Ventricular arrhythmias: from the electrophysiology laboratory to clinical practice. Part I: malignant ventricular arrhythmias.
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ABSTRACT: After myocardial infarction, patients are at increased risk for sudden cardiac death. A number of noninvasive and invasive risk stratification techniques have been used to define the risk and to protect the high-risk population with an ICD.Hellenic journal of cardiology: HJC = Hellēnikē kardiologikē epitheōrēsē 07/2013; 54(4):301-315. · 1.23 Impact Factor
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ABSTRACT: 1 Επειδή η κοιλιακή τα-χυκαρδία/μαρμαρυγή (ΚΤ/ΚΜ) προκα-λεί ΑΚΘ, η οντότητα του ΑΚΘ προβλή-θηκε και ως ένα υποκατάστατο/ισοδύνα-μο επεισοδίου ταχυαρρυθμίας και χρησι-μοποιήθηκε ως καταληκτικό σημείο για την ταξινόμηση των ασθενών στις σχετι-κές κλινικές μελέτες. 2 Εντούτοις, πολλές άλλες παθοφυσιολογικές καταστάσεις οι οποίες εξελίσσονται ραγδαία μπορούν εξίσου να οδηγήσουν σε ξαφνικό θάνα-το με αποτέλεσμα η κλινική διάγνωση του ΑΚΘ να μην είναι ισοδύναμη και με ΚΤ/ ΚΜ στην περίπτωση όλων των ασθενών που πληρούν κάθε φορά τα κριτήρια αυ-τής της κλινικής διάγνωσης. 3 Επιπροσθέ-τως, πρόσφατες μελέτες σε ασθενείς που φέρουν Εμφυτευμένο Αντιταχυκαρδιακό Βηματοδότη Απινιδωτή (ΕΑΒΑ) δείχνουν ότι αρκετοί εκ των θανάτων οι οποίοι εί-χαν συμβατικά προσδιοριστεί ως ΑΚΘ στην πράξη δεν οφειλόταν σε ταχυαρρυθ-μία. 4 Ως εκ τούτων, όταν κανείς εξισώνει τον ΑΚΘ με τις κοιλιακές ταχυαρρυθμίες οφείλει να λαμβάνει υπ όψιν τον παρα-κάτω εννοιολογικό περιορισμό: ότι δηλα-δή, ο ΑΚΘ, ενώ συνήθως στην προέλευ-ση του είναι αρρυθμιολογικός, εντούτοις τούτο δεν ισχύει πάντα. Το παρόν κείμε-νο διαπραγματεύεται με περιεκτικό τρό-πο το θέμα του αρρυθμιολογικού ΑΚΘ σε ασθενείς οι οποίοι πάσχουν από Στεφα-νιαία Νόσο (ΣΝ). Το παθοφυσιολογικό υπόστρωμα και οι μηχανισμοί πρόκλησης αρρυθμίας συνδέονται με τις σύγχρονες στρατηγικές διαστρωμάτωσης κινδύνου οι οποίες περιγράφονται με έμφαση ως προς την κλινική τους εφαρμογή. Επιδημιολογικά δεδομένα συσχετισμού ΣΝ και ΑΚΘΕλληνική Καρδιολογική Επιθεώρηση. 01/2013; 54:89-105.
(Hellenic Journal of Cardiology) HJC • 525
Hellenic J Cardiol 2011; 52: 525-535
October 1, 2010;
April 18, 2011.
P.O. Box 175
19009 Drafi Attikis
Key words: Risk
Ventricular Arrhythmias: From the
Electrophysiology Laboratory to Clinical Practice
Part I: Malignant Ventricular Arrhythmias
Konstantinos a. Gatzoulis, stefanos archontaKis, Polychronis Dilaveris,
Dimitrios tsiachris, Petros arsenos, sKevos siDeris, christoDoulos stefanaDis
Electrophysiology Laboratory and First University Department of Cardiology, Hippokration General Hospital,
University of Athens, Athens, Greece
tice.1-5 Apart from being commonly asym-
ptomatic, they may manifest with a vari-
ety of clinical symptoms, such as palpita-
tions, “strong” precordial beats, “missing”
heart beats, chest pounding, or occasion-
ally episodes of long-lasting tachycardia
accompanied with dyspnoea, chest dis-
comfort, hypotension and syncope. How-
ever, most concerns are directed towards
the risk of sudden cardiac death (SCD)
due to the unpredictable occurrence of
sustained ventricular tachyarrhythmias.4
Thus, risk stratification for SCD should
always be among the first priorities for all
patients presenting with ventricular ar-
rhythmias.6-7 According to the findings of
this risk stratification process and of the
clinical presentation, the most appropriate
treatment plan will be selected, including
simple measures such as regular follow up
with psychological support and symptom-
atic treatment with antiarrhythmic medi-
cation, as well as more complex therapeu-
tic interventions, such as endocardial cath-
eter ablation of the arrhythmogenic fo-
ci and prophylactic insertion of automat-
ic implantable cardioverter defibrillators
(AICD) with adequate treatment of all co-
entricular arrhythmias represent
a common problem for the clini-
cal cardiologist in everyday prac-
existing haemodynamic or ischaemic ab-
The electrophysiology (EP) labora-
tory provides us with great opportunities
in patients with potential life-threatening
ventricular arrhythmias who are at risk
for SCD, in terms of completing the risk
stratification, implementation of all inter-
ventional therapies previously mentioned
and effective suppression of ventricular
arrhythmias in cases where antiarrhyth-
mic pharmacological treatment has failed.
On the other hand, the role of the electro-
physiological study (EPS) is limited to re-
search purposes when ventricular arrhyth-
mias are considered to be “benign”, af-
ter non-invasive electrocardiographic and
Classification of ventricular arrhythmias
Ventricular arrhythmias could be clas-
sified into 3 diagnostic groups, depend-
ing on their complexity in ambulatory as
well as in 12-lead electrocardiography.3
This classification, however, mainly re-
flects the needs of the medical community
for a common methodological approach
to these conditions and consequently the
implementation of the best diagnosis and
treatment plan. In reality, they represent a
526 • HJC (Hellenic Journal of Cardiology)
K.A. Gatzoulis et al
continuous spectrum ranging from the “benign” spo-
radic ventricular ectopic beats to the malignant ven-
tricular arrhythmias, such as sustained ventricular
tachycardia (VT) and ventricular fibrillation (VF). In
between there is the group of potentially malignant
arrhythmias, such as very frequent premature ventric-
ular contractions, ventricular couplets and episodes
of non-sustained VT (i.e. VT lasting less than 30 s,
usually in the form of 3 to 10 consecutive ventricular
complexes) (Table 1).
The degree of SCD risk depends mainly on the
nature of the underlying heart disease, the extent
of the ventricular dysfunction, the presence of isch-
aemia or haemodynamic instability, the functional
condition of the autonomic nervous system, and the
presence of sites of slow ventricular conduction in
the right or left ventricle. Prior to classifying ventric-
ular arrhythmias as “benign”, potentially malignant
or malignant, a non-invasive electrophysiological as-
sessment should take place, including the patient’s
medical history, echocardiographic findings, exer-
cise testing, and signal-averaged electrocardiogram
(SAECG) results. Thus, even sporadic and rare ven-
tricular ectopic beats without complex morphology
should be considered as potentially malignant ven-
tricular arrhythmias in patients with severe ventricu-
lar dysfunction, positive late potentials and a histo-
ry of pre-syncopal and/or syncopal attacks, while on
the other hand, the presence of idiopathic sustained
monomorphic VT is associated with a relatively low
risk of SCD. The clinical value of this complex sys-
tem of non-invasive assessment and risk stratifica-
tion is important, thus limiting the invasive electro-
physiological diagnostic approach and treatment to
those patients with potentially life-threatening or
malignant ventricular arrhythmias. Moreover, pro-
grammed ventricular stimulation (PVS), aiming to
reveal a well-organised electrophysiological substrate
responsible for a future episode of sustained ventric-
ular tachyarrhythmia, should be selectively imple-
mented in those patients with ventricular arrhyth-
mias in whom the pharmacological or non-pharma-
cological antiarrhythmic intervention would probably
result in not only a better life expectancy, but also a
better quality of life.
In the present paper, the electrophysiological
methods for investigating malignant ventricular ar-
rhythmias will be reviewed as they currently apply to
the EP laboratory. In the second part of this paper we
will present the different electrophysiologically guid-
ed approaches to investigate the great variety of ven-
tricular arrhythmias, ranging from the benign to po-
Malignant ventricular arrhythmias
Coronary heart disease (CHD) is the commonest
cause of sustained ventricular arrhythmias. In most
cases, VF or polymorphic VT is the consequence of
acute coronary ischaemia, whereas sustained mono-
morphic VT in patients with structural heart disease is
usually due to a myocardial scar resulting from a prior
infarct, or other causes of non-ischaemic cardiomyopa-
thies, through re-entry mechanisms.27
Sustained monomorphic VT that is not related
to structural heart disease can be successfully treated
with endocardial ablation of its site of origin through
radiofrequency current intracardiac catheters (radio-
frequency catheter ablation, RCA).8,9,19-21 The site
of origin is usually located in the right ventricular
outflow tract, and occasionally in other locations of
the right ventricle (RV) or in the posterior inferior
septal wall of the left ventricle (LV). When deriving
from the RV, ventricular tachycardia is characterised
by a left bundle branch block (LBBB) pattern with a
varying axis depending on the site of origin, whereas
Table 1. Classification of ventricular arrhythmias.
Sustained VT or VF
Non-sustained VT, frequent
(≥ 30/hour) PVCs and
Organic heart disease Usually present Most commonly present Absent
Prognosis and risk of
sudden cardiac death
Impaired in the presence of
organic heart disease
Depending on EPS
results and severity of underlying
organic heart disease
VT – ventricular tachycardia; VF – ventricular fibrillation; PVCs – premature ventricular contractions; EPS – electrophysiological study.
(Hellenic Journal of Cardiology) HJC • 527
when deriving from the LV, it demonstrates a right
bundle branch block (RBBB) morphology with left
axis. In order for the electrophysiological mapping to
be completed, reproducible induction of the arrhyth-
mia with PVS is required. The site of origin of the
ventricular arrhythmia is identified by recording pre-
systolic electrograms during the induced tachycar-
dia or by reproducing the 12-lead morphology of the
arrhythmia when pacing from the presumptive tar-
get site while in sinus rhythm. In cases where the un-
derlying mechanism is ventricular re-entry, determi-
nation of the exact site of origin is feasible by meet-
ing the entrainment criteria, an electrophysiological
technique that contributes to the safest and most ef-
fective ablation by limiting the number of unneces-
sary lesions applied.11,17,18 RCA in idiopathic VT is
reserved for patients who do not respond to medical
treatment and is performed successfully in more than
80% of the cases, with a low rate of complications or
The effectiveness of VT RCA in patients with
structural heart disease is lower, varying from 50% to
80%.27 Ablation in disorders other than post-infarc-
tion cardiomyopathy is often more difficult and re-
currence of VT more frequent.27 In patients present-
ing with sustained VT or VF the optimal treatment
is AICD implantation.27-29 However, it is not uncom-
mon for recurrent episodes of VT that are not con-
trolled with antiarrhythmic agents to lead to repeat
AICD activation, resulting in a deterioration in the
patient’s quality of life. Furthermore, AICDs do not
provide absolute protection against SCD, with an es-
timated incidence of non-response of 5%.30 These pa-
tients, in addition to those with incessant VT, could
be treated effectively by modification of the arrhyth-
mological substrate by RCA.10-17,27,31,32 RCA might
also be an alternative to AICD implantation in cer-
tain population subgroups such as the elderly.33,34 In
a recent trial, patients who received AICD plus VT-
ablation, often described as hybrid therapy, dem-
onstrated a lower incidence of appropriate AICD
activation.35 In another recent study, prophylactic
RCA before AICD implantation was suggested in
post myocardial infarction (MI) patients who man-
ifested VT and a reduced left ventricular ejection
fraction (LVEF) ≤50%.36 In these cases, the under-
lying structural cardiac disease—which is most usu-
ally post-infarction CHD, but not infrequently dilated
cardiomyopathy, operated congenital heart disease
or arrhythmogenic right ventricular cardiomyopa-
thy/dysplasia—leads to the formation of one or more
sites of ventricular re-entry (scar-related VT), from
which frequent or even unsuppressed ventricular ec-
topic activity may originate. The morphology of VT
in the 12-lead electrocardiogram (ECG) provides us
with important information about the approximate
anatomical location of origin of the arrhythmia. In
cases where more than one morphology of VT is rec-
ognised, it is possible that multiple foci of VT, or al-
ternatively an extended myocardial scar resulting in
a re-entry circuit with more than one exit tract, are
present (Figure 1).
Reproduction of the 12-lead morphology of the
VT during pacing, at the presumptive site of origin,
is of great importance for the exact localisation of
the target site (Figure 2). Furthermore, detection
of pre-systolic or, even better, mid-diastolic electro-
grams during mapping is of great help in identify-
ing the ideal target site (Figures 3 & 4).9,10,27 Meet-
ing the entrainment criteria of VT when pacing from
the slow conduction area, and specifically from its
exit tract site, is reassuring evidence for exact locali-
Figure 1. Localisation of the site of origination of sustained ven-
tricular tachycardia (VT) by means of the electrocardiogram
(ECG). A 12-lead ECG of a 70-year-old, post-myocardial infarc-
tion patient, showing two different types of sustained VT, not sup-
pressed with amiodarone. Based on the electrocardiographic mor-
phology and the axis of the sustained VT, its exit tract sites can be
localised at the apex of the left ventricle and the middle section of
the intraventricular septum (S or CIL position and 2AC position
according to Kuchar and Josephson, respectively).
528 • HJC (Hellenic Journal of Cardiology)
K.A. Gatzoulis et al
Figure 2. Electrophysiological study. Reproduction of the 12-lead
morphology of the ventricular tachycardia (VT) during pacing.
Pacing from the apex of the left ventricle, at a cycle length similar
to that of the clinical tachycardia, results in reproduction of the
12-lead electrocardiographic morphology of the sustained VT.
Figure 3. Identification of the arrhythmogenic site with presystolic
electrograms during the electrophysiological study. Presystolic elec-
trograms 120 ms and 90 ms before the tachycardia complex are
recorded in the two different exit tract sites of the sustained ven-
tricular tachycardia. From top to bottom, surface leads I, II, III and
V1 are shown, followed by the endocardial electrograms of the right
ventricle (RV), the high right atrium (HRA), the His bundle (HBE)
and the zone surrounding the infarction area of the left ventricle
Figure 4. Entrainment of ventricular tachycardia during electrophysiological study. During the sustained ventricular tachycardia
(VT), in the slow conduction site (LV) of the zone surrounding the infarction area, low amplitude, long duration multi-fragmented
electrical activity is observed in the middle of the cardiac cycle (mid-diastolic electrograms). Pacing from this site, while the patient
remains in sustained VT, results in entrainment of the VT at the paced cycle length (acceleration from 440 ms to 400 ms) without
any changes in the surface lead morphology. From top to bottom, surface leads I, II, aVF and V1 are shown, followed by the en-
docardial electrograms of the right ventricular outflow tract (RVOT), the high right atrium (HRA), the apex of the right ventricle
and the zone surrounding the infarction area of the left ventricle (LV).
(Hellenic Journal of Cardiology) HJC • 529
sation and hence for safe and effective ablation (Fig-
ure 4).9-11,16-18 Specifically, when pacing from the slow
conducting area of the ventricular VT site of origin,
at a cycle length shorter to that of the induced sus-
tained VT, we entrain the VT at the pacing rate with-
out changing its 12-lead ECG morphology and axis,
while when the pacing is interrupted the returning
cycle length remains identical to that of the induced
VT. When ablating at the corresponding entrain-
ment site, there is a higher success rate compared to
lesions applied in areas of early pre-systolic activa-
tion and pace-mapping reproduction of the 12-lead
ECG VT morphology. However, in focal VT demon-
strating a point source of endocardial activation, the
entrainment criteria cannot be used and distinction
from macro–re-entrant VT is important because the
ablation site characteristics are very different.37 On
occasion, it is interesting to observe an atrioventric-
ular-node–like behaviour with decremental proper-
ties within the slow conduction area of the VT site
of origin (Figure 5). Recently, numerous “modern”
mapping technologies have been developed, resulting
in increased success rates of VT catheter ablation.38
These techniques are based on colourful electro-an-
atomical reproduction of the ventricular cavity of in-
terest with either activation and/or voltage mapping
performed through specially designed recording and
ablation catheter systems introduced into the LV or
RV cavities. The mapping could be performed either
during sinus rhythm or during the induced VT. Thus,
areas of slow conduction and low voltage, as well as
of late potentials and mid-diastolic activity, can be
identified during sinus rhythm, representing abnor-
mal scar tissue sites of interest. Similarly, activation
mapping during spontaneous or induced ventricular
ectopy may identify early activation sites of interest.
All of these sites represent potential ablative lesion
areas which could be “modified” by “drawing” lines
between them until the target VT is either complete-
ly suppressed or more difficult to induce. Apart from
achieving higher success rates, such techniques signif-
icantly also limit the radiation exposure to both inva-
sive electrophysiologists and patients.
These observations, in addition to correspond-
ing findings from the SAECG supporting the forma-
tion of organised areas of slow ventricular conduc-
tion, probably explain the occurrence of episodes of
electrical storm in patients with a history of malig-
nant ventricular arrhythmias treated with an AICD
(Figure 6). Electrical storm, namely the non-predict-
able occurrence of at least 3 episodes of sustained
ventricular tachyarrhythmias in a period less than
24 hours, is a major arrhythmic event presenting as
a medical emergency in 1 out of 5 patients receiving
an AICD for the secondary prevention of SCD.38-41
Both short- and long-term prognoses seem to be im-
paired, although acute management with an antiar-
rhythmic drug combination regimen is effective in the
vast majority of patients affected (Figure 7).39-50 In
fact, an advanced New York Heart Association (NY-
HA) heart failure stage and the occurrence of electri-
cal storm emerge as the most important independent
mortality predictors among patients managed with an
AICD.41,44-46 Some authors, however, argue that elec-
trical storm is frequent but does not increase mortal-
ity in AICD recipients.40,43,48 At the present time, it is
difficult to predict the AICD recipient who is going
to be affected by electrical storm.48 Reversible isch-
aemic, metabolic, haemodynamic or electrolytic ab-
normalities are not usually detected during the acute
event. However the incidence of electrical storm may
be higher among AICD patients receiving the device
for the secondary prevention of SCD, with severe sys-
tolic dysfunction, when the presenting arrhythmia is
VT and not primary VF, or with coexisting renal dys-
function.40,41,43,44,48,51-53 The role of other well accept-
ed risk stratification factors from 12-lead electrocar-
Figure 5. Atrioventricular-node–like behaviour with decremen-
tal properties within the slow conduction area of the ventricular
tachycardia site of origin. Self-termination of sustained ventricular
tachycardia (VT). In the slow-conduction area of the intraven-
tricular re-entry circuit, prolongation of the distance between
the mid-diastolic and pre-systolic electrograms is observed oc-
casionally, before the former are blocked in the circuit, in the last
sustained VT complex. The sequence of the electrocardiographic
leads and electrograms is as in Figure 3.
530 • HJC (Hellenic Journal of Cardiology)
K.A. Gatzoulis et al
diography, ambulatory electrocardiography, SAECG
or T-wave alternans has not been studied. The combi-
nation of a lower LVEF with the presence of late po-
tentials is associated with a higher rate of both AICD
activation and cardiac mortality.54
The role of RCA in electrical storm, aiming to-
wards a favourable modification of the arrhythmolog-
ical substrate, remains unclear. However, a number of
studies have suggested that it not only results in a bet-
ter quality of life but may also improve the impaired
prognosis.55-58 On the other hand, in patients with di-
lated cardiomyopathy, RCA was less effective com-
pared with patients with CHD and arrhythmogenic
right ventricular cardiomyopathy/dysplasia.58 Recent
data suggest a reduction in the incidence of AICD ac-
tivation including electrical storm recurrence, favour-
ably affecting mortality, among AICD recipients on
optimal antiarrhythmic medication, when they under-
go RCA.58 Such a reduced incidence of AICD activa-
tion can also be achieved with antiarrhythmic drugs
such as b-blockers, sotalol, and amiodarone, especial-
ly when b-blockers are combined with amiodarone.27
The increased incidence of AICD activation, with
the associated depression, may lead to worsening of
quality of life. Thus, every effort to reduce it is highly
desirable. Such efforts may also include the appropri-
ate anti-tachycardia pacing capabilities of the device
Figure 6. Electrical storm revealed during interrogation of an
automatic implantable cardioverter defibrillator (AICD) in a
patient with coronary heart disease. Interrogation of the device in
a 65-year-old, post myocardial infarction patient, with a history of
sustained ventricular tachycardia (VT) and an AICD implantation
presenting four years later with multiple episodes of sustained
VT. The interrogation revealed multiple VT episodes within a
few days, successfully interrupted with anti-tachycardia pacing or
defibrillation shocks. Electrical storm was successfully treated by
means of a triple antiarrhythmic drug combination (amiodarone,
metoprolol and mexiletine).
Log rank test p=0.0004
Pts without ES (n=137)
Pts without ES (n=32)
Follow up (months)
Patients at risk
2040 6080100 120 140
Figure 7. Survival curve in electrical storm. Probability of survival
of automatic implantable cardioverter defibrillator (AICD) patients
according to the presence of electrical storm. (From: Gatzoulis KA,
Andrikopoulos GK, Apostolopoulos T, et al. Electrical storm is an
independent predictor of adverse long-term outcome in the era of
implantable defibrillator therapy. Europace 2005; 7: 184-192. Re-
produced with permission from Oxford University Press.)
(Hellenic Journal of Cardiology) HJC • 531
programming in order to interrupt silently even fast
episodes of VT.59 In these cases, as well as in patients
with idiopathic VT in whom it is not always possible
to induce sustained ventricular tachycardia, invasive
electrophysiology, using novel electro-anatomical
mapping techniques seems to be promising (Figure
8).42,57,58,60 Thus, short-duration episodes of VT or
even sporadic ventricular ectopic beats can be tracked
and ablated.22 The effectiveness and safety of these
techniques of endocardial ablation are currently un-
der investigation, not only expanding the treating op-
tions, but also limiting the radiation exposure for pa-
tients and invasive electrophysiologists.
Apart from RCA of the VT site of origin, in the
EP laboratory we safely and effectively perform AICD
implantations in high-risk cardiac patients who have
had a previous spontaneous sustained ventricular
tachyarrhythmia event (secondary prevention of SCD),
or whenever the risk stratification process defines such
a risk in the near future (primary prevention of SCD).
Detailed reviews regarding the clinical and laboratory
indications for the implantation of an AICD in high-
risk patients, the implantation techniques and the long
term follow up of these patients have been published in
the past.23-27,29,61,62 Recent technological improvements
in the field of endocardial defibrillation, the expanding
experience of the implantation centres, as well as the
well-documented positive impact of AICDs on survival
in patients with structural heart disease and a history
of spontaneous or/and induced malignant ventricular
arrhythmias, have resulted in a tremendous increase
in the number of AICD implantations worldwide, al-
though there are still striking differences between the
two sides of the Atlantic.63
Figure 8. Electroanatomical mapping in a patient with electrical storm. A 65-year-old patient with coronary heart disease presented with
repeat episodes of sustained ventricular tachycardia (electrical storm) prior to automatic implantable cardioverter defibrillator (AICD)
implantation. The episodes were treated with triple antiarrhythmic medication and subsequent ablation/modification of the arrhythmo-
genic substrate using a three-dimensional colour electro-anatomical mapping system (potential map). Five years later the patient remains
in stage II heart failure while the AICD has been successfully activated with anti-tachycardia pacing only once, three months after the abla-
tion and AICD implantation (Modified from: Gatzoulis KA, Sideris SK, Kallikazaros IE, Stefanadis CI. Electrical storm: a new challenge
in the age of implantable defibrillators. Hellenic J Cardiol. 2008; 49: 86-91.)
532 • HJC (Hellenic Journal of Cardiology)
K.A. Gatzoulis et al
The role of electrophysiological intervention,
however, is not limited only to the diagnosis and treat-
ment of high-risk patients. Occasionally, patients with
a history of malignant ventricular arrhythmias are
treated with non-antiarrhythmic or even antiarrhyth-
mic surgery, aiming at mechanical restoration of the
detected ischaemic or haemodynamic dysfunctions
and modification of the arrhythmia substrate. Pa-
tients with CHD, aneurysm of the left ventricle, val-
vular heart disease or idiopathic hypertrophic ob-
structive cardiomyopathy should be reassessed in the
postoperative period with PVS.64-67 It is not unusual
for a patient with CHD and a history of cardiac arrest
and induced ventricular fibrillation on PVS to remain
electrically stable after revascularisation, especially
when there is no severe left ventricular dysfunction
or presence of late potentials. Furthermore, aneurys-
mectomy of the left ventricle with disappearance of
the pre-existing late potentials may be associated with
an inability to re-provoke a previously easily triggered
VT on PVS (Figure 9).64,65 It is unlikely, however,
that this would occur in a patient with a history of sus-
tained monomorphic VT when severe dysfunction of
the left ventricle and the presence of late potentials
are still present postoperatively (Figure 10).
Figure 10. A signal averaged electrocardiogram (SAECG) and
electrophysiological study (EPS) in a patient with coronary heart
disease. An SAECG and EPS in a middle-aged post myocardial
infarction patient who presented with sustained ventricular tachy-
cardia (VT) and underwent a triple coronary artery bypass sur-
gery. Postoperatively, pre-existent positive late potentials persist-
ed and additionally sustained monomorphic VT was induced. The
patient remains alive and in good clinical condition (no angina,
left ventricular ejection fraction 40%, New York Heart Associa-
tion class II) 9 years later after the second automatic implantable
cardioverter defibrillator (AICD) replacement, with 6 episodes of
sustained VT interrupted by the device.
Figure 9. Elimination of late potentials in the signal averaged
electrocardiogram (SAECG) after aneurysmectomy. SAECG
performed in a 64-year-old post myocardial infarction patient with
left ventricular aneurysm before (fQRS = 191 ms, RMS-40 = 1
μV, LAS = 104 ms) and after (fQRS = 113 ms, RMS-40 = 16
μV, LAS = 35 ms) aneurysmectomy of the left ventricle showing
disappearance of the pre-existing late potentials. The presenting
sustained ventricular tachycardia (VT) (both spontaneous and
induced preoperatively) was not induced postoperatively.
(Hellenic Journal of Cardiology) HJC • 533
1. Morganroth J. Premature ventricular complexes. Diagnosis
and indications for therapy. JAMA. 1984; 252: 673-676.
2. Bigger JT. Identification of patients at high risk for sudden
cardiac death. Am J Cardiol. 1984; 54: 3D-8D.
3. Morganroth J, Bigger JT. Pharmacologic management of
ventricular arrhythmias after the cardiac arrhythmia suppres-
sion trial. Am J Cardiol. 1990; 65: 1497-1503.
4. Lown B, Wolf M. Approaches to sudden death from coronary
heart disease. Circulation. 1971; 44: 130-142.
5. Wellens HJ, Brugada P. Treatment of cardiac arrhythmias:
when, how and where? J Am Coll Cardiol. 1989; 14: 1417-
6. Horowitz ZN, Spielman SR, Greenspan AM, Josephson
ME. Role of programmed stimulation in assessing vulner-
ability to ventricular arrhythmias. Am Heart J. 1982; 103:
7. Morady F, Scheinman MM, Hess DS, Sung RJ, Shen E, Sha-
piro W. Electrophysiologic testing in the management of sur-
vivors of out-of-hospital cardiac arrest. Am J Cardiol. 1983;
8. Calkins H, Kalbfleisch SJ, el-Atassi R, Langberg JJ, Morady
F. Relation between efficacy of radiofrequency catheter abla-
tion and site of origin of idiopathic ventricular tachycardia.
Am J Cardiol. 1993; 71: 827-833.
9. Bogun F, Bahu M, Knight BP, et al. Comparison of effective
and ineffective target sites that demonstrate concealed en-
trainment in patients with coronary artery disease undergoing
radiofrequency ablation of ventricular tachycardia. Circula-
tion. 1997; 95: 183-190.
10. Morady F, Harvey M, Kalbfleisch SJ, el-Atassi R, Calkins H,
Langberg JJ. Radiofrequency catheter ablation of ventricular
tachycardia in patients with coronary artery disease. Circula-
tion. 1993; 87: 363-372.
11. Waldo AL, Henthorn RW. Use of transient entrainment dur-
ing ventricular tachycardia to localize a critical area in the re-
entry circuit for ablation. Pacing Clin Electrophysiol. 1989;
12. Blanck Z, Dhala A, Deshpande S, Sra J, Jazayeri M, Akhtar
M. Catheter ablation of ventricular tachycardia. Am Heart J.
1994; 127: 1126-1133.
13. Haissaguerre M, Warin JF, Lemétayer P, Guillem JP, Blan-
chot P. Fulguration of ventricular tachycardia using high cu-
mulative energy: results in thirty-one patients with a mean
follow-up of twenty-seven months. Pacing Clin Electrophysi-
ol. 1989; 12: 245-251.
14. Volkmann H, Kühnert H, Dannberg G, Heinke M. Bundle
branch reentrant tachycardia treated by transvenous catheter
ablation of the right bundle branch. Pacing Clin Electrophysi-
ol. 1989; 12: 258-261.
15. Willems S, Borggrefe M, Shenasa M, et al. Radiofrequency
catheter ablation of ventricular tachycardia following implan-
tation of an automatic cardioverter defibrillator. Pacing Clin
Electrophysiol. 1993; 16: 1684-1692.
16. Stevenson WG, Khan H, Sager P, et al. Identification of re-
entry circuit sites during catheter mapping and radiofrequen-
cy ablation of ventricular tachycardia late after myocardial in-
farction. Circulation. 1993; 88: 1647-1670.
17. Waldo AL. From bedside to bench: entrainment and other
stories. Heart Rhythm. 2004; 1: 94-106.
18. Waldo AL, Henthorn RW, Plumb VJ, MacLean WA. Dem-
onstration of the mechanism of transient entrainment and in-
terruption of ventricular tachycardia with rapid atrial pacing.
J Am Coll Cardiol. 1984; 3: 422-430.
19. Nogami A, Naito S, Tada H, et al. Demonstration of diastol-
ic and presystolic Purkinje potentials as critical potentials in
a macroreentry circuit of verapamil-sensitive idiopathic left
ventricular tachycardia. J Am Coll Cardiol. 2000; 36: 811-823.
20. Nakagawa H, Beckman KJ, McClelland JH, et al. Radiofre-
quency catheter ablation of idiopathic left ventricular tachy-
cardia guided by a Purkinje potential. Circulation. 1993; 88:
21. Ouyang F, Cappato R, Ernst S, et al. Electroanatomic sub-
strate of idiopathic left ventricular tachycardia: unidirectional
block and macroreentry within the purkinje network. Circula-
tion. 2002; 105: 462-469.
22. Della Bella P, Pappalardo A, Riva S, Tondo C, Fassini G,
Trevisi N. Non-contact mapping to guide catheter ablation
of untolerated ventricular tachycardia. Eur Heart J. 2002; 23:
23. A comparison of antiarrhythmic-drug therapy with implant-
able defibrillators in patients resuscitated from near-fatal
ventricular arrhythmias. The Antiarrhythmics versus Im-
plantable Defibrillators (AVID) Investigators. N Engl J Med.
1997; 337: 1576-1583.
24. Moss AJ, Hall WJ, Cannom DS, et al. Improved survival with
an implanted defibrillator in patients with coronary disease at
high risk for ventricular arrhythmia. Multicenter Automatic
Defibrillator Implantation Trial Investigators. N Engl J Med.
1996; 335: 1933-1940.
25. Connolly SJ, Hallstrom AP, Cappato R, et al. Meta-analysis
of the implantable cardioverter defibrillator secondary pre-
vention trials. AVID, CASH and CIDS studies. Antiarrhyth-
mics vs Implantable Defibrillator study. Cardiac Arrest Study
Hamburg. Canadian Implantable Defibrillator Study. Eur
Heart J. 2000; 21: 2071-2078.
26. Moss AJ, Zareba W, Hall WJ, et al. Prophylactic implantation
of a defibrillator in patients with myocardial infarction and re-
duced ejection fraction. N Engl J Med. 2002; 346: 877-883.
27. Koplan BA, Stevenson WG. Ventricular tachycardia and sud-
den cardiac death. Mayo Clin Proc. 2009; 84: 289-297.
28. ACC/AHA/HRS 2008 Guidelines for Device-Based Thera-
py of Cardiac Rhythm Abnormalities: a report of the Ameri-
can College of Cardiology/ American Heart Association Task
Force on Practice Guidelines (Writing Committee to Revise
the ACC/AHA/NASPE 2002 Guideline Update for Implan-
tation of Cardiac Pacemakers and Antiarrhythmia Devices)
developed in collaboration with the American Association
for Thoracic Surgery and Society of Thoracic Surgeons. J Am
Coll Cardiol. 2008; 51: e1-62.
29. Solomon SD, Zelenkofske S, McMurray JJ, et al. Sudden
death in patients with myocardial infarction and left ventric-
ular dysfunction, heart failure, or both. N Engl J Med. 2005;
30. Anderson KP. Sudden cardiac death unresponsive to im-
plantable defibrillator therapy: an urgent target for clinicians,
industry and government. J Interv Card Electrophysiol. 2005;
534 • HJC (Hellenic Journal of Cardiology)
K.A. Gatzoulis et al
31. Bella PD, Riva S. Hybrid therapies for ventricular arrhyth-
mias. Pacing Clin Electrophysiol. 2006; 29 Suppl 2: S40-47.
32. Sacher F, Tedrow UB, Field ME, et al. Ventricular tachy-
cardia ablation: evolution of patients and procedures over 8
years. Circ Arrhythm Electrophysiol. 2008; 1: 153-161.
33. Pedrinazzi C, Durin O, Agricola P, Romagnoli P, Inama G.
Efficacy and safety of radiofrequency catheter ablation in the
elderly. J Interv Cardiac Electrophisiol. 2007; 19: 179-85.
34. Dagres N, Piorkowski C, Kottkamp H, Kremastinos DT, Hin-
dricks G. Contemporary catheter ablation of arrhythmias in
geriatric patients: patient characteristics, distribution of ar-
rhythmias, and outcome. Europace. 2007; 9: 477-480.
35. Reddy VY, Reynolds MR, Neuzil P, et al. Prophylactic cath-
eter ablation for the prevention of defibrillator therapy. N
Engl J Med. 2007; 357: 2657-2665.
36. Kuck KH, Schaumann A, Eckardt L, et al. Catheter ablation
of stable ventricular tachycardia before defibrillator implan-
tation in patients with coronary heart disease (VTACH): a
multicentre randomised controlled trial. Lancet. 2010; 375:
37. Das MK, Scott LR, Miller JM. Focal mechanism of ventric-
ular tachycardia in coronary artery disease. Heart Rhythm.
2010; 7: 305-311.
38. Eckardt L, Breithardt G. Catheter ablation of ventricular
tachycardia. From indication to three-dimensional mapping
technology. Herz. 2009; 34: 187-196.
39. Villacastín J, Almendral J, Arenal A, et al. Incidence and
clinical significance of multiple consecutive, appropriate,
high-energy discharges in patients with implanted cardiovert-
er-defibrillators. Circulation. 1996; 93: 753-762.
40. Credner SC, Klingenheben T, Mauss O, Sticherling C, Hohn-
loser SH. Electrical storm in patients with transvenous im-
plantable cardioverter-defibrillators: incidence, management
and prognostic implications. J Am Coll Cardiol. 1998; 32:
41. Exner DV, Pinski SL, Wyse DG, et al. Electrical storm pres-
ages nonsudden death: the antiarrhythmics versus implant-
able defibrillators (AVID) trial. Circulation. 2001; 103: 2066-
42. Gatzoulis KA, Sideris SK, Kallikazaros IE, Stefanadis CI.
Electrical storm: a new challenge in the age of implantable
defibrillators. Hellenic J Cardiol. 2008; 49: 86-91.
43. Greene M, Newman D, Geist M, Paquette M, Heng D,
Dorian P. Is electrical storm in ICD patients the sign of a dy-
ing heart? Outcome of patients with clusters of ventricular
tachyarrhythmias. Europace. 2000; 2: 263-269.
44. Verma A, Kilicaslan F, Marrouche NF, et al. Prevalence, pre-
dictors, and mortality significance of the causative arrhythmia
in patients with electrical storm. J Cardiovasc Electrophysiol.
2004; 15: 1265-1270.
45. Gatzoulis KA, Andrikopoulos GK, Apostolopoulos T, et al.
Electrical storm is an independent predictor of adverse long-
term outcome in the era of implantable defibrillator therapy.
Europace. 2005; 7: 184-192.
46. Sesselberg HW, Huang DT, Zareba W, et al. Storms of ven-
tricular tachycardia/fibrillation in MADIT II patients. Heart
Rhythm. 2005; 2: S205.
47. Arya A, Haghjoo M, Dehghani MR, et al. Prevalence and
predictors of electrical storm in patients with implantable
cardioverter-defibrillator. Am J Cardiol. 2006; 97: 389-392.
48. Brigadeau F, Kouakam C, Klug D, et al. Clinical predictors
and prognostic significance of electrical storm in patients
with implantable cardioverter defibrillators. Eur Heart J.
2006; 27: 700-707.
49. Hohnloser SH, Al-Khalidi HR, Pratt CM, et al. Electrical
storm in patients with an implantable defibrillator: incidence,
features, and preventive therapy: insights from a randomized
trial. Eur Heart J. 2006; 27: 3027-3032.
50. Nayak HM, Verdino RJ, Russo AM, et al. Ventricular tachy-
cardia storm after initiation of biventricular pacing: inci-
dence, clinical characteristics, management, and outcome. J
Cardiovasc Electrophysiol. 2008; 19: 708-715.
51. Soman SS, Sandberg KR, Borzak S, Hudson MP, Yee J, Mc-
Cullough PA. The independent association of renal dysfunc-
tion and arrhythmias in critically ill patients. Chest. 2002;
52. McCullough PA, Soman SS, Shah SS, et al. Risks associated
with renal dysfunction in patients in the coronary care unit. J
Am Coll Cardiol. 2000; 36: 679-684.
53. Raitt MH, Klein RC, Wyse DG, et al. Comparison of ar-
rhythmia recurrence in patients presenting with ventricular
fibrillation versus ventricular tachycardia in the Antiarrhyth-
mics Versus Implantable Defibrillators (AVID) trial. Am J
Cardiol. 2003; 91: 812-816.
54. Gomes JA, Cain ME, Buxton AE, Josephson ME, Lee KL,
Hafley GE. Prediction of long-term outcomes by signal-av-
eraged electrocardiography in patients with unsustained ven-
tricular tachycardia, coronary artery disease, and left ventric-
ular dysfunction. Circulation. 2001; 104: 436-441.
55. Bänsch D, Oyang F, Antz M, et al. Successful catheter abla-
tion of electrical storm after myocardial infarction. Circula-
tion. 2003; 108: 3011-3016.
56. Silva RM, Mont L, Nava S, Rojel U, Matas M, Brugada J.
Radiofrequency catheter ablation for arrhythmic storm in pa-
tients with an implantable cardioverter defibrillator. Pacing
Clin Electrophysiol. 2004; 27: 971-975.
57. Schreieck J, Zrenner B, Deisenhofer I, Schmitt C. Rescue
ablation of electrical storm in patients with ischemic cardio-
myopathy: a potential-guided ablation approach by modify-
ing substrate of intractable, unmappable ventricular tachycar-
dias. Heart Rhythm. 2005; 2: 10-14.
58. Carbucicchio C, Santamaria M, Trevisi N, et al. Catheter ab-
lation for the treatment of electrical storm in patients with
implantable cardioverter-defibrillators: short- and long-term
outcomes in a prospective single-center study. Circulation.
2008; 117: 462-469.
59. Sweeney MO, Wathen MS, Volosin K, et al. Appropriate and
inappropriate ventricular therapies, quality of life, and mor-
tality among primary and secondary prevention implantable
cardioverter defibrillator patients: results from the Pacing
Fast VT REduces Shock ThErapies (PainFREE Rx II) trial.
Circulation. 2005; 111: 2898-2905.
60. Gepstein L, Hayam G, Ben-Haim SA. A novel method for
nonfluoroscopic catheter-based electroanatomical mapping
of the heart. In vitro and in vivo accuracy results. Circulation.
1997; 95: 1611-1622.
61. Bardy GH, Lee KL, Mark DB, et al. Amiodarone or an im-
plantable cardioverter-defibrillator for congestive heart fail-
ure. N Engl J Med. 2005; 352: 225-237.
62. Desai AS, Fang JC, Maisel WH, Baughman KL. Implantable
(Hellenic Journal of Cardiology) HJC • 535
defibrillators for the prevention of mortality in patients with
nonischemic cardiomyopathy: a meta-analysis of randomized
controlled trials. JAMA. 2004; 292: 2874-2879.
63. Camm AJ, Nisam S. European utilization of the implantable
defibrillator: has 10 years changed the ‘enigma’? Europace.
2010; 12: 1063-1069.
64. Simson MB. Effects of surgery for control of ventricular
tachycardia on late potentials. Circulation. 1981; 64 (IV): 88.
65. Breithardt G, Seipel L, Ostermeyer J, et al. Effects of antiar-
rhythmic surgery on late ventricular potentials recorded by
precordial signal averaging in patients with ventricular tachy-
cardia. Am Heart J. 1982; 104: 996-1003.
66. Marcus NH, Falcone RA, Harken AH, Josephson ME, Sim-
son MB. Body surface late potentials: effects of endocardial
resection in patients with ventricular tachycardia. Circulation.
1984; 70: 632-637.
67. Borggrefe M, Breithardt G. Is the implantable defibrillator
indicated in patients with hypertrophic cardiomyopathy and
aborted sudden death? J Am Coll Cardiol. 1998; 31: 1086-