European Heart Journal (2003) 24, 1104–1112

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The ajmaline challenge in Brugada syndrome:
Diagnostic impact, safety, and recommended
protocol
Sascha Rolf*, Hans-Jürgen Bruns, Thomas Wichter, Paulus Kirchhof,
Michael Ribbing, Kristina Wasmer, Matthias Paul, Günter Breithardt,
Wilhelm Haverkamp, Lars Eckardt
Hospital of the Westfälische Wilhelms-University, Department of Cardiology and Angiology, Institute for
Arteriosclerosis Research, Münster, Germany
Received 17 December 2002; revised 17 February 2003; accepted 26 February 2003

KEYWORDS Aims The diagnostic ECG pattern in Brugada syndrome (BS) can transiently normalize
Brugada syndrome; and may be unmasked by sodium channel blockers such as ajmaline. Proarrhythmic
Ajmaline challenge; effects of the drug have been well documented in the literature. A detailed protocol
Test protocol; for the ajmaline challenge in Brugada syndrome has not yet been described. There-
Proarrhythmia; fore, we prospectively studied the risks of a standardized ajmaline test.
Safety Methods and results During a period of 60 months, 158 patients underwent the
ajmaline test in our institution. Ajmaline was given intravenously in fractions (10 mg
every two minutes) up to a target dose of 1 mg/kg. In 37 patients (23%) the typical
coved-type ECG pattern of BS was unmasked. During the test, symptomatic VT
appeared in 2 patients (1.3%). In all other patients, the drug challenge did not induce
VT if the target dose, QRS prolongation >30%, presence/appearance of the typical
ECG, or the occurrence of premature ventricular ectopy were considered as end points
of the test. A positive response to ajmaline was induced in 2 of 94 patients (2%) with a
normal baseline ECG, who underwent evaluation solely for syncope of unknown origin.
Conclusion The ajmaline challenge using a protocol with fractionated drug adminis-
tration is a safe method to diagnose BS. Because of the potential induction of VT, it should
be performed under continuous medical surveillance with advanced life-support facili-
ties. Due to the prognostic importance all patients with aborted sudden death or
unexplained syncope without demonstrable structural heart disease and family members
of affected individuals should presently undergo drug testing for unmasking BS.
© 2003 Published by Elsevier Science Ltd on behalf of The European Society of
Cardiology.

Introduction (VT/VF) due to an acute ischemic event. It may also

Sudden cardiac death (SCD) frequently is the con-
sequence of ventricular tachycardia/fibrillation
* Corresponding author: Sascha Rolf, MD, Universitäts-
klinikum Münster, Medizinische Klinik und Poliklinik C, Kardio-
logie und Angiologie, Albert-Schweitzer-Str. 33, D-48145 Münster,
Germany. Tel.: +49-251-8347580; fax: +49-251-8348640
E-mail address: srolf@uni-muenster.de (S. Rolf).
occur in patients with various forms of structural
heart disease without a triggering ischemic event.
In approximately 5–10% of sudden cardiac deaths,
no overt structural heart disease can be demon-
strated. In 1992, Brugada et al.1 described a sub-
group of patients with a distinct ECG pattern
consisting of atypical right bundle branch block and

0195-668X/03/$ - see front matter © 2003 Published by Elsevier Science Ltd on behalf of The European Society of Cardiology.
doi:10.1016/S0195-668X(03)00195-7
The ajmaline challenge in Brugada syndrome
right precordial ST-elevation, later referred to as
‘Brugada syndrome’. It is now understood as a
genetically determined channelopathy with an
autosomal dominant pattern of transmission.2
Several mutations of the gene encoding for the

-subunit of the human cardiac SCN5A sodium
channel located on chromosome 3 causing a loss
of function of the sodium channel have been
described.3
Available multicenter data4 have confirmed the
malignant character of this syndrome showing that
it is associated with a high recurrence rate in sur-
vivors of cardiac arrest and in patients after a
syncopal episode. Due to the absence of therapeu-
tic alternatives, the implantation of a cardioverter-
defibrillator (ICD) is recommended in symptomatic
patients. However, conflicting evidence exists on
the prognosis of previously asymptomatic individ-
uals. Brugada et al.4 recommend ICD implantation
in asymptomatic patients with a spontaneously ab-
normal ECG, if sustained arrhythmia is inducible
during electrophysiological study, whereas Priori et
al.5 demonstrated an increased risk of death in
patients with a spontaneously abnormal ECG,
particularly if they have a history of syncope.
Since its first description, the identification of
patients with Brugada syndrome is increasing expo-
nentially. Affected individuals may present with in-
termittent electrocardiographic manifestations.6–8
Additionally, the ECG can be modulated by many
factors including body temperature, autonomic
tone, and drugs affecting ion channel function.8–10
Class IC and IA antiarrhythmic drugs (flecainide,
propafenone, ajmaline, disopyramide, procaina-
mide) accentuate ST-segment elevation and are
capable of unmasking concealed forms of the dis-
ease.6,7,11,12 Class IC antiarrhythmic drugs tend to
induce ST-segment changes in Brugada syndrome
more reliably than class IA drugs.6,7 Ajmaline,
which is available only for intravenous application
due to its poor oral bioavailability, seems to be the
best drug to unmask Brugada syndrome,13 possibly
because of its kinetics and strength of rate-
dependent sodium channel blocking effects. Ad-
ditionally, a short half-life and the brief duration
of its electrophysiological effects (minutes) render
it superior to other antiarrhythmic drugs.14
However, it is marketed only in selected European
countries and not available in the U.S. A potential
proarrhythmic effect of class I drugs has been
reported7,8,11,15–17 In a series reported by Brugada
et al.,7 one of 45 Brugada patients developed spon-
taneous VF after pharmacological provocation. In
addition, a case report of a 13-year-old survivor of
cardiac arrest with an intermittent Brugada-ECG
1105
who developed incessant hemodynamically toler-
able monomorphic VT after ajmaline administration
has been reported.16 Ventricular premature com-
plexes occurring in Brugada patients displaying a
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marked ST-elevation when exposed to class I drugs
were reported by others.7,8,11 Additionally, marked
Brugada-type ECG changes preceding or following
premature ventricular contractions, VT or VF have
been described in the literature.8,12 This may sug-
gest a link between the effect of antiarrhythmic
agents on the ECG abnormalities and their potential
proarrhythmic effects. Ajmaline administration
might also cause lethal arrhythmias in patients not
affected with Brugada syndrome.18 Furthermore,
termination of VT/VF might be rendered more dif-
ficult after administration of class I drugs.19 The
described side effects of the pharmacological chal-
lenge may be of particular importance because
many physicians wish to perform this test on an
outpatient basis.
In order to quantify VT/VF occurrence during the
ajmaline challenge and to identify factors associ-
ated with it, we prospectively analysed the ajma-
line challenges performed at our institution. We
intended to outline an ajmaline test protocol,
which is safe without loss of power with regard to
diagnostic purposes.
Methods
Patient characteristics
The study population consisted of 158 consecutive
caucasian patients, mean age 42 (11–89) years,
with one or more of the following clinical presen-
tations (Table 1): (1) aborted cardiac arrest (n=21),
(2) syncope of unknown origin (n=95), (3) docu-
mented VT (n=18), (4) asymptomatic individuals
with a family history of sudden cardiac death,
syncope (n=47) or Brugada syndrome (n=9) or
with (5) a suspicious but not diagnostic ECG
(incomplete/complete bundle branch block pat-
tern, ‘saddle-type’ ECG with ST-segment elevation
less than 0.2 mV) during routine examination
(n=64). Structural heart disease was excluded
by clinical history and noninvasive and invasive
methods.
Twelve-lead ECG acquisition, data analysis
and drug administration
The ECG was defined as typical ‘coved-type’ if
displaying a right bundle branch block (RBBB) pat-
tern with a terminal r wave and a J-point elevation
1106 S. Rolf et al.

Table 1 Clinical characteristics and test results of patients undergoing the ajmaline challenge
n Positive ajmaline Suspicious Positive ajmaline
challenge total baseline challenge and
(n) ECG (n) suspicious baseline

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ECG (n)
Syncope 67 9 (13%) 22 (33%) 7
Family history 23 3 (13%) 9 (38%) 3
Syncope and family history 16 4 (25%) 6 (40%) 4
Aborted SCD* 11 5 (45%) 7 (64%) 5
Other 11 5 (45%) 6 (55%) 5
BS family 5 3 (60%) 4 (80%) 3
Documented VT 5 2 (40%) 2 (40%) 2
Documented VT and family history 4 — 1 (25%) —
Syncope and documented VT 3 — — —
Aborted SCD, syncope and documented VT 2 — — —
Aborted SCD and syncope 2 1 (50%) 2(100%) 1
Syncope and BS family 2 2(100%) 2(100%) 2
Aborted SCD, syncope, documented VT and family 1 — 1(100%) —
history
Aborted SCD, syncope and family history 1 — — —
Aborted SCD, documented VT and family history 1 — — —
Aborted SCD and BS family 1 1(100%) 1(100%) 1
Aborted SCD and family history 1 1(100%) 1(100%) 1
Aborted SCD and documented VT 1 — — —
Syncope, documented VT and BS family 1 1(100%) — —
158 (100%) 37 (23%) 64 (41%) 34
*
SCD: sudden cardiac death; BS: Brugada syndrome; VT: ventricular tachycardia; family history: family history of SCD and/or
syncope; BS family: family history of Brugada syndrome; other: recurrent presyncope of unknown origin, frequent polymorphic
ventricular extrasystoles.

of at least 0.2 mV with a slowly descending ST-
segment in continuation with a flat or negative T
wave in leads V1 to V3 (Fig. 1) either spontaneously
or after the administration of ajmaline. Heart rate,
PQ, QRS and QTc (Bazett formula) duration on ECG
were measured before, during and after drug
administration in all patients (Table 2). We admin-
istered the drug in fractions of 10 mg every two
minutes up to a target dose of 1 mg/kg.
End points
The test was considered positive if the abnormal
coved-type ECG pattern appeared in more than one
right precordial lead (V1–V3; Fig. 1). We initially
terminated the ajmaline challenge before reaching
the target dose only if QRS prolongation exceeded
30% compared to baseline interval. After the per-
formance of 32 tests, we also stopped ajmaline
administration before reaching the target dose
when a typical Brugada-type ECG or premature
ventricular beats occurred. This was because major
side effects had occurred (see results).
Statistical analysis
Data were analysed with the SPSS package for
paired and unpaired data. The student's t-test for
unpaired data was used to compare differences
between patients with positive and negative
ajmaline test. A value of p<0.05 (p<0.001 where
specified) was considered statistically significant.
Quantitative data are presented as mean±SD.
Results
ST-segment changes during ajmaline test
The ST segment pattern was worsened (further
elevation >2 mm) in 28 of 58 patients (48%) with
suspicious ECG abnormalities who initially had not
met the criteria of a typical ‘coved-type’ ECG pat-
tern (n=6 had an initially coved-type ECG). Of
those, n=17 patients were previously symptomatic
(SCD (n=6) or syncope (n=11)) with or without a
family history of Brugada syndrome (n=2), SCD or
syncope of unknown origin (n=4). In the group of
asymptomatic patients with nondiagnostic ECG
abnormalities (n=11), VT had been documented in
n=2 patients and the family history was remarkable
of Brugada syndrome in n=3 patients and of SCD or
syncope of unknown origin in n=3 patients.
A diagnostic coved-type ECG pattern was in-
duced in 3 of 94 patients (3%) with a normal base-
line ECG. Two of these patients solely underwent
The ajmaline challenge in Brugada syndrome 1107

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Fig. 1 Surface ECG (leads V1-6) shows the right precordial ECG changes during the fractionated application of ajmaline in one of our
first patients with Brugada syndrome. A ‘saddle-type’ ECG at baseline dynamically changes into the typical ECG pattern of right
bundle-branch block and ST-segment elevation of the ‘coved-type'. Note that the drug challenge could have been stopped after
20–30 mg of ajmaline without loss of diagnostic power to reduce the potential risk of VT.

Table 2
Before After Difference p-value
A: ECG parameters before and after the ajmaline challenge (n=158 total patients)
Heart Rate (/min) 69±15 78±13 8±10 p<0.001
PQ (ms) 160±29 195±31 35±19 p<0.001
QRS (ms) 96±16 116±18 21±11 p<0.001
QTc (ms) 415±28 442±32 28±23 p<0.001

B: ECG parameters before and after the ajmaline challenge (n=37 patients with positive ajmaline challenge)
Heart Rate (/min) 74±15* 83±15* 7±10 p<0.001
PQ (ms) 175±36† 212±32† 38±14 p<0.001
QRS (ms) 99±15 125±16* 27±14† p<0.001
†
QTc (ms) 419±34 467±36 47±24† p<0.001

C: ECG parameters before and after the ajmaline challenge (n=121 patients with negative ajmaline challenge)
Heart Rate (/min) 68±14* 76±12* 8±9 p<0.001
PQ (ms) 156±25† 191±29† 35±20 p<0.001
QRS (ms) 96±16 114±18* 19±9† p<0.001
QTc (ms) 414±26 445±27† 23±21† p<0.001
*
p<0.05 (B vs. C).
†
p<0.001 (B vs C); mean value±standard deviation.

evaluation for syncope of unknown origin, the other The test was negative in 30 of the 64 patients
underwent family screening for Brugada syndrome (47%) with suspicious baseline ECG and in n=91 of 94
and had additionally experienced syncope and patients (97%) without ECG abnormalities before
documented VT. the test. QRS duration was prolonged in all patients
1108
Fig. 2 Surface leads V1–V6 of a female patient with Brugada syndrome during ajmaline challenge. Arrow indicates the sudden
transition of a normal to a classical ‘coved-type’ Brugada-ECG after 40 mg ajmaline. Short-coupled premature ventricular contrac-
tions occur after 40 mg of ajmaline degenerating into a nonsustained polymorphic and later monomorphic VT after 60 mg ajmaline.
after drug administration. Mean QRS (PQ) prolon-
gation was 21±11 (35±19) ms vs. baseline (Table 2).
QTc intervals did not increase more than 12% in any
patient (including n=4 patients with suspected Long
QT syndrome). Patients with a positive ajmaline
test result had an additional prolongation of the
QTc interval (27 ms QRS prolongation vs 47 ms QTc
prolongation). Heart rate before and after the test
(pre test 74 vs 68/min, post test 83 vs 76/min,
p<0.05) and PQ interval (pre test 175 vs 156 ms,
post test 212 vs 191 ms, p<0.001) and increase in
QRS (27 vs 19 ms, p<0.001) and QTc (47 vs 23 ms,
p<0.001) intervals were significantly greater in
patients with positive reaction to ajmaline. Follow-
ing discontinuation of the drug, the ECG changes
returned to baseline within 20–30 min.
Adverse events during the ajmaline
challenge
The most remarkable events observed during
ajmaline challenge were symptomatic VT which
occurred in two of our first 32 patients (6%). Both
had a coved-type ECG after ajmaline injection.
The first patient was a 53-year old sister of a
patient with Brugada syndrome who had been
asymptomatic prior to testing. Her baseline ECG
showed a J-point elevation less than 0.1 mV in the
right precordial leads. Following the fractionated
application of 40 mg ajmaline, further J-point el-
S. Rolf et al.
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evation in the right precordial leads which switched
over to the typical coved-type ECG in a beat-to-
beat fashion was observed (Fig. 2). Subsequently
short-coupled ventricular extrasystoles occurred.
Two more injections of ajmaline were given and
hemodynamically relevant repetitive nonsustained
polymorphic VT developed. These VT finally degen-
erated in a monomorphic VT with RBBB configur-
ation (Fig. 2). No significant QRS prolongation was
seen before VT initiation. The VT cluster termi-
nated within 5 min. The second patient was a 40-
year-old male survivor of sudden cardiac arrest and
a positive family history of syncope with a classic
coved-type ECG before the test. He underwent an
ajmaline challenge and received 80 mg in a frac-
tionated and dose-limited manner. His baseline
coved-type ECG was aggravated and premature
ventricular contractions occurred after 50 mg
ajmaline. VT runs up to six consecutive beats were
seen after the full dose. A few days later a body
surface potential map was performed at rest and
after administration of ajmaline.17 Before the tar-
get dose was reached, short-coupled premature
ventricular contractions preceded the sudden onset
of sustained polymorphic VT (Fig. 3). Multiple defi-
brillations were required to terminate the arrhyth-
mia. In these two patients, the diagnostic ECG
pattern was already overt when drug ad-
ministration was continued and the formation of
premature ventricular contractions preceded the
The ajmaline challenge in Brugada syndrome 1109

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Fig. 3 Surface leads V1–V6 in a male patient with Brugada syndrome during ajmaline challenge. Induction of initially nonsustained
and later sustained polymorphic VT by short-coupled ventricular extrasystoles after administration of 60 mg of ajmaline which
required 5 defibrillation shocks for termination.

Table 3 Ajmaline test — suggested standardized protocol

Indication Aborted SCD in patients without structural heart disease. Syncope of unknown origin in patients
without structural heart disease. Polymorphic VT in patients without structural heart disease. Family
history of BS, sudden cardiac death and/or recurrent syncope of unknown origin. Suspicious ECG
(saddle-back or coved J-point elevation or ST-segment elvation <2 mm in at least one right precordial
lead) in asymptomatic patients without structural heart disease.
Environment Patient in fasting, resting and drug-free state. Presence of physician with experience in
intensive-care medicine. Advanced cardiopulmonary life-support facilities available including
external defibrillator, intubation set and drugs (atropine, isoproterenole). Safe venous access. 12
lead standard ECG. Blood pressure monitoring.
Performance Fractionated intravenous ajmaline application (10 mg every 2 min) up to target dose of 1 mg/kg.
Continuous ECG documentation at paper speed of 10 mm/s (one strip at 50 mm/s every 2 min).
Patient and ECG supervision until normalization of ECG.
Termination criteria Reached target ajmaline dose. Occurrence of J-point elevation or ST-segment elevation >2 mm in at
least one right precordial lead. Occurrence of premature ventricular beats, VT, sinus arrest or
AV-block (Type II or III). QRS prolongation >30%.

occurrence of VT. Since then, we adapted our pro- Discussion

tocol (see methods). The end points were not only
the full target dose or significant QRS prolongation,
but now included the unmasking of the typical ECG
pattern during the test and the occurrence of ven-
tricular extrasystoles (Table 3). We performed 126
ajmaline tests with this altered protocol without
any further induction of tachyarrhythmias.
Using this standardized protocol, PQ-, QRS-
and QTc-intervals were always prolonged without
clinical relevance. After administration of the full
ajmaline dosage, neither second/third degree SA/
AV-block nor polymorphic VT of the torsade de
pointes type15 were observed. The ECG changes
entirely resolved within a time period of 30 min
after the test. Only few patients (n=7) reported
minor complaints such as nausea or headache.
The present study underlines the ability of ajmaline
to confirm an ECG pattern compatible with Brugada
syndrome in individuals in whom the disease
is suspected due to a positive family history of
Brugada syndrome, syncope or sudden cardiac
death, previous syncope, documented VT or a sus-
picious but not diagnostic ECG.7 We were able to
demonstrate that the fractionated application of
ajmaline in otherwise healthy patients was safe if
certain criteria for test termination were fulfilled
(Table 3). These criteria comprised QRS prolon-
gation exceeding 30% compared to baseline inter-
val, the occurrence of a classic coved-type ECG
or the occurrence of premature ventricular
contractions. The low degree of proarrhythmia
1110 S. Rolf et al.

may be explained by the fractionated drug ap- but not Ito (flecainide, ajmaline and procainamide)
plication which is likely to be superior to bolus can further diminish sodium current already re-
administration. duced by Brugada mutations. This hypothesis may
explain the potential of sodium channel blockers to

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unmask concealed forms of the Brugada syndrome
Electrocardiographic features of Brugada and the potential proarrhythmic adverse ef-
syndrome fects.7,8,11,16 Further evidence for this hypothesis is
yielded by the observation of marked ST-segment
In Brugada syndrome, two different electrocardio-
elevation just prior or following the onset of poly-
graphic patterns exist: the ‘coved-type’ ECG and
morphic VT in Brugada syndrome. In addition, we
the ‘saddle-like’ ECG. Transition between the
have recently demonstrated that the body surface
two types has been described in some patients
area of ST elevation without drug provocation cor-
with Brugada syndrome. According to current
related to the inducibility of VT in Brugada syn-
literature2,4,7 the diagnosis of Brugada syndrome
drome.17 Due to the dynamic nature of the ECG
requires a ‘coved-type’ ECG pattern either spon-
changes concern may raise about the significance
taneously or drug-induced in more than one
of negative test results. It has been shown in studies
right precordial lead. Although affected Brugada
utilizing high-resolution body surface potential
patients – as proven by genetic testing may not
mapping, that recordings outside the positions of
show the typical ECG spontaneously or after the
the standard ECG leads — high right precordial
ajmaline challenge, no false positive drug chal-
leads in the second or third intercostal space — may
lenge has been reported so far. We consider an ECG
show more pronounced ECG changes typical of
compatible with Brugada syndrome if a ‘coved-
Brugada syndrome compared to the standard right
type’ pattern with ST-segment elevation of al least
precordial leads in the fourth intercostals
2 mm is expressed. Since we studied a selected
space.21,22 The present study underlines the poten-
patient population, we did not aim at proving sen-
tial of ajmaline to induce the above mentioned ST
sitivity or specifity of the drug test in the diagnosis
segment changes in the right precordial leads in
of Brugada syndrome.
Brugada syndrome.
The exact electrophysiologic mechanism of this
Of note, one patient required five defibrillation
syndrome has not yet been fully elucidated. Three
shocks until sustained polymorphic VT was termi-
mechanisms are proposed for ST segment elevation
nated. This is compatible with reports in the liter-
in Brugada syndrome: local conduction abnormal-
ature,19 that termination of VT might be rendered
ity, local ventricular depolarization and early re-
more difficult after administration of class I drugs.
polarization abnormality. The latter hypothesis9,20
Possibly due to conduction slowing,19 sodium chan-
postulates an accentuation of the action potential
nel blockers can provoke incessant VT/VF, which
notch in the right ventricular epicardium carried by
are difficult or impossible to terminate.23 Addition-
the transient outward current (Ito) via reduction of
ally, blocking cardiac sodium channels in animals is
the fast sodium inward current (INa). A genetic
reported to increase the amount of energy required
sodium channel defect, which may lead to such
to defibrillate a fibrillating heart.24 In parallel to
reduction of the sodium current has been linked to
previous observations,25 the PQ interval challenge
the Brugada syndrome.3 The resulting transmural
was significantly increased in patients with a
voltage gradient, normally responsible for the in-
positive ajmaline test, presumably reflecting the
scription of the J wave, may give rise to a
presence of a HV-conduction delay.
saddleback-form of ST-segment elevation if the
epicardial repolarization precedes repolarization in
mid- and endocardial regions. Further accentuation Clinical implications of the ajmaline
of the notch accompanied by a prolongation of the challenge
epicardial action potential may lead to the devel-
opment of a coved-type ST-segment elevation. Ul- Due to prognostic implication for the affected indi-
timately, a loss of the action potential dome at vidual, it is important to recognize the suspect ECG
some epicardial sites may result. As a consequence, pattern which is the cornerstone for the diagnosis
marked intramural dispersion of repolarization may of Brugada syndrome. However, there are certain
be responsible for local re-excitation via phase 2 circumstances mimicking the Brugada-ECG, that
re-entry. Through this mechanism very closely should be ruled out carefully.20 Transient normal-
coupled extrasystoles capable of initiating circus ization of the ECG signature of this syndrome may
movement reentry arrhythmias can be trig- lead to failed recognition. This could have negative
gered.9,20 The use of agents that primarily block INa consequences on the management of these patients
The ajmaline challenge in Brugada syndrome
at high risk for recurrence of lethal arrhythmias.
In this regard, inspection of previous ECGs and
performing a baseline and a follow-up ECG in all
patients to whom class I antiarrhythmic drugs are
prescribed and carefully reviewing it for appear-
ance of the typical pattern of right bundle branch
block and ST elevation seems good clinical prac-
tice, as it could unmask the disease in patients with
occult or borderline ECG patterns. Furthermore,
pharmacological interventions may facilitate de-
velopment of polymorphic VT/VF. A correct
diagnosis of a suspicious ECG pattern is of great
importance to save a patient's life and to avoid
medico-legal consequences. Suspicion of Brugada
syndrome should therefore lead to the performance
of a pharmacological challenge.8,20
In patients with a typical Brugada like ECG pat-
tern either spontaneously or after administration of
ajmaline we recommend programmed electrical
stimulation at two ventricular sites with up to three
premature beats26 and genetic testing.
Conclusion
At present, the provocative tests are not utilized
routinely and a standardized protocol has not been
published yet. Especially institutions without ex-
perience with the drug challenge may be cautious
because of the suspected likelihood of VT induction
and difficulty of VT termination. Brugada et al.7
already emphasized the need to perform adminis-
tration of ajmaline for diagnostic or investigational
purposes in an appropriate environment under
strict medical surveillance with advanced life-
support facilities available. The present study dem-
onstrated, that the acute proarrhythmic effect of
ajmaline in Brugada syndrome can be controlled if
the proposed requirements are fulfilled during the
drug challenge (Table 3).
Acknowledgements
Deutsche Forschungsgemeinschaft, Bonn, Germany
(Schu 1082/2-2, later Sonderforschungsbereich 556;
projects A1, C4), and grants from Interdisciplinary
Center for Clinical Research Münster, Germany
(BMBF, AZ 01 KS 9604), Alfried Krupp. Von Bohlen
und Halbach-Stiftung, Essen, Germany the Franz
Loogen Foundation, Düsseldorf, Germany.
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