Advances in Arrhythmia and Electrophysiology
How to Perform and Interpret Provocative Testing for the
Diagnosis of Brugada Syndrome, Long-QT Syndrome, and
Catecholaminergic Polymorphic Ventricular Tachycardia
Manoj N. Obeyesekere, MBBS; George J. Klein, MD; Simon Modi, MBBS; Peter Leong-Sit, MD;
Lorne J. Gula, MD, MSc; Raymond Yee, MD; Allan C. Skanes, MD; Andrew D. Krahn, MD
S udden cardiac death (SCD) is predominantly related to
coronary artery disease and its sequelae, cardiomyopathy,
and congenital or valvular heart disease. No structural abnor-
malities are detectable in 5– 8% of SCDs.1 Identified ion
channelopathies such as Brugada syndrome, long-QT syn-
drome (LQTS), and catecholaminergic polymorphic ventric-
ular tachycardia (CPVT) contribute to this incidence. The
diagnosis requires a high level of suspicion because of a
resting ECG that is often borderline, intermittently normal, or
frankly normal. Genetic testing does not provide a simple
solution to this issue, as it is often neither sensitive nor
specific even when the phenotype points to a specific entity
and may yield results that are difficult to interpret (ie, variants
of unknown significance). Pharmacological and/or exercise
testing by manipulation/stressing the cardiac action potential
can accentuate the desired abnormality or provoke a charac-
teristic arrhythmia response. A systematic approach to clini-
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cal testing that includes drug provocation results in unmask-
ing of the cause of apparently unexplained aborted SCD in
⬎50% of patients and is very helpful in directing genetic
testing of the index case and family to diagnose genetically
mediated arrhythmia syndromes.2 This review will seek to
highlight the clinical utility of provocative testing and de-
scribe how to perform and interpret provocative testing for
the diagnosis of Brugada syndrome, LQTS, and CPVT.
Performing Provocative Testing
Pharmacological challenge should be performed in an area
that has comprehensive monitoring and resuscitation equip-
ment (including an external cardioverter-defibrillator). Test-
ing should be performed with continuous monitoring of the
patient by adequately trained/experienced personnel in an
area equipped with advance resuscitation equipment (includ-
ing external defibrillator) and personnel trained in advance
resuscitation and an expert physician promptly available.
Given the potential risk for hemodynamically compromising
ventricular arrhythmias during exercise stress testing (partic-
ularly when exercise stress testing for CPVT), we advise the
presence of physically capable personnel to prevent the
patient from falling, should hemodynamic collapse occur.
Received July 6, 2011; accepted October 17, 2011.
From the University of Western Ontario, Division of Cardiology, London, Ontario, Canada.
Correspondence to Andrew D. Krahn, MD, 339 Windermere Rd, C6-110, London, Ontario, Canada, N6A 5A5. E-mail akrahn@uwo.ca
(Circ Arrhythm Electrophysiol. 2011;4:958-964.)
© 2011 American Heart Association, Inc.
Circ Arrhythm Electrophysiol is available at http://circep.ahajournals.org
958
Continuous monitoring of the ECG should be undertaken,
and 12-lead ECGs should be recorded at 1- to 10-minute
intervals, depending on the rate and nature of the drug
infused. Frequent blood pressure monitoring should be per-
formed. After drug administration, the ECG should be mon-
itored for another 30 minutes or until it normalizes. Physi-
cians and staff should be familiar and knowledgeable
regarding the pharmacodynamics and pharmacokinetics of
the agents used (Tables 1 and 2).
Provocative testing may not always produce the classic
ECG response, given the varied test accuracies. Therefore,
the absence of a classic response or the presence of borderline
changes should not supplant clinical evidence (that includes
genetic testing). Even a clearly normal or abnormal provoc-
ative test result must be carefully reviewed within the clinical
context. Therefore, provocative testing should be viewed as
another part of the diagnostic workup and in the context of the
pretest probability, not as a binary positive or negative test.
When provocative testing yields borderline changes or the
absence of a classic response despite high clinical suspicion
(high pretest probability), an alternative provocative test may
be useful (eg, exercise stress testing plus catecholamine
infusion for LQTS/CPVT, an alternative sodium channel
blocker used to test for Brugada syndrome).
Long-QT Syndrome
Up to 50% of patients with LQTS display a nondiagnostic
resting QTc (⬍460 ms),3 and overlap of the resting QTc
intervals between healthy persons and patients with LQTS
makes the diagnosis challenging. Genetic testing may be defin-
itive but can often show a variant of unknown significance and
only detects a mutation in approximately 75% of patients with
LQTS. Clinical criteria such as the Schwartz criteria4 identified
a high probability of LQTS (score ⬎4) with a sensitivity of only
19% and specificity of 99%. The Keating criteria5 had 36%
sensitivity and 99% specificity. This highlights the need for
provocative testing to enhance diagnostic accuracy.
The QT interval is defined as the interval from the beginning
of the QRS complex to the end of the T wave. The authors favor
the maximum slope technique wherein the end of the T wave is
DOI: 10.1161/CIRCEP.111.965947
 Obeyesekere et al Provocative Testing for Channelopathies 959

Table 1. Drug Infusion Doses for Provocation

Channelopathy Drug Infusion
Brugada syndrome Flecainide 2 mg/kg (maximum, 150 mg) over
10 min
Brugada syndrome Ajmaline 1 mg/kg over 10 min
Brugada syndrome Procainamide 10 mg/kg over 20–30 min
Brugada syndrome Pilsicainide 1 mg/kg over 10 min
LQTS and CPVT Epinephrine Infusion started at 0.05 ␮g/kg per min
and increased every 5 min to 0.1 and
0.2 ␮g /kg per min for 5 min at
each dose
LQTS Adenosine Rapid bolus adenosine injected at 6 mg
incremental doses (maximum single dose
of 24 mg) until atrioventricular block or
sinus pauses lasting 3 s occurs
LQTS indicates long-QT syndrome; CPVT, catecholaminergic polymorphic
ventricular tachycardia.

marked by the intersection point of the tangent line representing

the maximal downward or upward slope of a positive or negative
T wave, respectively, and the isoelectric baseline (Figure 1).
Despite its imperfections, the Bazett formula (QT divided by the
square root of the R-R interval) remains widely used to correct
for heart rate. QT and QTc measurement during atrial fibrillation
should be averaged over 10 consecutive beats. Significant sinus
arrhythmia may also complicate assessment of QTc intervals
because of relatively larger changes in the R-R intervals com-
pared with lesser corresponding changes in the QT interval. QT
and QTc intervals may be averaged over 10 consecutive beats in
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an attempt to correct for this. The longest QT intervals are Figure 1. Examples of positive provocative tests. LQTS indi-
generally measured in the precordial leads. The standard leads to cates long-QT syndrome; CPVT, catecholaminergic polymorphic
ventricular tachycardia.
measure the QT are V5 and lead II. U waves should not be
included in the measurement.
a loss of function mutation in the slowly (IKs) and rapidly (IKr)
Mechanism of LQTS activating delayed rectifier potassium channel leads to LQT1
Eighty-five percent to 95% of all LQTS are due to LQT1, LQT2, and LQT2, respectively. This leads to failure of adrenergic
and LQT3. A decreased outward potassium current mediated by stimulation to shorten the action potential duration and hence the
QT interval. The IKr channels represent a smaller fraction of
Table 2. Procainamide and Epinephrine Infusion Protocols potassium channels responsible for repolarization compared
Progress Test Instructions with IKs channels. Furthermore, IKr is activated rapidly in low
Procainamide adrenergic circumstances and IKs gradually at higher adrenergic
Baseline ECG*/Vitals Start procainamide 1 g over 30 min
states. Because of the intact IKs channels in LQT3 (INa defect),
no QT lengthening is characteristically observed with adrenergic
10 min ECG/Vitals
stimulation (Figure 2B).
20 min ECG/Vitals
30 min ECG*/Vitals Stop procainamide
Provocative Testing in LQTS
40 min ECG/Vitals Evaluation of the QT response to the brisk tachycardia induced
60 min ECG/Vitals by standing provides important information that aids in the
90 min ECG/Vitals diagnosis of LQTS.6 Despite similar heart rate acceleration in
Epinephrine response to brisk standing in patients (n⫽68) and control
Baseline ECG/Vitals Start epinephrine 0.05 ␮g/kg per min subjects (n⫽82), on average, the QT interval of control subjects
0:05 min ECG/Vitals Increase to 0.10 ␮g/kg per min shortened by 21⫾19 ms, whereas the QT interval of LQTS
patients increased by 4⫾34 ms (P⬍0.001). Additionally, the QTc
0:10 min ECG/Vitals Increase to 0.20 ␮g/kg per min
interval increased by 50⫾30 ms in the control group and by 89⫾47
0:15 min ECG/Vitals Stop epinephrine
ms in the LQTS group (P⬍0.001). Receiver-operating characteris-
0:25 min ECG/Vitals 10 min after epinephrine
tic curves showed that the test added diagnostic value and the
0:35 min ECG/Vitals 20 min after epinephrine response was particularly impaired in patients with LQT2.
0:45 min ECG/Vitals 30 min after epinephrine Exercise stress testing has also been used for differentiating
*ECG should include high precordial leads. LQT1, LQT2, and unaffected individuals. End-of-recovery QTc
 960 Circ Arrhythm Electrophysiol December 2011
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may have clinical use in distinguishing patients with LQTS from
healthy individuals—a QTc ⬎445 ms at the end of recovery (4
minutes after cessation of exercise) had a sensitivity of 92% and
specificity of 88% at identifying LQT1 and LQT2 individuals.7
Furthermore, early-recovery QTc may be used to distinguish
LQT1 from LQT2 patients: early recovery QTc ⬍460 ms had a
sensitivity of 79% and specificity of 92% at identifying LQT2
patients (from LQT1).7,8 Increased QT hysteresis may be a
unique feature of LQT2 syndrome. QT hysteresis is calculated as
the QT interval difference between exercise and 1 to 2 minutes
into recovery at similar heart rates (within 10 bpm) at heart rates
of approximately 100 bpm.9 In LQT2 patients, the QT fails to
shorten at intermediate heart rates in early exercise. However,
recruitment of IKs at higher heart rates is associated with
appropriate QT shortening, which persists into the recovery
phase. This consequently leads to an exaggerated QT difference
between exercise and recovery, which manifests as increased QT
hysteresis. QT hysteresis of ⬎25 ms has a sensitivity and
specificity of 73% and 68%, respectively, at identifying patients
with LQT2 over LQT1.10
Two major protocols have evolved for epinephrine infusion:
the bolus and brief infusion (Shimizu protocol)11 and the
gradually escalating dose protocol (Mayo protocol).12 Both are
well tolerated, with a low incidence of adverse events. Gradually
Figure 2. Proposed algorithmic approach
to investigating for long-QT syndrome
(LQTS; A) and schematic depiction of heart
rate zones (B) when abnormal QTc intervals
are most likely observed during provocative
testing for LQTS. LQT1 indicates late exer-
cise and recovery; LQT2, early exercise and
recovery; and LQT3, rest.
increasing doses of epinephrine (0.05, 0.1, 0.2, and 0.3 ␮g/kg per
minute) can distinguish healthy control subjects from patients
with concealed LQT1. In one study of 147 genotyped patients,3
the median change in QT interval during low-dose epinephrine
infusion was ⫺23 ms in the gene negative group, ⫹78 ms in
LQT1, ⫺4 ms in LQT2, and ⫺58 ms in LQT3. The paradoxical
QT response was observed in 92% of patients with LQT1
compared with 18% of gene-negative, 13% LQT2, and 0%
LQT3 patients. Overall, the paradoxical QT response had a
sensitivity of 92.5%, specificity of 86%, positive predictive
value of 76%, and negative predictive value of 96% for LQT1
status. Patients receiving ␤-blocker therapy at the time of testing
are likely to have lower diagnostic accuracy.
Graded infusions of epinephrine in normal subjects can be
associated with QTc prolongation. Up to 79% of normal
subjects may show an abnormally prolonged QTc interval at
1 or more infusion levels of epinephrine.12,13 This may lead to
an inappropriate diagnosis of LQTS. However, an absolute
QT prolongation by more than 20 –30 ms is not typically seen
at any dose level of epinephrine.
A positive test is defined if a paradoxical QT/QTc response is
identified (Figure 1). Studies have proposed an increase in the
absolute QT by 30 ms (at 0.05 ␮g/kg per minute epinephrine),12
an increase in absolute QT by 35 ms11 or QTc prolongation by
 Obeyesekere et al
30 ms14 (at 0.10 ␮g/kg per minute epinephrine), or an increase
in QTc by 65 ms15 or to a value above 600 ms13 during
epinephrine infusion (up to 0.4 ␮g/kg per minute) as useful
criteria for diagnosing LQTS (Figure 2). The authors favor the
Mayo definition of an absolute QT prolongation of ⱖ30 ms at
0.10 ␮g/kg per minute epinephrine but take into account the
other parameters, particularly if there is a dramatic change at
0.20 ␮g/kg per minute epinephrine or a strong clinical suspicion
of LQTS. QT measurement during adrenaline infusion can be
challenging to interpret in the context of dynamic T-wave
morphology changes, particularly when prominent U waves are
present, the T wave is flattened or when notching of the T wave
occurs. Assessing the ECG in all 12 leads may assist in defining
the QT interval.
Adenosine-induced, sudden bradycardia and subsequent
tachycardia have also been investigated to identify QT changes
of diagnostic value in patients with LQTS. Adenosine challenge
resulted in dissimilar response in LQT patients (n⫽18) and
control subjects (n⫽20) in one study.16 A QT of ⬎410 ms at
maximal bradycardia had a sensitivity of 0.94 and a specificity
of 0.9 to detect LQTS. A QTc of ⬎490 ms at maximal
bradycardia had a sensitivity of 0.94 and a specificity of 0.85 to
detect LQTS. The small number of genotyped patients in this
study series precludes reaching reliable conclusions regarding
the utility of adenosine testing, but it is promising.
Data on the utility of Holter monitoring for the diagnosis
and prognosis of LQTS are unclear. Some studies have
reported the minimal diagnostic and prognostic utility of
Holter monitoring in evaluating LQTS.17,18 However, studies
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have also reported the value of Holter monitoring in diagnos-
ing LQTS, and in particular the utility of diurnal repolariza-
tion dynamics.19 Holter monitoring may be more useful in
LQTS2 and LQTS3 due to the more pronounced QT prolon-
gation observed compared with LQTS1 at slow heart rates in
these patients (particularly at night).20
Provocative testing can be useful in patients with a suspected
diagnosis of LQT1/LQT2 who have not been genotyped, in
patients who have been genotyped with a diagnosis of LQT1/
LQT2—if the patient’s resting ECG is unremarkable— or if the
LQT1/LQT2-associated mutation is novel. The test is not rec-
ommended for patients with type 3 LQTS (Figure 2). The test
can also be of diagnostic value in other LQTS that involve the
IKs and IKr channels and other channels that are sensitive to
sympathetic stimulation (eg, IK1 channel in LQT7), although the
rarity of these mutations make systematic study challenging.
During provocation, epinephrine infusion should be
stopped if systolic blood pressure rises above 200 mm Hg,
there is an increase in premature ventricular contractions or
nonsustained ventricular tachycardia or polymorphic VT
occurs, T-wave alternans develops, or the patient becomes
intolerant to the test. Intravenous ␤-blocker therapy can be
used to suppress ventricular arrhythmia and should be avail-
able for resuscitative efforts in the event of sustained ventric-
ular arrhythmias.
Catecholaminergic Polymorphic
Ventricular Tachycardia
CPVT is characterized by adrenergically induced ventricular
arrhythmias associated with syncope and SCD. The resting
Provocative Testing for Channelopathies 961
ECG is usually normal, and the QT interval is usually normal
or borderline, making diagnosis difficult. The diagnosis is
based on exercise/catecholamine-induced polymorphic or
bidirectional VT in the absence of structural heart disease or
a prolonged QT interval.21
Mechanism of CPVT
In CPVT, a gain-of-function mutation of the ryanodine
receptor leads to a premature release of calcium from the
sarcoplasmic reticuluum.22 Cardiac calsequestrin mutations
can also contribute to abnormal regulation of cellular cal-
cium.23 Abnormal calcium handling can lead to arrhythmias
mediated by delayed afterdepolarizations.24
Arrhythmia is induced by sympathetic stimulation by
exercise or by epinephrine infusion. Ventricular ectopy,
bidirectional VT, and polymorphic VT may occur in a
progressively predictable order with increasing heart rate.
Continuation of provocative testing may lead to syncope. The
tachyarrhythmias disappear with discontinuation of testing.
Intravenous ␤-blocker therapy can be used to suppress
ventricular arrhythmias in CPVT after provocative testing.
Provocative Testing in CPVT
A positive test is defined when complex ventricular ectopy,
bidirectional VT, and/or polymorphic VT occurs (Figure 1).
CPVT should not be diagnosed if simple isolated monomorphic
ectopy is induced. However, CPVT patients often have outflow
tract ectopy at the onset of induced arrhythmia at a relatively
predictable heart rate threshold.25 Polymorphic or bidirectional
VT is provoked with exercise in 63% and epinephrine in 82% of
patients with CPVT.25 Therefore, a normal provocative test does
not exclude the diagnosis. In a large series of CPVT patients
(n⫽101), exercise testing was negative in 12 (of 17) asymptom-
atic family members with a positive CPVT genotype.26 In
another study involving 30 mutation carriers, exercise stress
testing induced ventricular arrhythmias in only 23.27 Holter
monitoring may also be useful in active patients for the evalu-
ation of CPVT by bringing out the progressive arrhythmia with
exercise.21 However, compared with noninvasive monitoring
alone, provocation testing significantly improves the diagnostic
yield (by approximately 4-fold).25
Suppression of exercise-induced ventricular arrhythmias with
␤-blocker therapy does not necessarily translate into long-term
effectiveness of therapy.27 Furthermore, the absence of effort-
induced symptoms and/or ventricular arrhythmia on stress test-
ing may be observed in more than one-third of pathogenic RyR2
mutation carriers who still remain at future risk for SCD.26,28
However, repeated exercise tests on therapy have been used to
titrate ␤-blocker, verapamil, and flecainide dosage.29,30
Brugada Syndrome
The prevalence of fluctuations between diagnostic and nondiag-
nostic ECGs in patients with Brugada syndrome is high.31 In a
study of 176 Brugada syndrome patients in whom repetitive
baseline ECGs were recorded, only 90 patients had at least 1
positive baseline ECG for a type 1 pattern.32 The typical ECG
features can be unmasked with sodium channel blockers. Auto-
nomic tone can also modulate the ECG phenotype: isoproterenol
attenuates and acetylcholine accentuates the ECG changes in
 962 Circ Arrhythm Electrophysiol December 2011
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Figure 3. Proposed algorithmic approach to investigating for Brugada syndrome (A) and high precordial lead placement (B).
affected patients.33 In a series of 334 patients, 30% could only be
diagnosed with pharmacological challenge.34 The sensitivity of
provocative pharmacological testing may vary, depending on the
sodium channel blocker used, ECG lead position, the type and
severity of the mutation, baseline autonomic tone, and genetic
polymorphisms.35 Standard genetic testing is not universally
feasible and has a low sensitivity (Table 1).
It is important to distinguish patients who are asymptom-
atic with a Brugada pattern ECG from Brugada syndrome, in
which a type 1 ECG pattern is associated with symptoms. In
one study, the cardiac event rate per year was 7.7% in patients
with aborted SCD, 1.9% in patients with syncope, and 0.5%
in asymptomatic patients.36
The type 1 Brugada ECG pattern is characterized by a
complete or incomplete right bundle-branch block pattern with a
coved morphology ST-segment elevation of at least 2 mm in the
right precordial leads (V1–V3) followed by a negative T wave.
The type 2 ST-segment elevation has a saddleback appearance
with a high takeoff ST-segment elevation of ⬎2 mm, a trough
displaying ⬎1-mm ST-elevation followed by a positive or
biphasic T. Type 3 has an ST-segment morphology that is either
saddleback or coved with an ST-segment elevation of ⬍1 mm.
Type 2 and type 3 ECGs are not diagnostic of the Brugada
syndrome. Patients with a Brugada type 1 pattern on ECG
diagnosed with leads placed 2 intercostal spaces above the
standard position may have a similar prognosis to that of
individuals with a type 1 ECG recorded from the standard
position37 (Figures 1 and 3). When undertaking provocative
testing with a sodium channel blocker, the infusion should be
terminated when a type- 1 ECG develops, premature ventricular
beats or other arrhythmias develop, or the QRS widens to
⬎130% of baseline. QRS prolongation ⱖ130% occurs in ⬎50%
of all tests. In 40% of positive tests, it occurs before diagnostic
ECG changes. Always terminating the test when QRS prolongs
ⱖ130% could possibly result in loss of important diagnostic
information.38 Isoproterenol (by inhibiting Ito) can be effective in
normalizing the ECG changes and to treat ventricular
tachyarrhythmia.33
Large cohort studies indicate the low incidence of arrhythmic
events in asymptomatic patients with either the spontaneous or
 Obeyesekere et al
drug-induced type 1 ECG compared with symptomatic sub-
jects.39 Therefore, drug testing to unmask the type 1 ECG in
asymptomatic patients with a non–type 1 ECG does not appear
to have additional value for risk stratification. However, the
authors favor considering this to provide practical lifestyle
advice to patients with respect to treatment of fever, avoidance
of provocative drugs (www.brugadadrugs.org), and reporting of
syncope and seizures.
However, a drug-induced type 1 ECG is useful in symptom-
atic patients showing only the non–type 1 ECG for diagnosis,
prognosis, screening, and therapy. Additionally, screening of
asymptomatic family members can be undertaken with drug
testing for diagnosis and counseling. Drug challenge generally is
not performed in asymptomatic patients displaying the type 1
ECG at baseline because the additional diagnostic value is
considered to be limited, the added prognostic value is not clear,
and the test has a very small risk of provoking arrhythmic events.
Mechanism of Brugada Syndrome
The arrhythmogenic substrate in Brugada syndrome is believed
to relate to an increase in heterogeneity of the action potential
duration in cells residing in epicardial compared with endocar-
dial layers of the right ventricle. The reduction in the inward
sodium current (INa) allows the transient outward (Ito) current to
repolarize the cell in phase 1 beyond the voltage range in which
L-type Ca⫹2 channels are active. Inactivity of the Ca⫹2 channel
(along with the Ito repolarization current) results in loss of the
action potential plateau, predominantly in the subepicardial cells.
Conduction of the action potential from sites at which it is
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maintained (subendocardial) to sites at which it is abbreviated
(subepicardial) is believed to cause local reexcitation. This
situation may lead to closely coupled extrasystoles, thus trigger-
ing ventricular arrhythmias.
Provocative Testing in Brugada Syndrome
Varied potencies of inhibition of Ito and INa by various sodium
channel blockers contribute to the varied effectiveness in un-
masking Brugada syndrome. For example, flecainide and ajma-
line reduce the depolarizing INa current. However, these agents
also inhibit the repolarizing Ito current, which counters the INa
inhibition. In addition to reducing the peak amplitude of Ito,
ajmaline and flecainide also accelerate the decay of the Ito
current. Class IA antiarrhythmic agents display a more rapid
dissociation from the sodium channel. This may underlie their
lesser potency compared with class IC agents in unmasking the
ECG pattern. However in contrast to ajmaline and flecainide,
procainamide produces no block of Ito at clinically relevant drug
concentrations.40 A modest-sized study comparing the effect of
intravenous flecainide versus ajmaline reported disparate re-
sponses, with a failure of flecainide in 7 of 22 cases (32% versus
0% with ajmaline).41 In another study, pharmacological chal-
lenge with flecainide or ajmaline was unable to unmask most
silent gene carriers, with a positive predictive value of only
35%.35 Thus, sensitivity and specificity for pharmacological
provocation remains under dispute in the absence of a large
systematic study that exposes patients to serial drug testing with
varied agents. Nonetheless, there is inference that ajmaline and
flecainide are more sensitive than procainamide. Many countries
do not have access to all 3 drugs in intravenous form.
Provocative Testing for Channelopathies 963
Overall, the sensitivity of provocative tests in patients with
an SCN5A mutation (which represents only 20% of all
Brugada syndrome patients42,43) is estimated to be 71– 80%.
The available study by Brugada et al on the sensitivity in
non-SCN5A Brugada syndrome patients applies to patients
with documented but transitory type 1 ECGs resuscitated
from SCD; in this study, the sodium channel blocker test was
found to be 100% sensitive.44
Conclusions
Provocative drug and/or stress testing can unmask the diag-
nosis of Brugada syndrome, LQTS, and CPVT when the ECG
is not diagnostic. It is particularly useful when an inherited
arrhythmia is suspected in the context of syncope or cardiac
arrest, or in family screening, assisting in arriving at an
elusive diagnosis and in directing genetic testing of the index
case and family.
Disclosures
None.
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KEY WORDS: Brugada syndrome 䡲 long-QT syndrome 䡲 catecholaminergic
polymorphic ventricular tachycardia