundle-branch block
and ST-segment elevation in leads V1 through
V3. No structural heart disease could be demonstrated after
extensive investigation. During programmed ventricular
stimulation, ventricular fibrillation was inducible with
two premature stimuli. This patient received an implantable
defibrillator.
Methods
Top
Abstract
Introduction
Methods
Results
Discussion
Appendix 1
References
The population consisted of 56 men and 7 women with a mean
age at the time of diagnosis of 38±17 years. Twenty-seven patients had
a family history of sudden death, and 9 were family members of affected
individuals. These patients have been identified in 33 centers around
the world ("Appendix"). Only the patients in whom the physician
definitively excluded demonstrable structural heart disease after
extensive invasive and noninvasive tests were included. Noninvasive
tests included enzymatic and electrolytic profile in all,
echocardiogram in all, ergonovine test in 53 patients, stress test in
55 patients, and nuclear magnetic resonance imaging in 22 patients.
Invasive test included coronary angiography in 49 patients,
left ventriculography in 48 patients, right ventriculography in 43
patients, and endomyocardial biopsies in 17
patients. In none of these tests could structural heart disease be
demonstrated, and all were informed as normal. Patients were treated
depending on the physician preferences. Information about last
follow-up was obtained from the primary physician. 
2
analysis.
Results
Top
Abstract
Introduction
Methods
Results
Discussion
Appendix 1
References
In 41 patients, the abnormal ECG pattern was first identified
after an episode of aborted sudden death (n=32) or syncope of unknown
origin (n=9) (symptomatic patients). In 12 of the 32
patients with aborted sudden death, a previous history of recurrent
sincopal episodes was present before the cardiac arrest. In two of
these patients, nonsustained polymorphic ventricular
tachycardia was documented during such episodes. In the
remaining 22 patients, the abnormal ECG was identified during routine
ECG (n=13) or during screening after an episode of sudden death in a
family member (n=9) (asymptomatic patients). All patients
were not taking drugs when the abnormal ECG was identified. During
follow-up, 6 of these 22 asymptomatic patients developed
symptoms (4, sudden death; 2, aborted sudden death). Therefore, 47 of
the 63 patients have developed symptoms at least once in their
lifetime. The age of first arrhythmic event ranged from 2 to 77 years,
with a mean age of 41±18 years. ). During a mean follow-up of 34±32
months, an arrhythmic event was detected in 11 patients with an
implantable defibrillator (31%) (Fig 2),
5 patients in the pharmacological group (33%), and 4 patients in the
no therapy group (31%) (P=NS). No patient died in the
implantable defibrillator group, 4 patients died in the pharmacological
group, and 4 patients died in the no therapy group
(P<.002). All mortality was due to sudden death. In Figs. 3 and 4,
the Kaplan-Meier curves are shown for recurrent arrhythmic events and
mortality depending on the therapy group. No variable was found to
be predictable for a recurrent arrhythmic event (Table 2).
View this table:
[in a new window]
Table 1. Characteristics of Patient Population Depending
on Therapy
View larger version (21K):
[in a new window]
Figure 2. For the same patient as represented in
Fig 1 
, at 18 months after the implant, a syncopal episode was
experienced that was terminated by a discharge from the device. The
continuous stored electrogram of this episode shows that an spontaneous
premature ventricular beat during sinus rhythm initiates a
very rapid ventricular arrhythmia terminated by a
15-J discharge from the device.
View larger version (24K):
[in a new window]
Figure 3. Kaplan-Meier curves of recurrent
ventricular fibrillation (VF) or sudden death depending on
treatment. Incidence of recurrent arrhythmic events during follow-up
was similar in the three therapy groups. ICD indicates implantable
cardioverter defibrillator.
View larger version (22K):
[in a new window]
Figure 4. Kaplan-Meier curves of mortality depending on
treatment. Mortality was significantly different during follow-up in
patients with an implantable cardioverter defibrillator (ICD) compared
with patients with medical therapy or no therapy.
View this table:
[in a new window]
Table 2. Characteristics of Patients With and Without an
Arrhythmic Event During Follow-up , Kaplan-Meier curves of
recurrent arrhythmic event in symptomatic patients are
compared with the first arrhythmic event in asymptomatic
patients. During a mean follow-up of 37±31 months, 14 of the 41
symptomatic patients had recurrent arrhythmic events
compared with 6 of 22 asymptomatic patients who developed
symptoms (P=NS) during a mean follow-up of 27±32
months.
View larger version (24K):
[in a new window]
Figure 5. Kaplan-Meier curves of recurrent arrhythmic events
in symptomatic patients versus first
ventricular fibrillation (VF) or sudden death in
asymptomatic patients. During follow-up, the incidence of
arrhythmic events was similar in both groups.
Discussion
Top
Abstract
Introduction
Methods
Results
Discussion
Appendix 1
References
In this study, we present data on 63 patients recruited in 33
centers around the world in whom an abnormal ECG was documented
consisting of right bundle-branch block and ST-segment elevation in
leads V1 to V3. We have
previously shown that the administration of IV ajmaline or
procainamide can unmask the presence of such an ECG pattern in
patients previously recognized with the abnormal ECG but with transient
normalization or in family members of affected
individuals.6 7 Because we do not know whether
these patients are similar to those in whom the abnormal ECG is
documented spontaneously without pharmacological intervention, in the
present series only those with a basal off-drugs abnormal ECG were
included to have an homogeneous group of patients. Some
patients underwent extensive noninvasive and invasive evaluation,
specially the symptomatic ones, whereas others (specially
the asymptomatic ones) underwent a more limited evaluation
including, however, in all cases, at least an echocardiogram; in most
cases, a stress test and an ergonovine test; and in a large group,
coronary angiography, left and right ventriculography, and
electrophysiological study. Because not all
tests were performed in all patients, we cannot exclude that some minor
forms of structural heart disease might have remained undiagnosed.
However, the fact that follow-up failed to show any progression to some
form of right or left cardiomyopathy argues against
it.
Appendix 1
Top
Abstract
Introduction
Methods
Results
Discussion
Appendix 1
References
Physicians and Centers
A. Asso, Hospital Miguel Servet, Zaragoza, Spain; J.
Atié, Universidad Federal Rio de Janeiro, Brasil; J.
Brugada, L. Mont, Hospital Clínic, Universidad de
Barcelona, Spain; P. Brugada, OLV Hospital, Aalst,
Belgium; J. Cabrera, Hospital NaSra. del Pino, Las Palmas, Spain; J.R. Carmona, Hospital de
Navarra, Pamplona, Spain; J.P. Cebron, Saint Henri Hospital,
Nantes, France; L. De Roy, Mont-Godine Hospital, Yvoir,
Belgium; P. Della Bella, Università degli Studi di
Milano, Italy; A. Ebagosti, CHG Martigues, France; J.
Farré, Fundación Jimenez Diaz, Madrid, Spain; M.
Fromer, CHU Vaudois, Lausanne, Switzerland; R. Hauer,
University Hospital Utrecht, The Netherlands; C.
Lafuente, Hospital General Albacete, Spain; J. Martinez, F.
Picó, Hospital Virgen de la Arrixaca, Murcia, Spain;
J. Metzger, Hopital Cantonal, Geneva, Switzerland; C. Moro,
Hospital Ramón y Cajal, Madrid, Spain; A. Moya,
Hospital Vall d'Hebró, Barcelona, Spain; J.
Ollitrault, Hospital Saint Joseph, Paris, France; M.
Pavón, Hospital Virgen de la Macarena, Sevilla, Spain;
J. Pelegrin, Hospital Clínico Zaragoza, Spain; D.
Potenza, San Giovanni Rotondo, Italy; S. Priori,
Università di Milano, Italy; J. Rodriguez,
Hospital Virgen de Valme, Sevilla, Spain; X. Sabaté,
Hospital Bellvitge, Barcelona, Spain; P. Scanu,
CHU Caen, France; E. Sosa, INCOR, Sao Paolo,
Brasil; W. Stevenson, Brigham and Women's Hospital, Boston,
Mass; R. Stroobandt, St Jozef Hospital, Oostende,
Belgium; V. Taramasco, CHU Marseille, France; J.K.
Triedman, Children's Hospital, Boston, Mass; P. Vanzini,
Asociación Española, Montevideo, Uruguay; J.
Villacastin, Hospital Gregorio Marañon, Madrid, Spain.
References
Top
Abstract
Introduction
Methods
Results
Discussion
Appendix 1
References
1.
Brugada P, Brugada J. Right bundle branch block,
persistent ST segment elevation and sudden cardiac death: a distinct
clinical and electrocardiographic syndrome. J Am Coll
Cardiol. 1992;20:1391–1396.[Abstract]
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N. Patruno, D. Pontillo, A. Achilli, G. Ruggeri, and G. Critelli Electrocardiographic pattern of Brugada syndrome disclosed by a febrile illness: clinical and therapeutic implications Europace, January 1, 2003; 5(3): 251 - 255. [Abstract] [Full Text] [PDF]
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M. H. Dinckal, V. Davutoglu, I. Akdemir, S. Soydinc, A. Kirilmaz, and M. Aksoy Incessant monomorphic ventricular tachycardia during febrile illness in a patient with Brugada syndrome: fatal electrical storm Europace, January 1, 2003; 5(3): 257 - 261. [Abstract] [Full Text] [PDF]
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J. M Morgan PATIENTS WITH VENTRICULAR ARRHYTHMIAS: WHO SHOULD BE REFERRED TO AN ELECTROPHYSIOLOGIST? Heart, December 1, 2002; 88(5): 544 - 550. [Full Text] [PDF]
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J. P. P. Smits, L. Eckardt, V. Probst, C. R. Bezzina, J. J. Schott, C. A. Remme, W. Haverkamp, G.u. Breithardt, D. Escande, E. Schulze-Bahr, et al. Genotype-phenotype relationship in Brugada syndrome: electrocardiographic features differentiate SCN5A-related patients from non-SCN5A-related patients J. Am. Coll. Cardiol., July 17, 2002; 40(2): 350 - 356. [Abstract] [Full Text] [PDF]
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S. Nagase, K. F. Kusano, H. Morita, Y. Fujimoto, M. Kakishita, K. Nakamura, T. Emori, H. Matsubara, and T. Ohe Epicardial electrogram of the right ventricular outflow tract in patients with the brugada syndrome: Using the epicardial lead J. Am. Coll. Cardiol., June 19, 2002; 39(12): 1992 - 1995. [Abstract] [Full Text] [PDF]
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D. J. Callans Management of the Patient Who Has Been Resuscitated From Sudden Cardiac Death Circulation, June 11, 2002; 105(23): 2704 - 2707. [Full Text] [PDF]
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M. Kanda, W. Shimizu, K. Matsuo, N. Nagaya, A. Taguchi, K. Suyama, T. Kurita, N. Aihara, and S. Kamakura Electrophysiologic characteristics andimplications of induced ventricular fibrillationin symptomatic patients with brugada syndrome J. Am. Coll. Cardiol., June 5, 2002; 39(11): 1799 - 1805. [Abstract] [Full Text] [PDF]
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K. Nademanee Prognostic value of electrophysiologic studies in brugada syndrome J. Am. Coll. Cardiol., June 5, 2002; 39(11): 1806 - 1807. [Full Text] [PDF]
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H.-J. Bruns, L. Eckardt, C. Vahlhaus, E. Schulze-Bahr, W. Haverkamp, M. Borggrefe, G. Breithardt, and T. Wichter Body surface potential mapping in patients with Brugada syndrome: right precordial ST segment variations and reverse changes in left precordial leads Cardiovasc Res, April 1, 2002; 54(1): 58 - 66. [Abstract] [Full Text] [PDF]
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S. G. Priori, C. Napolitano, M. Gasparini, C. Pappone, P. D. Bella, U. Giordano, R. Bloise, C. Giustetto, R. De Nardis, M. Grillo, et al. Natural History of Brugada Syndrome: Insights for Risk Stratification and Management Circulation, March 19, 2002; 105(11): 1342 - 1347. [Abstract] [Full Text] [PDF]
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S. G. Priori, E. Aliot, C. Blomstrom-Lundqvist, L. Bossaert, G. Breithardt, P. Brugada, J. A. Camm, R. Cappato, S. M. Cobbe, C. Di Mario, et al. TASK FORCE ON SUDDEN CARDIAC DEATH, EUROPEAN SOCIETY OF CARDIOLOGY: Summary of Recommendations Europace, January 1, 2002; 4(1): 3 - 18. [Abstract] [PDF]
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J. Brugada, R. Brugada, C. Antzelevitch, J. Towbin, K. Nademanee, and P. Brugada Long-Term Follow-Up of Individuals With the Electrocardiographic Pattern of Right Bundle-Branch Block and ST-Segment Elevation in Precordial Leads V1 to V3 Circulation, January 1, 2002; 105(1): 73 - 78. [Abstract] [Full Text] [PDF]
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R. Brugada and R. Roberts Brugada Syndrome: Why Are There Multiple Answers to a Simple Question? Circulation, December 18, 2001; 104(25): 3017 - 3019. [Full Text] [PDF]
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S H Wong, N T Mulvihill, M Norton, and R. HALL Assessing the risk of sudden cardiac death Heart, December 1, 2001; 86(6): 624 - 625. [Abstract] [Full Text] [PDF]
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Y. Miyasaka, H. Tsuji, K. Yamada, S. Tokunaga, D. Saito, Y. Imuro, N. Matsumoto, and T. Iwasaka Prevalence and mortality of the Brugada-type electrocardiogram in one city in Japan J. Am. Coll. Cardiol., September 1, 2001; 38(3): 771 - 774. [Abstract] [Full Text] [PDF]
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B. Surawicz Brugada syndrome: manifest, concealed, "asymptomatic," suspected and simulated J. Am. Coll. Cardiol., September 1, 2001; 38(3): 775 - 777. [Full Text] [PDF]
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S.G. Priori, E. Aliot, C. Blomstrom-Lundqvist, L. Bossaert, G. Breithardt, P. Brugada, A.J. Camm, R. Cappato, S.M. Cobbe, C. Di Mario, et al. Task Force on Sudden Cardiac Death of the European Society of Cardiology Eur. Heart J., August 2, 2001; 22(16): 1374 - 1450. [PDF]
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M Furuhashi, K Uno, K Tsuchihashi, D Nagahara, M Hyakukoku, T Ohtomo, S Satoh, T Nishimiya, and K Shimamoto Prevalence of asymptomatic ST segment elevation in right precordial leads with right bundle branch block (Brugada-type ST shift) among the general Japanese population Heart, August 1, 2001; 86(2): 161 - 166. [Abstract] [Full Text] [PDF]
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H. Atarashi, S. Ogawa, K. Harumi, T. Sugimoto, H. Inoue, M. Murayama, J. Toyama, H. Hayakawa, and for the Idiopathic Ventricular Fibrillation Invest Three-year follow-up of patients with right bundle branch block and ST segment elevation in the right precordial leads: Japanese registry of Brugada syndrome J. Am. Coll. Cardiol., June 1, 2001; 37(7): 1916 - 1920. [Abstract] [Full Text] [PDF]
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T. Ikeda, H. Sakurada, K. Sakabe, T. Sakata, M. Takami, N. Tezuka, T. Nakae, M. Noro, Y. Enjoji, T. Tejima, et al. Assessment of noninvasive markers in identifying patients at risk in the brugada syndrome: insight into risk stratification J. Am. Coll. Cardiol., May 1, 2001; 37(6): 1628 - 1634. [Abstract] [Full Text] [PDF]
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S. G Priori, C. Napolitano, and M. Grillo Concealed arrhythmogenic syndromes: the hidden substrate of idiopathic ventricular fibrillation? Cardiovasc Res, May 1, 2001; 50(2): 218 - 223. [Abstract] [Full Text] [PDF]
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G. Gronefeld and S. H Hohnloser What do implantable cardioverter/defibrillators teach us about the mechanisms of sudden cardiac death? Cardiovasc Res, May 1, 2001; 50(2): 232 - 241. [Abstract] [Full Text] [PDF]
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D. Corrado, C. Basso, and G. Thiene Sudden cardiac death in young people with apparently normal heart Cardiovasc Res, May 1, 2001; 50(2): 399 - 408. [Abstract] [Full Text] [PDF]
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J.A. Towbin Early repolarization syndrome and the Brugada syndrome: forme frustes? Eur. Heart J., March 2, 2001; 22(6): 448 - 449. [PDF]
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M Bianco, S Bria, A Gianfelici, N Sanna, V Palmieri, and P Zeppilli Does early repolarization in the athlete have analogies with the Brugada syndrome? Eur. Heart J., March 2, 2001; 22(6): 504 - 510. [Abstract] [PDF]
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C.A Remme, E.F.D Wever, A.A.M Wilde, R Derksen, and R.N.W Hauer Diagnosis and long-term follow-up of the Brugada syndrome in patients with idiopathic ventricular fibrillation Eur. Heart J., March 1, 2001; 22(5): 400 - 409. [Abstract] [PDF]
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D. Corrado, C. Basso, G. Buja, A. Nava, L. Rossi, and G. Thiene Right Bundle Branch Block, Right Precordial ST-Segment Elevation, and Sudden Death in Young People Circulation, February 6, 2001; 103(5): 710 - 717. [Abstract] [Full Text] [PDF]
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M. Kakishita, T. Kurita, K. Matsuo, A. Taguchi, K. Suyama, W. Shimizu, N. Aihara, S. Kamakura, F. Yamamoto, J. Kobayashi, et al. Mode of onset of ventricular fibrillation in patients with Brugada syndrome detected by implantable cardioverter defibrillator therapy J. Am. Coll. Cardiol., November 1, 2000; 36(5): 1646 - 1653. [Abstract] [Full Text] [PDF]
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D. W. Wang, N. Makita, A. Kitabatake, J. R. Balser, and A. L. George Jr Enhanced Na+ Channel Intermediate Inactivation in Brugada Syndrome Circ. Res., October 13, 2000; 87 (8): e37 - e43. [Abstract] [Full Text] [PDF]
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S Viskin, R Fish, M Eldar, D Zeltser, M D Lesh, A Glick, and B Belhassen Prevalence of the Brugada sign in idiopathic ventricular fibrillation and healthy controls Heart, July 1, 2000; 84(1): 31 - 36. [Abstract] [Full Text] [PDF]
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W. G. Stevenson and H. T. Aretz Case 20-2000- A 61-Year-Old Man with a Wide-Complex Tachycardia N. Engl. J. Med., June 29, 2000; 342(26): 1979 - 1987. [Full Text] [PDF]
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C Wren, J J O'Sullivan, and C Wright Sudden death in children and adolescents Heart, April 1, 2000; 83(4): 410 - 413. [Abstract] [Full Text]
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R. Brugada, J. Brugada, C. Antzelevitch, G. E. Kirsch, D. Potenza, J. A. Towbin, and P. Brugada Sodium Channel Blockers Identify Risk for Sudden Death in Patients With ST-Segment Elevation and Right Bundle Branch Block but Structurally Normal Hearts Circulation, February 8, 2000; 101(5): 510 - 515. [Abstract] [Full Text] [PDF]
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C. Bezzina, M. W. Veldkamp, M. P. van den Berg, A. V. Postma, M. B. Rook, J.-W. Viersma, I. M. van Langen, G. Tan-Sindhunata, M. Th. E. Bink-Boelkens, A. H. van der Hout, et al. A Single Na+ Channel Mutation Causing Both Long-QT and Brugada Syndromes Circ. Res., December 3, 1999; 85(12): 1206 - 1213. [Abstract] [Full Text] [PDF]
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J. D. Fisher, D. Krikler, and K. A. Hallidie-Smith Familial polymorphic ventricular arrhythmias: A quarter century of successful medical treatment based on serial exercise-pharmacologic testing J. Am. Coll. Cardiol., December 1, 1999; 34(7): 2015 - 2022. [Abstract] [Full Text] [PDF]
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M. B. Rook, C. Bezzina Alshinawi, W.A. Groenewegen, I. C. van Gelder, A. C.G. van Ginneken, H. J. Jongsma, M. M.A.M. Mannens, and A. A.M. Wilde Human SCN5A gene mutations alter cardiac sodium channel kinetics and are associated with the Brugada syndrome Cardiovasc Res, December 1, 1999; 44(3): 507 - 517. [Abstract] [Full Text] [PDF]
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R. Dumaine, J. A. Towbin, P. Brugada, M. Vatta, D. V. Nesterenko, V. V. Nesterenko, J. Brugada, R. Brugada, and C. Antzelevitch Ionic Mechanisms Responsible for the Electrocardiographic Phenotype of the Brugada Syndrome Are Temperature Dependent Circ. Res., October 29, 1999; 85(9): 803 - 809. [Abstract] [Full Text] [PDF]
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G.-X. Yan and C. Antzelevitch Cellular Basis for the Brugada Syndrome and Other Mechanisms of Arrhythmogenesis Associated With ST-Segment Elevation Circulation, October 12, 1999; 100(15): 1660 - 1666. [Abstract] [Full Text] [PDF]
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C. WREN Cardiac causes for syncope or sudden death in childhood Arch. Dis. Child., October 1, 1999; 81(4): 289 - 291. [Full Text]
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X. Jouven, M. Desnos, C. Guerot, and P. Ducimetiere Predicting Sudden Death in the Population : The Paris Prospective Study I Circulation, April 20, 1999; 99(15): 1978 - 1983. [Abstract] [Full Text] [PDF]
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K. Matsuo, T. Kurita, M. Inagaki, M. Kakishita, N. Aihara, W. Shimizu, A. Taguchi, K. Suyama, S. Kamakura, and K. Shimomura The circadian pattern of the development of ventricular fibrillation in patients with Brugada syndrome Eur. Heart J., March 2, 1999; 20(6): 465 - 470. [Abstract] [PDF]
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J. Brugada, P. Brugada, and R. Brugada The syndrome of right bundle branch block ST segment elevation in V1 to V3 and sudden death--the Brugada syndrome Europace, January 1, 1999; 1(3): 156 - 166. [Abstract] [PDF]
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G. Baroudi, S. Acharfi, C. Larouche, and M. Chahine Expression and Intracellular Localization of an SCN5A Double Mutant R1232W/T1620M Implicated in Brugada Syndrome Circ. Res., January 11, 2002; 90 (1): e11 - e16. [Abstract] [Full Text] [PDF]
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