REViEWS

The diagnosis and management

of ventricular arrhythmias
Kurt C. Roberts-Thomson, Dennis H. Lau and Prashanthan Sanders
abstract | The term ‘ventricular arrhythmias’ incorporates a wide spectrum of abnormal cardiac rhythms, from
single premature ventricular complexes to sustained monomorphic ventricular tachycardia (VT), polymorphic
VT, and ventricular fibrillation. Sustained ventricular arrhythmias are the most common cause of sudden
cardiac death. These arrhythmias occur predominantly in patients with structural heart disease, but are
also seen in patients with no demonstrable cardiac disease. The diagnosis of VT can be made reliably using
electrocardiographic criteria, and a number of algorithms have been proposed. Among patients with VT and
a structurally normal heart, the prognosis is usually benign and treatment is predominantly focused on the
elimination of symptoms. Patients who have VT in the presence of structural heart disease are often managed
with implantable cardioverter-defibrillators. These devices are effective for both primary and secondary
prevention of VT and sudden cardiac death. Pharmacological therapy for VT has limited efficacy and is
associated with a high incidence of adverse effects. Radiofrequency catheter ablation is useful for controlling
recurrent episodes of monomorphic VT; however, research is needed to define the role of catheter ablation in
the treatment of other ventricular arrhythmias.
Roberts-Thomson, K. C. et al. Nat. Rev. Cardiol. advance online publication 22 February 2011; doi:10.1038/nrcardio.2011.15

Introduction
sustained ventricular arrhythmias are an important cause
of morbidity and the most common cause of sudden
cardiac death, accounting for 75–80% of cases.1–3 the term
‘ventricular arrhythmias’ incorporates a wide spectrum of
abnormal cardiac rhythms, from single premature ven­
tricular complexes (PvCs) to sustained monomorphic
ventricular tachycardia (vt), polymorphic vt, and ven­
tricular fibrillation. these arrhythmias predominantly
occur in patients with structural heart diseases, such as
ischemic and dilated cardiomyopathies. However, benign
forms of vt can also occur among individuals without
evidence of cardiac disease. evaluation of the underlying
disease substrate is important, as the etiology not only
provides clues to the mechanism of the arrhythmia, but
also determines the patient’s prognosis and the appro­
priate therapy, which differ between the various forms of
ventricular arrhythmia.
Patients with vt most commonly present with a wide
Qrs complex during tachycardia. the electrocardio­
graphic characteristics of the arrhythmia can indicate
potential mechanisms and the nature of the underlying
etiology. sustained monomorphic vt has a repetitive
sequence of ventricular activation and, therefore, a Qrs
competing interests
K. C. Roberts-Thomson declares an association with the
following company: St Jude Medical. P. Sanders declares
associations with the following companies: Bard
Electrophysiology, Biosense-Webster, Medtronic, Merck Sharp
& Dohme, Sanofi-Aventis and St Jude Medical. See the article
online for full details of the relationships. D. H. Lau declares
no competing interests.
morphology that does not change from beat to beat. this
pattern can indicate a single focus that initiates ventricular
activation, or a stable substrate capable of supporting a re­
entrant circuit. Both mechanisms can occur in patients
with or without structural heart disease.
By contrast, polymorphic vt has continuously chang­
ing Qrs morphology representing beat­to­beat altera­
tions in ventricular activation. this pattern can be seen
in patients without structural heart disease who have
genetically based ion channel disorders, such as long Qt
syndromes, Brugada syndrome, catecholaminergic poly­
morphic vt syndrome, or idiopathic ventricular fibrilla­
tion. However, myocardial ischemia is the most common
underlying etiology of polymorphic vt. in this review,
we discuss the mechanisms and diagnosis of ventricular
arrhythmias and the management of these patients,
focusing on monomorphic vts.
Diagnosis of VT
Medical history and clinical examination
the presentation of a patient with a wide­complex tachy­
cardia (Qrs >120 ms) is a common diagnostic dilemma Cardiovascular
Research Center,
in clinical practice. several arrhythmias can present Department of
as wide­complex tachycardia, including vt, supra­ Cardiology, Royal
Adelaide Hospital,
ventricular tachycardia (svt) with aberrancy or bundle North Terrace, Adelaide,
branch block (BBB), and svt with antegrade conduction SA 5000, Australia
over an accessory pathway (pre­excited tachycardia). in (K. c. roberts‑Thomson,
d. H. lau, P. Sanders).
addition, Qrs widening can be seen with other condi­
tions, such as repaired congenital heart disease, drug toxi­ Correspondence to:
P. Sanders
cities, and electrolyte imbalances. However, pre­excited prash.sanders@
tachycardias, and drug­induced and electrolyte­induced adelaide.edu.au

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Key points
■ The diagnosis of ventricular arrhythmias can be accurately made using
electrocardiographic algorithms
■ The underlying heart disease determines the prognosis of patients with
ventricular arrhythmias
■ in patients without structural heart disease, the treatment of ventricular
arrhythmias is focused on the elimination of symptoms
■ in patients with structural heart disease, implantable cardioverter-defibrillators
can prevent sudden death
■ Antiarrhythmic therapy has limited efficacy in patients with ventricular
arrhythmias and can have substantial adverse effects
■ Catheter ablation is useful to prevent recurrences of ventricular arrhythmia
Box 1 | Electrocardiographic findings that suggest VT
■ Atrioventricular dissociation
■ Fusion or capture beats
■ QRS width (LBBB >160 ms, RBBB >140 ms)
■ Northwest axis
■ Concordance
■ LBBB morphology with right axis deviation
■ Absence of RS complexes in precordial leads
Abbreviations: LBBB, left bundle branch block; RBBB, right bundle
branch block; VT, ventricular tachycardia.
tachycardias account for only a small minority (1–5%) of
wide­complex tachyarrhythmias and, therefore, the clini­
cally relevant differential diagnosis is between vt and
svt with aberrancy.4
in the assessment of a patient with wide­complex
tachycardia, medical history and physical examination
can aid in the diagnosis. a history of angina, myocardial
infarction, or congestive cardiac failure all carry a positive
predictive value (PPv) for vt of >95%, but have a poorer
sensitivity.5 Young patients (aged <35 years) are less likely
than older patients to have vt. age above this threshold
carries a PPv of 85% and a sensitivity of 92% for vt diag­
nosis,5 which is to be expected given that a ventricular
scar is the basis of the arrhythmia in the majority of
patients with vt. Many physicians use the clinical status
of the patient to help in the diagnosis of a wide­complex
tachycardia; however, hemodynamic tolerance for the
arrhythmia is a poor guide to diagnosis. although vt is
more likely than svt to cause hypotension and hemo­
dynamic collapse, these signs are not useful in differenti­
ating between vt and svt, and many patients with vt
present with palpitations alone.
Clinical examination of the patient can provide
information complementary to the electrocardiogram
(eCG). the clinical features of atrioventricular (av)
dissociation—the independent activation of the atria
and ventricles—almost always indicate the presence of
vt. Clinical signs of av dissociation include ‘cannon’
a waves in the jugular venous pulse, variability in the
intensity of the first heart sound, and variability in arte­
rial blood pressure. these signs have reasonably good
sensitivity (61–96%) and specificity (71–100%) for the
identification of av dissociation.6 vagal maneuvers,
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such as the valsalva maneuver or carotid sinus massage,
that result in termination of tachycardia indicate the
presence of svt, but some vts can also terminate with
these maneuvers, which are, therefore, not reliable
diagnostic tests.
Ecg criteria
the 12­lead eCG is the most reliable means of differenti­
ating vt from svt. as mentioned above, patients with
vt usually present with a wide Qrs complex during
tachycardia. However, a wide­complex tachycardia with a
Qrs morphology consistent with either BBB or fascicular
block is indicative of svt with aberrancy, because this
arrhythmia conducts through part of the His–Purkinje
system. aberrations associated with sustained tachy­
cardias are just as likely to have a right BBB (rBBB)
pattern as a left BBB (LBBB) pattern. vt is likely to be
present if the Qrs morphology is incompatible with these
patterns.7 therefore, the physician needs to be familiar
with these Qrs morphologies.8 in a few of the eCG leads,
vt can seem to have a fairly narrow Qrs complex and
the appearance of such a narrow­complex tachycardia on
a single lead does not exclude the possibility of vt. thus,
obtaining a full 12­lead eCG in patients with tachycardia
is essential.
a number of eCG criteria have been used to differenti­
ate vt from svt with aberrancy (Box 1). Heart rate is not
usually a useful criterion, as both vt and svt can occur
over a wide range of heart rates. vt and svt usually
have a regular rate; a wide­complex tachycardia that is
irregular is most likely to represent atrial fibrillation with
BBB or antegrade conduction over an accessory pathway
(Figure 1). However, irregularity of heart rate does not
exclude vt. in particular, focal idiopathic vt can mani­
fest with periods of acceleration and deceleration, and so
can be irregular (Figure 2).
the most useful eCG feature that differentiates vt
from svt is the presence of av dissociation. Complete
av dissociation is present in 10–50% of vts and only
in exceedingly rare cases of svt (Figure 3). 4,9–11 in
addition, variable retrograde conduction, in a 2:1 or
wenckebach pattern, can be seen in patients with
vt. wenckebach retrograde conduction is characterized
by prolonged ventricular–atrial intervals followed by a
beat with av block. the presence of av dissociation is
dependent upon the rate of the vt, and detection of this
sign is dependent upon the experience of the clinician in
interpreting the eCG. Fusion and capture beats during
a wide­complex tachycardia imply the presence of av
dissociation (Figure 4). a fusion beat is a Qrs complex
arising from two different sources within the ventricle,
one usually from a sinus beat propagating down the
normal conduction system and one beat from the vt. a
capture beat is a sinus beat that conducts down the His–
Purkinje system producing a narrow Qrs complex during
tachycardia. Both beats usually require the presence of a
slow vt to affect ventricular activation.
the width of the Qrs complex has also been shown
to be useful in diagnosing vt. in 1978, wellens et al.
observed that almost 70% of vts had a Qrs >140 ms,
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whereas all svts had Qrs duration of <140 ms, although

no patients in this study had pre­existing BBB.11 in the late
1980s, akhtar and colleagues demonstrated that, because
the Qrs duration is slightly longer with LBBB, the diag­
nostic accuracy of using a Qrs >140 ms with rBBB
morphology and a Qrs >160 ms with LBBB morphology
is excellent, with PPvs of 100% and 96%, respectively.10
However, a relatively narrow Qrs (<120 ms) does not
absolutely exclude the diagnosis of vt, as can be seen
when the tachycardia involves the Purkinje system. the
Qrs axis alone is fairly poor at differentiating vt from
svt, because block in the anterior and posterior fascicles
can produce vectors between ­90o and +150o, which are
also commonly seen during vt. the one exception is the Figure 1 | 12-lead electrocardiogram of atrial fibrillation with ventricular pre-
combination of LBBB morphology and right­axis devia­ excitation over a left-sided accessory pathway. The morphology is right bundle
tion, which is almost always the result of vt.10 a right branch block and Northwest axis, suggestive of ventricular tachycardia. However,
superior (‘northwest’) axis, which is a clear sign of vt, is the rhythm is irregular. The concordance suggests a basal location in the left
present in approximately one quarter of patients.10 ventricle for the origin of the arrhythmia.
single criteria are not particularly useful for differenti­
ating between vt and svt; therefore, a number of algo­ a
rithms have been proposed for diagnostic purposes.4,9,12
the most widely used and cited is the algorithm pro­ I aVR V1 V4
posed by Brugada and collegues.12 this algorithm com­
prises four steps, with the first two steps involving the II aVL V2 V5
assessment of an rs complex in the precordial leads
(Figure 5a). the investigators reported that this sign III aVF V3 V6
had a sensitivity and specificity for the diagnosis of vt
of 99% and 97%, respectively.12 Other researchers4,9 have VI
found this algorithm to be useful, but to be less accurate
than originally reported by Brugada and co­workers. in
II
2008, vereckei et al. provided a simpler algorithm for
the identification of vt (Figure 5b), which involves the
assessment of lead avr only.9 in a blinded comparison, V5

this new model was found to have greater sensitivity and

specificity (97% and 75%, respectively) than the widely b
quoted Brugada algorithm.6 I aVR V1 V4
although eCG criteria are predominantly used for
diagnosing vt, for cases in which doubt exists about the
type of arrhythmia, an electrophysiological study can
provide the diagnosis. in patients with coronary artery II aVL V2 V5
disease and vt, a high likelihood exists of inducing the
clinical arrhythmia with reasonable reproducibility. 13
in other disease states, however, this likelihood is much
III aVF V3 V6
lower. isoproterenol is useful in provoking idiopathic
PvCs and vt.14

Diagnosis of structural heart disease II

Once the diagnosis of vt has been confirmed, the prog­
nosis of the patient and the treatment they should be
given depends on the type of underlying heart disease.
as will be discussed in the next section, patients without
structural heart disease generally have a benign prog­
nosis compared with patients who have various forms
of cardiomyopathy.13
as a first­line investigation, transthoracic echocardio­
graphy should be performed to evaluate left and right
ventricular structure and function, including left ven­
tricular ejection fraction (LveF). regional wall motion
abnormalities in a coronary artery distribution suggest
coronary artery disease that, as the most common etiology
Figure 2 | A patient with focal idiopathic ventricular tachycardia. a | On the 12-lead
electrocardiogram (ECG), the morphology is right bundle branch block ventricular
tachycardia with a left superior axis. Note the irregularity of the tachycardia, which
is particularly seen with focal ventricular tachycardias. This ventricular tachycardia
arose from the posterior papillary muscle in the left ventricle. b | The patient’s ECG
during sinus rhythm is normal with no evidence of prior infarction.
of vt, needs to be excluded. exercise stress testing, or
more­commonly coronary angiography, is employed to
evaluate the presence of coronary artery disease. right
ventricular abnormalities can indicate arrhythmo­
genic right ventricular cardiomyopathy (arvC)
or sarcoidosis.15

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rEviEwS
I aVR V1 V4
II aVL
V2 V5
III aVF V3 V6
25 mm/s; 1 cm/mV
Figure 3 | 12-lead electrocardiogram of broad complex tachycardia. The diagnosis
of ventricular tachycardia (VT) is made using the Brugada criteria12 and the aVR
criteria.9 Note that no RS complexes are present in the precordial leads,
suggesting VT. The lead aVR has an initial R wave, suggesting VT. Note the
atrioventricular dissociation.
I aVR
V1 V4
II aVL V2 V5
III aVF V3 V6
II
Figure 4 | 12-lead electrocardiogram of fascicular ventricular tachycardia. Note
the atrioventricular dissociation, with the P waves shown with arrows. The star
indicates a capture beat. This ventricular tachycardia has right bundle branch
block morphology with left superior axis. The QRS is fairly narrow owing to the
involvement of the Purkinje system in the mechanism of the tachycardia. Note
the similar morphology to that of the focal ventricular tachycardia arising from the
posterior papillary muscle (Figure 2).
Cardiac Mri can provide detailed structural and func­
tional information and is often useful, particularly in the
diagnosis of arvC and infiltrative cardiomyopathies.
Myocardial fibrosis can be identified with delayed gado­
linium enhancement, even in patients without prior myo­
cardial infarction.16 in addition to providing diagnostic
information, cardiac Mri can also provide prognostic
information17 and has been shown to be beneficial in
planning mapping and radiofrequency catheter ablation
strategies.16 Myocardial biopsy and signal­averaged eCGs
can also provide useful information in certain situations. in
particular, myocardial biopsy can assist in the identification
of arvC or myocarditis when the diagnosis is unclear.18
the various mechanisms of vt, the prognoses and the
appropriate treatments for this condition, determined by
the presence or absence of structural heart disease, will be
discussed separately in the following sections.
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VT in the normal heart
‘idiopathic’ vt refers to any vt that is not associated with
structural heart disease. this etiology accounts for up to
25% of patients undergoing catheter ablation of vt in the
usa.19 several forms of idiopathic vt exist, with various
underlying mechanisms. idiopathic vts have been clas­
sified in a number of different ways, including location
of origin, mechanisms, and response to pharmacological
agents. Broadly, idiopathic vts can be classified mecha­
nistically into two groups: focal vts, which are predomi­
nantly triggered or automatic arrhythmias, and fascicular
vts, which are predominantly re­entrant arrhythmias
within the Purkinje system.
Focal vT
the most common form of idiopathic vt is focal vt
arising from the right ventricular outflow tract, which
accounts for approximately 60–70% of idiopathic vts.20
these focal vts can manifest as recurrent PvCs or paroxys­
mal monomorphic vt, usually with LBBB morphology
and marked inferior axis. Patients, who are typically aged
30–50 years, often present with palpitations and, occasion­
ally, presyncope. Focal vt is also observed on the eCGs
of asymptomatic patients. exercise testing reproduces
the patient’s clinical vt in 25–50% of cases.21,22 in some
patients, vt is suppressed by exercise and appears during
the recovery phase whereas, in other patients, vt initiates
during exercise. although the right ventricular outflow
tract is the origin of the majority of focal vts, many other
sites (particularly the structures around the outflow tract
regions) can also produce PvCs or paroxysmal vt (Box 2).
in addition, the papillary muscles, particularly in the left
ventricle, have been recognized as a fairly common site of
focal vt.23–26 the main differential diagnosis that needs to
be excluded in patients with suspected focal vt is arvC,
which can also present as a vt with repetitive LBBB
morphology. t­wave abnormalities in leads v1–v3 on
the baseline eCG, multiple vts with LBBB morphology,
a family history of arvC, and right ventricular structural
abnormalities support a diagnosis of arvC.18,27
Mechanisms
the majority of focal vts seem to be caused by cyclic
adeno sine monophosphate (aMP)­related activity,
although the evidence for this mechanism, which was
presented by Lerman and colleagues, 14,28,29 is limited.
Catecholamine stimulation of the β­adrenergic receptor
results in a rise in intracellular cyclic aMP, producing an
increase in the levels of intracellular calcium and release
of calcium from the sarcoplasmic reticulum. this process
then gives rise to delayed after­depolarizations and vt.
Focal vts can be induced with isoproterenol, atropine,
aminophylline, and rapid pacing, but not usually with
programmed ventricular stimulation.14 Other than the
work by Lerman and his group, very little research has
been carried out into the mechanisms of focal vt.
Management
the treatment of patients with focal vt depends on the
frequency and severity of symptoms, as this condition has
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a Brugada algorithm b aVR algorithm

Absence of RS complex in all precordial leads Presence of an initial R wave

Yes No Yes No

VT diagnosed VT Diagnosed

The longest RS interval >100 ms in any precordial lead Presence of an initial R or Q wave >40 ms

Yes No Yes No

VT diagnosed VT diagnosed

AV dissociation Presence of notch on descending limb of a

negative onset and predominantly negative QRS

Yes No
Yes No

VT diagnosed
VT diagnosed

Morphology criteria for VT present in leads V1–2 and V6 Vi/Vt ≤1

Yes No Yes No

VT diagnosed SVT diagnosed VT diagnosed SVT diagnosed

Figure 5 | Electrocardiographic algorithms of broad complex tachycardia to differentiate between VT and SVT. a | Brugada
algorithm. From Brugada, P. et al. A new approach to the differential diagnosis of a regular tachycardia with a wide QRS
complex. Circulation 83, 1649–1659 (1991) with permission from Wolters Kluwer Health. b | aVR algorithm. Reprinted from
Heart Rhythm, 5, Vereckei, A. et al. New algorithm using only lead aVR for differential diagnosis of wide QRS complex
tachycardia. 89–98, copyright (2008), with permission from Elsevier. vi /vt measures the vertical excursion (in mV) recorded
on the electrocardiogram during the initial (vi) and terminal (vt) 40 ms of the QRS complex. Abbreviations: AV, atrioventricular;
SVT, supraventicular tachycardia; vi /vt, ventricular activation velocity ratio; VT, ventricular tachycardia.

a benign course in the vast majority of patients, with an
extremely low incidence of sudden cardiac death.21,30,31
Patients with minimal symptoms do not necessar­
ily need treatment. For those with severe symptoms or
those who have developed a tachycardia­mediated cardio­
myopathy, the options include pharmacological therapy or
radiofrequency catheter ablation.
acute termination of focal vt can be achieved by vagal
maneuvers, such as carotid sinus massage. adenosine,
lidocaine, and verapamil are also effective; both adenosine
and verapamil terminate tachycardia in approximately
75% of cases.32 First­line antiarrhythmic therapy for symp­
tomatic focal vt is usually a β­blocker, often propranolol,
which is effective in approximately 50% of patients. 33
Other options include calcium­channel blockers, such as
verapamil and diltiazem, which are effective in 25–50%
of patients,33–36 and class i antiarrhythmic agents, such
as flecainide, which is slightly more efficacious.35,37 the
most effective medications are the class iii antiarrhythmic
agents sotalol and amiodarone, both of which alone can
eliminate symptoms in 75–90% of patients.33,35,38
radiofrequency catheter ablation is an alternative to
antiarrhythmic medication in patients with symptomatic
focal vt, given that many of these patients are fairly young
and would otherwise require lifelong medical therapy. For
vts that arise from the right ventricular outflow tract,
ablation is successful in >90% of patients.39 ablation at
other sites can be more challenging and occasionally is
prevented by proximity to a coronary artery, resulting in
slightly lower success rates. ideally, activation mapping
should be performed, but pace mapping can also be
used. activation mapping involves identifying the earli­
est region ‘activated’ during a PvC or vt. Pace mapping
involves pacing the ventricle from various sites, compar­
ing the Qrs morphology to that of the spontaneous PvC,
and targeting the site with the best match. Pace mapping is
predominantly used when PvCs are infrequent; however,
pace map matches can often be seen over a large area,
which sometimes necessitates more­extensive ablation.
Complications of catheter ablation are infrequent, but
include cardiac perforation and tamponade, as well as
coronary artery occlusion.39,40 reversal of tachycardia­
mediated cardiomyopathy can be seen following success­
ful catheter ablation.41,42 Catheter ablation of focal vt is
primarily used in patients without structural heart disease.
However, ablation is also used in patients with struc­
tural heart disease and focal vt, in whom it can reduce
frequent episodes of vt and improve quality of life.43
Fascicular vT
Fascicular vt, which is less common than focal vt, arises
from the left ventricle and presents with a rBBB morph­
ology and predominantly left­axis deviation (Figure 4).
Fascicular vt usually manifests in patients aged between

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Box 2 | Common locations of focal VT
■ Right ventricular outflow tract
■ Left ventricular outflow tract
■ Aortic cusps
■ Pulmonary artery
■ Mitral annulus
■ Tricuspid annulus
■ Papillary muscles
■ Epicardium
Abbreviation: VT, ventricular tachycardia.
15 and 40 years, with most episodes occurring while at
rest. as with focal vt, symptoms include palpitations
and presyncope. recurrent fascicular vt can lead to
tachycardia­mediated cardiomyopathy, but sudden cardiac
death is very rare.44,45
Mechanism
the majority of evidence regarding fascicular vt comes
from mapping studies and the response of tachycardia
to pacing maneuvers, and indicates that the underlying
mechanism is re­entry.46,47 During vt, the retrograde
limb of the circuit is usually the posterior fascicle, with
the antegrade limb comprising abnormal tissue in the left
ventricular septum, which exhibits slow and decremental
conduction. in rare cases, however, the anterior fascicle
can be involved and produces right axis deviation.48
Management
the prognosis of patients with fascicular vt is good and
treatment is aimed at controlling symptoms. verapamil
is useful as acute therapy 49,50 although, as long­term
maintenance therapy, this drug predominantly reduces
symptoms rather than completely abolishing them. 44
Catheter ablation is appropriate when medications fail
or are undesirable, such as among patients who cannot
tolerate drug therapy, those who have comorbidities or
are taking incompatible medications, and individuals who
do not wish to receive medical therapy indefinitely. Long­
term success rates for catheter ablation are >90%, with
a low incidence of complications.51–53 Catheter ablation
is, therefore, the preferred strategy to avoid long­term
medical therapy in patients with fascicular vt.
VT in structural heart disease
Sustained monomorphic vT
the structural changes in the ventricles of patients
with cardiac disease can create the substrate for ventri­
cular arrhythmias. the most common substrate for vt
is ventricular scarring related to ischemic heart disease,
which is present in approximately 60% of patients.19
However, patients with dilated cardiomyopathies, arvC,
prior cardiac surgery (particularly for correction of con­
genital anomalies or valve surgery), sarcoidosis, or hyper­
trophic cardiomyopathy can also have ventricular scarring
and vt.
ventricular scars consist of dense fibrosis, with surviv­
ing myocardial bundles traversing the scar and creating
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channels. these channels often have interstitial fibrosis,
which can create separations between the muscle bundles
and, therefore, circuitous patterns of activation through the
bundles.54 in addition, cell­to­cell coupling between
the myocytes is reduced.55 this combination creates slow
conduction through the channels. in concert with the fixed
anatomical obstacles created by dense fibrosis, the appro­
priate substrate for re­entry is set. Large ventricular scars
seem to predispose the patient to the development of
vt by supporting a greater number of channels than do
smaller scars.56 Patients with structural heart disease and
vt tend to have numerous channels, as evidenced by
multiple inducible morphologies of scar­related vt.57,58
Bundle branch re­entry is a unique form of re­entrant
monomorphic vt that occurs predominantly in patients
with dilated cardiomyopathy. this condition comprises
a macro re­entrant circuit that involves the Purkinje
system. the most common form of bundle branch re­
entry features the right bundle as the antegrade limb and
the left bundle as the retrograde limb, leading to an LBBB
morphology during vt. rarely, the circuit can occur in
the opposite direction, giving rise to an rBBB pattern.
Commonly, these patients have evidence of conduction­
system disease. importantly, this form of vt responds
poorly to pharmacological therapy, but can be eliminated
by catheter ablation of the right bundle.59–61
Primary prevention
For the primary prevention of sudden cardiac arrest in
patients with depressed left ventricular function, implant­
able cardioverter­defibrillators (iCDs) have been shown
to reduce mortality compared with conventional and
antiarrhythmic drug therapy. the MaDit ii study,62
which included patients with ischemic cardiomyopathy
and an LveF ≤30%, found that iCD use reduced mortal­
ity compared with conventional therapy, with an abso­
lute risk reduction of 5.6% and a relative risk reduction of
31%. the sCD­HeFt trial63 included patients with both
ischemic and nonischemic cardiomyopathies, an LveF
of ≤35%, and nYHa class ii or iii heart failure. Patients
were randomly assigned to receive an iCD, amiodarone,
or conventional therapy. although no difference in sur­
vival was found between the amiodarone­therapy and
conventional­therapy groups, iCD use reduced mortality
by 7.2% over 5 years compared with conventional therapy,
which corresponds to a relative risk reduction of 23%.63
Acute management
the initial management of a patient with sustained mono­
morphic vt caused by underlying structural heart disease
is determined by the nature of the symptoms and the
patient’s hemodynamic state. regardless of the etiology,
direct­current cardioversion is warranted for sustained
vt, which produces symptomatic hypotension, pulmo­
nary edema, or myocardial ischemia. reversible causes
of vt, such as electrolyte imbalances, acute ischemia,
hypoxia, and drug toxicities should be corrected.
in patients who are hemodynamically stable, pharmaco­
logical reversion of vt can be attempted. Lidocaine has
often been regarded as a first­line antiarrhythmic agent,
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and can be useful in vt associated with ischemia or
myocardial infarction.64 However, in patients with slow
and stable vt, the efficacy of lidocaine is limited.65–67
intravenous procainamide is an appropriate therapy in
these patients, as it rapidly slows and terminates vt.65
although procainamide is successful for acute arrhyth­
mia termination in around 75% of patients with sustained
monomorphic vt, its use can be limited by hypotension,
which occurs in approximately 20% of these indivi­
duals.68,69 amiodarone is also useful, but its onset of action
is slower than lidocaine or procainamide, and the results
of acute termination studies have been variable. 67,70–72
However, amiodarone is less likely to produce hypotension
than procainamide.68 in some areas of the world, intrave­
nous sotalol (australia, europe) and ajmaline (europe)
are available and have been shown to be effective.66,73
transvenous catheter pace termination, by application
of ventricular pacing at a faster rate than the vt, can
also be performed to treat sustained vt. this approach
is often effective and can be used in combination with
antiarrhythmic agents.74,75
Secondary prevention
recurrence of vt is frequent, with approximately 50% of
patients having subsequent episodes in the 2­year period
following the initial event.76–79 Patients who have been
resuscitated from a cardiac arrest, or who have experienced
vt that has produced hemodynamic compromise, have
a death rate in the first year post­event of approximately
20%.80,81 in 1997, the aviD study 82 demonstrated that iCD
use reduced this risk by 31% over 3 years compared with
amiodarone. whether iCDs should be used in patients
who have sustained vt without hemodynamic compro­
mise and LveF >35% is controversial, and currently little
data are available to answer this question. although iCDs
effectively treat ventricular arrhythmias, shocks from these
devices can have substantial psychological consequences
and may increase the risk of death.83,84
Medical therapy can also be beneficial in the secondary
prevention of vt. among patients with heart failure, who
are at high risk of vt, both angiotensin­converting­enzyme
inhibitors and β­blockers have been shown to reduce
mortality and the incidence of sudden death.85–88 the
class i antiarrhythmic drugs flecainide and propafenone
actually increase mortality in patients at risk of ventricu­
lar arrhythmias.89,90 in patients with an iCD, amiodarone
and sotalol can reduce the number of device therapies,
but do not reduce mortality.63,91 Connolly and colleagues
randomly assigned patients who had sustained ventricular
arrhythmia, an LveF of ≤40%, and an iCD, to receive a
β­blocker, sotalol, or amiodarone plus a β­blocker.78 Over
a 12­month follow­up period, iCD shocks occurred in 39%
of patients in the β­blocker group, 24% of those receiving
sotalol, and 10% of those assigned to the combination of
amiodarone and a β­blocker. in addition, discontinuation
rates were high in the sotalol and amiodarone groups.78
Mexiletine can be used as a second­line therapeutic agent
for recurrent ventricular arrhythmias, particularly in com­
bination with other antiarrhythmic medications, although
adverse effects can limit its use.92–94
nature reviews | cardiology
© 2011 Macmillan Publishers Limited. All rights reserved
rEviEwS
in patients with structural heart disease, catheter abla­
tion can prevent or reduce recurrent episodes of vt
without the adverse effects of antiarrhythmic therapy.
Catheter ablation can also be life­saving in patients with
incessant vt. as previously discussed, the arrhythmo­
genic regions of the ventricle are the slowly conduct­
ing channels within areas of ventricular scar. these
channels are the targets of catheter ablation and can be
identified in several ways. One approach is to use a com­
bination of activation and entrainment mapping during
vt. entrainment mapping can be used to evaluate the
response of the vt to pacing, to determine the relation­
ship between the pacing site and the circuit.95 this infor­
mation is useful for locating the critical portions of the
circuit implicated in the arrhythmia. However, in many
patients, vt is poorly tolerated or unstable and for these
individuals other mapping techniques should be used
during sinus rhythm. ventricular scars can be identified
by low­amplitude electrograms. this technique is used to
create 3­dimensional voltage maps during sinus rhythm,
which reconstruct the anatomy of the ventricle and
the region of scar. thus, abnormal electrograms within the
scar, such as fractionated and late potentials representing
regions of slow conduction, can be targeted during sinus
rhythm allowing ablation of vts in hemodynamically
unstable patients.
the majority of evidence supporting the use of cath­
eter ablation comes from patients with ischemic cardio­
myopathies and vt. in this group, success rates range
from 50% to 80%, with the incidence of major compli­
cations being up to 10%.57,58 Procedure­related mortality
is low, and most deaths result from failure of the proce­
dure to control life­threatening arrhythmias.58 Catheter
ablation is also beneficial in controlling recurrent vt in
patients with dilated cardiomyopathies and arvC.96–100
in these patients, regions of scarring are often midmyo­
cardial or epicardial and, therefore, ablation can be chal­
lenging. epicardial access in these patients is possible
using a percutaneous subxiphoid approach, in which a
needle designed to enter potential spaces is passed into
the pericardium, under fluoroscopic guidance, followed
by a sheath advanced over a wire.101 the ablation cath­
eter can then be introduced, and radiofrequency applied,
although care is needed to avoid the coronary arteries and
phrenic nerve.101–104
the concept of preventive catheter ablation in patients
with an iCD has been evaluated in two trials in the past
4 years. 76,77 reddy et al. randomly assigned patients
who received an iCD for secondary prevention of ven­
tricular arrhythmias to catheter ablation or conventional
therapy.76 Catheter ablation reduced the incidence of
ventricular arrhythmias requiring iCD therapy from
33% to 12% (P = 0.007). in addition, despite the trial not
being adequately powered to assess this outcome, a trend
towards a reduction in mortality was reported.76 Kuck
et al. randomly assigned patients presenting with hemo­
dynamically stable monomorphic vt, prior myocardial
infarction, and an LveF ≤50% to catheter ablation plus
an iCD or to an iCD alone.77 Patients receiving catheter
ablation had a reduction in the number of appropriate
aDvanCe OnLine PuBLiCatiOn | 7
rEviEwS
iCD shocks (27% versus 47%) and a longer time to recur­
rence of vt (median 19 months versus 6 months).77 to
date, no randomized trials comparing catheter ablation
with antiarrhythmic therapy in the prevention of vt have
been conducted.
Pvcs and nonsustained vT
PvCs and nonsustained vt are common among patients
with structural heart disease. the mechanisms of these
arrhythmias can be focal automaticity or triggered activ­
ity, as in patients without structural heart disease, or
scar­related re­entry.105,106 early studies suggested that
frequent and repetitive ventricular ectopy, in associ­
ation with a reduced LveF, predicted an increased risk
of sudden death among patients with myocardial infarc­
tion.107,108 However, more recently, this relationship has
been questioned and the increased mortality risk is now
thought to be related to the extent of structural heart
disease. 109 ambulatory monitoring of patients with
heart failure has indicated that nonsustained ventricular
arrhythmias do not seem to predict an increased risk of
sudden death.110
in patients with nonischemic cardiomyopathy, deter­
mining whether PvCs are the cause of tachycardia­
mediated cardiomyopathy or the consequence of a primary
cardiomyopathy is important. this distinction is essential,
as the former condition can be reversible, particularly with
the use of catheter ablation. Clinical clues that indicate
tachycardia­mediated cardiomyopathy include very fre­
quent PvCs (more than 10,000 per day, and often more
than 20,000 per day 42,111,112), monomorphic PvCs arising
from the outflow tract (LBBB or rBBB morphology with
marked inferior axis), and a young, otherwise healthy,
patient.113 improvement in left ventricular function with
suppression of PvCs, with either antiarrhythmic medi­
cation (such as amiodarone) or catheter ablation, confirms
the diagnosis of tachycardia­mediated cardiomyopathy.
Management
in most patients with structural heart disease, PvCs and
nonsustained vt are asymptomatic. these arrhythmias
do not reliably predict sudden death and no evidence
exists that their suppression prolongs life. therefore,
treatment of these arrhythmias is not indicated. in a
small proportion of patients, PvCs and nonsustained
vt can produce symptoms and, in such cases, treatment
with antiarrhythmic drug therapy or catheter ablation is
appropriate. First­line antiarrhythmic therapy for sympto­
matic patients consists of β­blockade. if this approach
fails, amiodarone or sotalol are appropriate.3 sarrazin
et al. demonstrated that patients with prior myocardial
infarction and frequent PvCs also have a component
of tachycardia­mediated cardiomyopathy that can be
reversible with catheter ablation.114 assessment of the
morphology of the PvCs or nonsustained vt should be
performed to ensure that their site of origin is related to
an area of scar, and not the result of a focal mechanism,
such as would be the case with right ventricular outflow
tract PvCs or vt, which are particularly amenable to
catheter ablation.
8 | aDvanCe OnLine PuBLiCatiOn
© 2011 Macmillan Publishers Limited. All rights reserved
Polymorphic vT
Polymorphic vt is defined by a changing Qrs morph­
ology from beat to beat, which can be sustained—often
requiring emergency cardioversion—or self­limiting.
evaluation of the underlying substrate for polymorphic
vt is important. although the most common cause of
polymorphic vt is acute ischemia, patients with other
conditions such as long Qt syndrome, Brugada syndrome,
catecholaminergic polymorphic vt, and idiopathic vF
can also present with polymorphic vt.
Coronary angiography should be performed to
exclude ischemia in patients with recurrent poly­
morphic vt. Correction of electrolyte abnormalities
and stabilization of heart failure are also important.
intravenous administration of a β­blocker is the treat­
ment of choice for these patients3 and improves mortality
in those with myocardial infarction and recurrent poly­
morphic vt.115 amiodarone is also effective in control­
ling episodes of polymorphic vt.116,117 in patients with
myocardial infarction, PvCs arising from the Purkinje
system in the scar border zone can trigger episodes of
polymorphic vt. Catheter ablation can be used to target
these sites and suppress vt.118 Catheter ablation can
also be successful in other substrates causing PvCs and
polymorphic vt.119,120
Conclusions
ventricular arrhythmias are the most common cause
of sudden cardiac death. they usually occur in patients
with structural heart disease, but are also occasionally
seen in patients without demonstrable cardiac disease. a
number of electrocardiographic criteria and algorithms
exist to accurately diagnose vt. Patients with structur­
ally normal hearts have benign prognoses and treat­
ment is predominantly aimed at reducing symptoms.
Most patients with scar­related vt receive an iCD for
the prevention of sudden cardiac death; antiarrhythmic
therapy can prevent vt recurrence but does not reduce
mortality. Catheter ablation is useful in preventing vt
recurrence, but research is still required to fully define
its role in disease management. Currently several clini­
cal trials are underway comparing catheter ablation
with antiarrhythmic therapy, in particular amiodarone
therapy, for the management of vt. the results of these
studies will clarify the optimal management strategies for
patients with vt. Clearly, research is required to deter­
mine why some patients develop vt and others remain
arrhythmia­free. ideally, preventing the development of
ventricular scarring with improvements in the manage­
ment of ischemic heart disease would be the preferable
management strategy.
Review criteria
The PubMed database was searched to select
articles for inclusion in this Review. Search terms
included “ventricular tachycardia”, “diagnosis”,
“electrocardiogram”, “management”, “treatment”, and
“catheter ablation”. No date limit was set, but only full-
text articles in English were included.
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acknowledgments
K. C. Roberts-Thomson and P. Sanders are supported
by the National Heart Foundation of Australia.
author contributions
K. C. Roberts-Thomson researched data for the
article. All the authors contributed to the discussion
of content, wrote the article, and reviewed/edited the
manuscript before submission and after peer-review.
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