Download Nonsustained ventricular tachycardia

European Heart Journal (2004) 25, 1093–1099
Review
Nonsustained ventricular tachycardia: where do
we stand?
Demosthenes G. Katritsis*, A. John Camm
Department of Cardiology, Athens Euroclinic, 9 Athanassiadou Street, Athens 11521, Greece
Department of Cardiological Sciences, St. George’s Hospital Medical School, London, UK
KEYWORDS
The clinical approach to the patient with nonsustained ventricular tachycardia
(NSVT) should always be considered within the particular clinical context in which
the arrhythmia occurs. In the documented absence of heart disease, spontaneous
NSVT does not carry any adverse prognostic significance. Exercise-induced NSVT may
predict increased cardiac mortality. In ischaemic patients with a left ventricular
ejection fraction (LVEF)<40%, NSVT has an adverse prognostic significance and
electrophysiologic testing is indicated with a view to ICD implantation. In patients
with LVEF>40% the independent prognostic significance of NSVT is unknown. The
prognostic value of NSVT in patients with dilated cardiomyopathy is not known.
NSVT in young patients with hypertrophic obstructive cardiomyopathy carries an
adverse prognostic significance. The prognostic value of NSVT in conditions such as
the long-QT syndromes, primary ventricular fibrillation, and Brugada syndrome, as
well as in patients with hypertension and valvular disease, has not been
established.
c 2004 Published by Elsevier Ltd on behalf of The European Society of Cardiology.
Ventricular tachycardia;
Nonsustained
Introduction
Nonsustained ventricular tachycardia (NSVT) is one of the
most common problems encountered in modern clinical
cardiology. The term, defined as 3 or more consecutive
beats arising below the atrioventricular node with a rate
>120 beats/min and lasting less than 30 s,1–3 denotes an
electrocardiographic finding that can be associated with
an extremely wide range of clinical conditions, from
patients with significant heart disease and annual mortality rates exceeding 50% to asymptomatic, apparently
healthy, young individuals. In several clinical settings
NSVT is a marker of increased risk for subsequent sustained tachyarrhythmia and sudden cardiac death.3
However, even today it is not known whether NSVT has a
* Corresponding author. Tel.: þ30-210-641-6600; fax: þ30-210-6819779.
E-mail address: [email protected] (D.G. Katritsis).
cause-and-effect relationship with sustained ventricular
tachyarrhythmias or is merely a surrogate marker of left
ventricular dysfunction and electrical instability. Even in
the case where it does hold prognostic significance, NSVT
is not necessarily involved in the mechanism of death.
There are certain patient groups with a high mortality
due to progress of their disease. Death in these patients
may be arrhythmic but this does not mean that merely
preventing NSVT will unconditionally prolong life significantly. In several trials, reduction of arrhythmias or even
arrhythmic death was not associated with a concomitant
reduction in total mortality.4–6
The physician attending a patient presenting with an
episode of NSVT has two tasks. First, to establish whether underlying occult pathology is responsible for the
arrhythmia and, in the case of diagnosed heart disease,
to risk-stratify the patient for appropriate management
and therapy. The clinical approach to the patient with
NSVT should always be considered within the particular
0195-668X/$ - see front matter c 2004 Published by Elsevier Ltd on behalf of The European Society of Cardiology.
doi:10.1016/j.ehj.2004.03.022
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Received 11 December 2003; revised 5 March 2004; accepted 18 March 2004
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clinical context in which the arrhythmia occurs. In several settings the patient with NSVT is a clinical challenge
insofar as proper management is concerned, and several
questions remain unanswered.
Novel data on NSVT
those detected in age-matched populations without the
arrhythmia.16;17 Tachycardia originating from the right
ventricular outflow tract (RVOT), one of the commonest
causes of NSVT in apparently healthy individuals, may
cause symptoms but the risk of death is very low.18;19
Thus, recording of spontaneous NSVT in apparently
healthy individuals does not imply an adverse prognosis,
provided that occult cardiomyopathy and genetic arrhythmia disorders are excluded. These conditions may
remain latent for several years and although apparently
healthy individuals presenting with NSVT can be reassured about their prognosis, long-term follow-up is advisable. There is continually accumulating evidence for
occult pathology in apparently normal subjects who
develop ventricular arrhythmia.20–22 Patients with RVOT
ventricular tachycardia might have subtle structural and
functional abnormalities of the outflow tract as detected by magnetic resonance imaging20 and the diagnosis of RVOT ventricular tachycardia needs to be
differentiated from the diagnosis of arrhythmogenic
right ventricular dysplasia23 and right ventricular myocarditis.
The occurrence of premature ventricular depolarisation during exercise in apparently healthy subjects has
not been associated with an increase in cardiovascular
mortality and was considered to be a normal response to
exertion.24–27 It appears now that the long-term prognostic implications of exercise-induced ventricular arrhythmias may be adverse. Recently, the Paris
Prospective Study28 has confirmed earlier data29 and
reported that runs of two or more consecutive ventricular depolarisations during exercise or at recovery may
occur in up to 3% of healthy men and indicate an increase
in cardiovascular mortality within the next 23 years by a
factor of more than 2.5. This increased relative risk
persisted even after adjusting for other characteristics
and known predisposition to coronary artery disease.
Interestingly, among subjects with a positive exercise
test for ischaemia, only 3% had ectopy, whereas among
subjects with exercise-induced ectopy only 6% had a
positive exercise test for ischaemia. Thus, although the
precise mechanism of arrhythmia is unknown in this
setting and various forms of occult cardiomyopathy
cannot be excluded, it does not appear to be a direct
consequence of ischaemia. This study argues that exercise-induced nonsustained ventricular arrhythmia may
predict coronary artery disease even in the absence of
evidence of ischaemia in asymptomatic individuals.
Exercise testing may also induce catecholaminergic
polymorphic ventricular tachycardia.30;31 When recognised, this condition requires aggressive management.
Clinical approach
Patients with heart disease
Apparently healthy individuals
Initial reports indicated that the presence of complex
ventricular ectopy and NSVT increase the risk of subsequently observed heart disease.14;15 However, when the
presence of occult ischaemia or structural heart disease
was excluded, NSVT was not found to adversely influence prognosis, with cardiac event rates not exceeding
Ischaemic heart disease
The occurrence of NSVT during the first day of acute
myocardial infarction, although frequent (40% to 70% of
patients), is not associated with increased risk for subsequent long-term mortality.32 Following the first 24 h
postinfarction, NSVT is detected in approximately 5–10%
of the patients, particularly during the first months, and
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Reliable epidemiologic data on NSVT are difficult to obtain. Most of the available information comes from older
studies based on Holter monitoring. Usually, although
not invariably, patients remain asymptomatic; the reproducibility of NSVT recordings is documented in only
half of the patients with this arrhythmia.7 The advent of
implantable permanent pacemakers and implantable
cardioverter defibrillators (ICD) with extensive ECG
monitoring capabilities has made it possible to compile
considerable information from patients with heart disease. There is emerging evidence from ICD data that
NSVT is a distinct tachyarrhythmia that may cause syncope without causing death in patients with heart disease, and that the incidence of polymorphic NSVT
relative to sustained arrhythmia is greater than previously believed.8 Reports from the Analysis of the Multicenter UnSustained Tachycardia Trial (MUSTT)9
substudies have provided valuable information regarding
the prevalence and prognostic significance of NSVT in the
context of different clinical settings. It seems that not
only the frequency of NSVT but the circumstances under
which it occurs are important. MUSTT data have shown
prognostic differences in patients with in-hospital, as
opposed to out-of-hospital, identified NSVT.10 Overall
mortality rates at two and five years of follow-up were
24% and 48%, respectively, for inpatients and 18% and
38% for outpatients (adjusted p ¼ :018). In patients undergoing surgical coronary revascularisation, the occurrence of NSVT within the early (first 10 days)
postrevascularisation period portends a far better outcome than when it occurs later after CABG (10–30 days)
or in nonpostoperative settings.11 Indeed, the approximate 2-year mortality rates for patients with early
postrevascularisation NSVT, late postrevascularisation
NSVT, and nonpostoperative NSVT were 14%, 23%, and
24%, respectively.11 However, when sustained ventricular tachycardia is inducible in patients with early postoperative NSVT, the outcome is worse than in
noninducible patients.12 In the MUSTT, racial differences
have also been shown to influence the outcome of patients with NSVT and reduced left ventricular function.13
D.G. Katritsis, A.J. Camm
Nonsustained ventricular tachycardia: where do we stand?
heart failure survival trial of antiarrhythmic therapy
(CHF-STAT) despite the elimination of ventricular
ectopy.46
Nonsustained ventricular tachycardia can be detected
in approximately 5% of ischaemic patients with preserved
left ventricular function, apparently excluding previous
myocardial infarction, but does not appear to indicate an
adverse clinical outcome.47;48 However, NSVT appears
now to occur in the majority of ischaemic patients with
reduced left ventricular function,49;50 Induction of sustained arrhythmia by programmed electrical stimulation51;52 still appears to retain predictive power in
ischaemic patients with impaired left ventricular function (LVEF<40%).50 Recently, the MUSTT investigators
analysed the relation of ejection fraction and inducible
ventricular tachyarrhythmias to mode of death in 1791
patients enrolled in MUSTT who had not already received
antiarrhythmic therapy. Total and arrhythmic mortality
were higher in patients with an ejection fraction <30%
than in those whose ejection fractions were 30% to 40%.
Inducibility of tachyarrhythmia identified patients for
whom death was significantly more likely to be arrhythmic. This study therefore suggested that the major utility
of electrophysiologic testing may be restricted to patients having an ejection fraction between 30% and
40%.50 In ischaemic patients with relatively well preserved left ventricular function (LVEF[40%), the role of
programmed electrical stimulation is not established.
There are cases, however, where programmed electrical
stimulation tests may reveal monomorphic ventricular
tachycardia in the postinfarction patient.
Noninducible patients may not have a lower risk for
arrhythmic events. Both the MUSTT9 and the Multicenter
Automatic Defibrillator Implantation Trial (MADIT) II53
have suggested that patients noninducible by electrophysiologic testing have a risk for sudden cardiac death
similar to that of inducible patients. In the MUSTT, the
inducible group had a 2-year total mortality rate of 28%,
whereas the noninducible group had 21%. The mortality
rate in noninducible patients is high enough to question
the need for programmed electrical stimulation. Actually, data from MADIT II suggest an even higher rate of
appropriate ICD shocks in patients who were noninducible at electrophysiologic testing.53 These findings are
consistent with analyses of stored ICD data, which have
clearly shown that there was little association between
spontaneous and induced ventricular arrhythmias.54
Thus, electrophysiology testing cannot select patients
with a favourable outcome.
The value of signal-averaged ECG and autonomic
markers, such as heart rate variability and depressed
baroreflex sensitivity, for determining prognosis and selecting high-risk patients with NSVT is not established.3;40
Analysis of ATRAMI patients has shown that NSVT, heart
rate variability, and depressed baroreflex sensitivity
were all significantly and independently associated with
increased mortality. Depressed baroreflex sensitivity, in
particular, identified a subgroup with the same mortality
risk as patients with NSVT and reduced LVEF.40 Recently,
the Multiple Risk Factor Analysis Trial (MRFAT) showed
that in the beta-blocking era the common arrhythmia risk
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has been considered to have adverse prognostic significance.33–35
Previous studies have emphasised the importance of
NSVT as an important prognostic determinant for arrhythmic death, even independent of left ventricular
ejection fraction (LVEF).36;37 It now appears that in the
patient with ischaemic heart disease, NSVT no longer
appears to be an independent predictor of death if other
factors such as the ejection fraction are taken into account. In the Gruppo Italiano per lo Studio della Sopravvivenza nell’Infarto Miocardico-2 (GISSI-2, Italian
Group for the Study of Survival after Myocardial Infarction-2) trial, NSVT was a significant predictor of mortality
in univariate analysis, but not independently in multivariate analysis involving other clinical variables.35
Similarly, in the electrophysiologic study versus electrocardiographic monitoring (ESVEM) trial, although univariate analysis suggested that there was an association
between the presenting arrhythmia and outcome, multivariate analysis failed to establish the predictive value
of the presenting arrhythmia.38 Left ventricular ejection
fraction was the single most important predictor of
arrhythmic death or cardiac arrest in patients with lifethreatening arrhythmias who were treated with antiarrhythmic drugs. Over a 6-year follow-up period, 285 of
the 486 patients enrolled in the ESVEM trial had an arrhythmia recurrence. Patients with LVEF>40% had a 5%
risk of developing a malignant arrhythmia, whereas for
each decrease of 5% in LVEF, the risk of cardiac arrest or
arrhythmic death increased by 15%.38 In another study in
which most patients (78%) had revascularisation of the
infarct-related artery, NSVT early after myocardial infarction (4–16 days) had a low prevalence (9%) and
carried a significant but low relative risk for the composite endpoint of cardiac death, ventricular tachycardia, or ventricular fibrillation, but not for arrhythmic
events considered alone.39 Interestingly, in a recent
analysis of 1071 ATRAMI patients, many of which underwent thrombolysis (63%), NSVT (with a prevalence of
13.4%) was found to adversely influence prognosis, independent of reduced LVEF.40
Although Holter monitoring is a valuable diagnostic
tool in detecting patients with NSVT, its usefulness for
the subsequent follow-up and evaluation of treatment is
questionable. First, the prognostic significance of the
frequency of NSVT runs or other ECG variables such as
heart rate and complex ventricular ectopy is unknown.
Recent trials in postinfarction patients have yielded
conflicting evidence with regards to the relationship
between the frequency of ventricular ectopy and heart
rate with cardiac mortality.41;42 It seems that in the betablocking era, all common arrhythmia risk variables, including NSVT, have diminished predictive power in
identifying postinfarction patients at risk of sudden cardiac death.43 Second, the suppression of frequent ventricular ectopy or NSVT runs following beta-blockade or
amiodarone therapy does not imply a favourable diagnosis. Mortality was increased in the cardiac arrhythmia
suppression trials (CAST and CAST II), despite reduced
ectopic activity,44;45 whereas mortality was not reduced
by amiodarone in the Veterans administration congestive
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Nonischaemic heart disease
In conditions other than ischaemic heart disease the independent prognostic significance of NSVT, at least as far
as sudden arrhythmic death is concerned, is even less
established. There has been some evidence regarding its
prognostic significance in patients with hypertrophic
cardiomyopathy in the young,56;57 but several questions
remain in patients with dilated cardiomyopathy46;58–60
and other congenital or idiopathic arrhythmogenic conditions.61–64 Clearly, more data are needed for risk
stratification of these patients and ongoing trials are
eagerly awaited in this respect.65;66
The high prevalence of ventricular arrhythmias on
Holter monitoring in patients with dilated cardiomyopathy (up to 80%)46;58;60;67;68 makes their prognostic significance difficult to assess and the prognostic value of NSVT
in this setting is questionable. The GESICA trial has provided evidence that in patients with NSVT the risk of
sudden death compared to nonsudden death was significantly increased;59;60 this was not confirmed in the CHFSTAT.46 Furthermore, although amiodarone therapy was
associated with decreased mortality in the GESICA trial,
no such effect was observed in the CHF-STAT trial, despite the higher prevalence of NSVT in this cohort.60;46 No
advantage of ICD implantation over amiodarone was
shown in the AMIOVIRT trial in patients with LVEF<35%
and NSVT,69 despite suggestions that NSVT patients may
require an ICD as badly as patients with a history of
previous ventricular fibrillation.70 Similarly, disappointing results with the use of ICDs for primary prevention in
patients with nonischaemic cardiomyopathy (LVEF<30%)
have been recently reported by the CAT investigators.71
The Marburg Cardiomyopathy Study72 has recently
reported on noninvasive arrhythmia risk stratification in
patients with dilated cardiomyopathy. Although NSVT
and frequent ventricular premature beats showed a significant association with a higher arrhythmia risk on
univariate analysis, on multivariate analysis only LVEF
was found to be a significant predictor of major arrhythmic events with a relative risk of 2.3 per 10% decrease of LVEF. Signal-averaged ECG, baroreflex
sensitivity, heart rate variability, and T-wave alternans
were not helpful for arrhythmia risk stratification. Results of subanalyses from the still ongoing DEFINITE and
SCD-HeFT trials should also provide data on the prognostic value of NSVT in this setting.
In hypertrophic cardiomyopathy 20–30% of patients
may have NSVT, whereas in patients with a history of
cardiac arrest this proportion approaches 80%.56;73;74 It
has been suggested that NSVT only has prognostic importance in patients with hypertrophic cardiomyopathy
when it is repetitive, prolonged, or associated with
symptoms.3 In a recent study on 531 patients with hypertrophic cardiomyopathy, no relation between the
Table 1 Clinical significance of NSVT
Clinical setting
Apparently normal heart
Random finding
During or postexercise
Ischemic heart disease
Acute MI < 24 h
Acute MI > 24 h
Chronic IHD with LVEF > 40%
Chronic IHD with LVEF < 40%
Significance
No adverse prognostic significance in the absence of
occult pathology
May predict IHD and increased cardiac mortality
No adverse prognostic significance
Adverse prognostic significance
Prognostic significance unknown
Adverse prognostic significance
DCM
Independent prognostic significance
not established, as opposed to LVEF
HOCM
Probable adverse prognostic significance, especially in
the young
Primary VF, congenital long-QT, Brugada syndrome, ARVD,
repaired congenital abnormalities, valvular disease, hypertension
Prognostic significance unknown
IHD: ischaemic heart disease, MI: myocardial infarction, LVEF: left ventricular ejection fraction, DCM: dilated cardiomyopathy, HOCM: hypertrophic cardiomyopathy, VF: ventricular fibrillation, ARVD: arrhythmogenic right ventricular dysplasia.
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variables, particularly autonomic and standard ECG
markers, have limited predictive power in identifying
patients at risk of sudden cardiac death.43 In a 43 ± 15month follow-up of 675 patients, sudden cardiac death
was weakly predicted only by reduced LVEF (<40%),
NSVT, and abnormal signal-averaged ECG, but not by
autonomic markers or ECG variables. The positive predictive accuracy of these markers (low LVEF, NSVT, and
abnormal signal-averaged ECG), however, was low, 8%,
12%, and 13%, respectively.43 More data are clearly
needed to establish the clinical utility of autonomic
markers, particularly in the setting of NSVT.
Based on the MUSTT and MADIT results, patients with
LVEF below 40% and NSVT should undergo electrophysiologic testing with a view to ICD implantation. Guided
antiarrhythmic drug therapy no longer has a role in the
treatment of these patients.55 Patients with LVEF less
than 30% should be considered high-risk for arrhythmic
death, regardless of the presence of NSVT, according to
MADIT II. So far, no hard data exist to guide the management of ischaemic patients with NSVT and LVEF>40%.
D.G. Katritsis, A.J. Camm
Nonsustained ventricular tachycardia: where do we stand?
Conclusions
Based on the evidence presented as well as on our
own experience, we can make the following statements
(Table 1).
In the documented absence of heart disease, spontaneous NSVT does not appear to carry any adverse prognostic significance. Exercise-induced or postexercise
NSVT may predict the future development of coronary
artery disease and increased cardiac mortality.
In ischaemic patients with LVEF<40%, NSVT has an
adverse prognostic significance and electrophysiologic
testing with a view to ICD implantation is indicated. In
patients with LVEF>40%, the independent prognostic
significance of NSVT is unknown and the role of electrophysiologic testing not established, although we do
advocate its use in this setting.
The independent prognostic value of NSVT in patients
with dilated cardiomyopathy has never been proven.
NSVT in patients with hypertrophic obstructive cardiomyopathy probably carries an adverse prognostic significance, particularly in the young.
The prognostic value of NSVT in conditions such as the
long-QT syndromes, primary ventricular fibrillation, and
Brugada syndrome, as well as in patients with hypertension and valvular disease, is not established.
Thus, the clinical approach to the patient with NSVT
should always be considered within the particular clinical
context in which the arrhythmia occurs.
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frequency, duration, or rate of NSVT episodes could be
demonstrated.57 However, NSVT was associated with a
substantial increase in sudden death risk in young patients with hypertrophic cardiomyopathy.57 The presence of high-risk factors, including NSVT in the young,
may justify defibrillator implantation as primary prevention in patients with hypertrophic cardiomyopathy.75
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on Holter or exercise testing has no predictive value to
guide appropriate therapy, although ICD implantation is
recommended, at least in symptomatic patients.61;63;76
In patients with valvular disease the incidence of NSVT
is considerable (up to 25% in aortic stenosis and in significant mitral regurgitation) and appears to be a marker
of underlying left ventricular pathology.77;78 Up to 65% of
patients with surgical repair of tetralogy of Fallot have
ventricular ectopy, whereas NSVT occurs in up to 17% of
patients either at rest or during exercise.79;80 In patients
with arterial hypertension, NSVT is correlated to the
degree of cardiac hypertrophy and subendocardial fibrosis.81;82 Approximately 15% of patients with hypertension and left ventricular hypertrophy present NSVT, as
opposed to 6% of patients with hypertension alone.81–83
No convincing evidence exists to prove that NSVT is an
independent predictor of sudden death in patients with
valve disease, repaired congenital abnormalities, or hypertension. In these conditions, therefore, the approach
to the patient from the point of view of arrhythmias
currently remains empirical.
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