Supraventricular tachycardia

European Heart Journal (1996) 17 (Supplement Q, 21-25
Supraventricular tachycardia
Occasional nuisance or frequent threat?
R. W. F. Campbell
University of Newcastle upon Tyne and Freeman Hospital, Newcastle upon Tyne, U. K.
Supraventricular tachycardias (SVTs) are common and are
widely regarded as a nuisance. They are often repetitive and
persistent, and cause more upset than is currently acknowledged although only rarely do they threaten life.
Surprisingly, they are ill-defined. A modern approach to
SVT requires an accurate diagnosis and a readiness to
abandon obsolete therapies in favour of effective new
strategies, whether pharmacological or ablative.
(Eur Heart J 1996; 17 (SuppI Q : 21-25)
Introduction
Prevalence of SVT
Key Words: Supraventricular tachycardia, propafenone,
flecainide, amiodarone, RF ablation.
There is only sketchy information about the prevalence
of supraventricular tachycardias regardless of how they
are defined. In the Tromso Study131 a population were
asked 'Have you observed sudden changes in your heart
rate or heart rhythm during the preceding year?' The 43
who replied 'yes' to this question and 54 who replied 'no'
were examined by 24 h ambulatory ECG recordings and
the arrhythmia prevalence examined. Perhaps not surprisingly, 98% of those replying 'yes' had some type of
arrhythmia on the recording but so too did 74% of those
replying 'no'. Few were important arrhythmias and none
qualified as a supraventricular tachycardia.
Further information is available from an examination of 400 factory workers known to have normal hearts and who underwent 24 h ECG recordings.
Supraventricular tachycardias were not found in this
population although supraventricular ectopic beats
were found in 25% of males and 39% of females[4]. Interestingly in that study only 20% of males and 29% of
females had no arrhythmic events on the recordings. In
another study151, 2000 Athenians aged between 18 and 81
years underwent Bruce Treadmill Testing. Seven per cent
developed arrhythmias, the majority being supraventricular or ventricular ectopic beats. There were no incidents of
supraventricular tachycardia. Finally, on exercise testing
of 1383 asymptomatic volunteers, 83 (6%) developed an
'SVT'[6]. In 13 the event was sustained more than 10 min
but only three were symptomatic (Fig. 1).
These studies show that whilst supraventricular
and
ventricular
ectopic beats are commonly found
Academic Cardiology is supported by the British Heart
in apparently normal populations, sustained supraFoundation.
ventricular tachycardias are not.
Correspondence: Professor R. W. F. Campbell, Professor of
The division between a salvo of supraventricular
Cardiology, University of Newcastle upon Tyne and Freeman
ectopic beats and a supraventricular tachycardia is
Hospital, Newcastle upon Tyne, U.K.
0195-668X/96/0C0021+05 $18.00/0
© 1996 The European Society of Cardiology
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The narrow QRS tachycardias or supraventricular
tachycardias (SVTs) as they are more popularly known,
generate considerable academic interest. In the last few
years the fundamental mechanism of each has been
elucidated and many have been shown to be based upon
reentry whether anatomical or functional. With that
understanding of mechanism has also come a more
logical approach to management'1'2'. As the ultimate in
management strategies, curative radiofrequency ablation has forced a reappraisal of what the aim of treatment should be and its success has focused attention on
our new knowledge of arrhythmia anatomy. Yet there is
much that remains to be established. Remarkably few
studies have examined the prevalence of supraventricular tachycardias and even fewer have provided a
longitudinal review of their impact upon the quality and
quantity of life.
The reasons for these deficiencies are not clear
but there are several potential explanations. Supraventricular tachycardias have not been considered
'serious' arrhythmias and have received much less attention than ventricular arrhythmias. Another factor may be
the difficulties of defining what constitutes a supraventricular tachycardia particularly when brief salvos of
supraventricular ectopic beats are a not uncommon
finding on 24 h ECG recordings. Finally, unlike some
diseases, follow-up needs 10, 20 or more years of
observation.
22
R W. F. Campbell
Heart rates 105-290
16%
4%
44%
> 10 min
symptomatic
at peak effort
Figure 1 Prevalence and characteristics of supraventricular tachycardia (SVT) provoked
by exercise in 1383 asymptomatic volunteers (Maurer et a/.161).
Eur Heart J, Vol. 17, Suppl C 1996
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the frequency of attacks and upon the susceptibility
of attacks to treatment whether prescribed on an 'as
required' basis (e.g. Valsalva manoeuvre etc.) or as
chronic prophylactic therapy. The advent of radiofrequency ablation for WPW syndrome has encouraged
a more aggressive non-pharmacological approach'11'121
although there are still many patients for whom chronic
oral antiarrhythmic therapy is a reasonable management
strategy. In that circumstance, therapy logically should
target the accessory pathway. No patients with WPW
Impact and patterns of specific SVTs
syndrome should suffer significant impairment in quality
The term supraventricular tachycardia is outmoded. It of life. If medical therapy is ineffective, not tolerated
does not accurately describe the arrhythmias commonly or inappropriate, radiofrequency ablation should be
included in this category and it encourages an un- pursued.
scientific grouping of arrhythmias. More information is
The major life-threatening complication of
available from considering each individual arrhythmia. WPW syndrome is atrial fibrillation in the presence of a
short antegrade refractory period accessory pathway.
There are no good estimates of the risk of this condition.
It almost certainly has been over-emphasised in the past,
SVT and WPW syndrome
but there are sufficient anecdotes in the literature to
WolfF-Parkinson-White (WPW) syndrome is variously underscore that for some, it is a potentially lethal
9 10 13 141
estimated to occur in up to two per 1000 of an appar- situation' ' ' ' . The risk appears greatest between
71
ently normal population' . This is a relatively high ages 8 and 20 years and there is circumstantial evidence
prevalence but it would seem likely that a sizable pro- that in some patients continuation of digoxin therapy
portion of affected patients, perhaps up to 50%, may not from infancy may have a contributory effect. Digoxin
experience arrhythmic events during their lifetime. Only should not be continued past the age of 8 years in a
a minority with WPW syndrome develop troublesome patient with WPW syndrome unless that therapy has
symptoms. Arrhythmias are most problematic in the been shown to be absolutely safe. This usually means
first year of life, in the teens and 20s and then in the 50s an accessory pathway capable of only retrograde
and 60s. Whilst it is not certain why this pattern occurs, conduction.
a plausible explanation is that in the first year of life the
Several studies have suggested that the overall
characteristics of the accessory pathway and the atrio- risk of death in WPW syndrome is small'15'161, but WPW
ventricular (AV) node are relatively well-matched, is a curable condition and any young lives lost with this
meaning that when reciprocating tachycardia occurs it condition are theoretically preventable. In one study,
may be particularly persistent. Fortunately, most re- there was an overall 2% mortality in up to 15 years of
spond to medical therapy181. In adolescence, the atria are follow-up1151. In at least half of those patients who died
of a size that can support atrial fibrillation with the the risk could have been defined by their ventricular
attendant arrhythmic problems that this brings in those response rate in induced atrial fibrillation. We do not yet
patients with short antegrade refractory period acces- have the mandate to screen for WPW syndrome in all
sory pathways19-101. In the later years of life, accessory individuals (e.g. newborns or young schoolchildren) but
pathways may change their conduction properties at a there is a growing opinion that in those in whom WPW
time when initiating supraventricular and ventricular syndrome has already been identified, tests should be
ectopic beats become more common.
performed to establish the risk of the pathway1'71. In
It is difficult to judge the detriment of reciprocat- situations considered high risk, radiofrequency ablation
ing tachycardia in WPW syndrome. Much depends upon should be offered.
important but has been neglected. A definition requiring
a sustained arrhythmia of 30 s might be appropriate but
there are many individuals with organic troublesome
forms of SVT which occur in briefer salvos. A working
definition of 10 or more consecutive tachycardia beats is
more practical. Only rarely in normal individuals would
such salvos of supraventricular ectopic beats be found.
Supraventricular tachycardia
Para A V nodal reentry tachycardia
Permanent form ofjunctional reciprocating
tachycardia (PJRT)
PJRT is an interesting arrhythmia seen almost
exclusively in a paediatric population. It is now known
to be based upon an accessory AV node and a right
postero septal accessory pathway1233. The tachycardia
associated with this abnormality can be near incessant
and affected individuals may present with significant
cardiac decompensation. Occasionally the primary
diagnosis may be overlooked and the tachycardia
considered secondary to heart failure. PJRT is medically treatable and is also amenable to radiofrequency
ablation.
Atrial flutter
Atrial flutter is a poorly researched arrhythmia.
Considerable experimental evidence of its mechanism
exists but much less is known of its clinical impact and
treatment susceptibility. Reprehensibly, atrial flutter is
often lumped with atrial fibrillation and the two arrhythmias considered variants of each other. Atrial flutter is
very different from atrial fibrillation. It is based probably on a single macro reentrant circuit within the right
atrium'241. It may present as brief paroxysms or as a
sustained event. It can be a very debilitating arrhythmia
as AV nodal conduction may permit 2:1 ventricular
responses (with a typical ventricular rate of 140-150
beats . min" 1 ) or worse, 1:1 conduction which is often
associated with haemodynamic collapse. The possibility
of such incapacitation resulting from atrial flutter is the
reason this arrhythmia disbars airline pilots from flying,
in contrast with the more tolerant licensing approach to
atrial fibrillation'251.
Atrial flutter is relatively rare but becomes more
common as age advances. Its prevalence is unlikely to be
more than 15 per 1000 of a population aged 70 years or
older. An important management strategy is to control
AV nodal transmission before tackling the basic flutter
mechanism. Atrial flutter is very resistant to medical
therapy. The flutter cycle may be slowed but restoration
and maintenance of sinus rhythm is a greater challenge.
Identification of the reentrant circuit and areas of slow
conduction in the medial right atrium have prompted
the development of crude but modestly successful
radiofrequency ablation approaches'261.
Atrial fibrillation
Of all the supraventricular tachycardias, atrial fibrillation is by far the most common and the most important. It may affect up to 4% of individuals aged 70 years
or more. The risk of AF is measured by the presence
of underlying cardiovascular disease including myocardial infarction and hypertension'271 (Fig. 2). It has an
immediate haemodynamic impact as ventricular rate
control is disturbed. Cardiac emptying and filling is
disadvantaged by the changing cycle lengths and atrial
transport is lost. In susceptible individuals, particularly
those with globally impaired left ventricular function,
atrial fibrillation may have profound haemodynamic
consequences. Paroxysmal atrial fibrillation can occur
in apparently normal individuals. Whilst it might be
surmised that they should tolerate the arrhythmia
well, the reverse is often true. Many such patients are
devastated by the abrupt change in cardiac rhythm and
many feel relatively incapable of undertaking normal
activities while the arrhythmia is present. Atrial fibrillation also brings a risk of thromboembolism. The level
of risk depends upon whether or not there is associated
structural heart disease1281. Overall, AF increases the risk
of stroke and heart failure but perhaps surprisingly, not
of total mortality1271 (Fig. 3).
Management should be directed to establishing
and maintaining sinus rhythm or if that fails, the ventricular response rate should be controlled. Restoring
sinus rhythm may be through DC electro-version or by
medical cardioversion. There is renewed interest in the
power of drugs to convert AF and impressive success
rates have been recorded for class Ic drugs such as
propafenone129"301, flecainide1311 and amiodarone1321. If
sinus rhythm can be obtained, a period of observation
with no prophylactic drug therapy is reasonable. In
the event of recurrence, sinus rhythm should be
re-established and chronic prophylactic antiarrhythmic
therapy with drugs such as propafenone1331, flecainide1341,
beta-blockersl3S] or amiodarone13*1, considered. In addition to targeting the arrhythmia, management must
also take account of the thromboembolic risk as this
threatens quality and quantity of life.
Eur Heart J, Vol. 17, Suppl C 1996
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In adult reviews of SVTs, para AV nodal reentry tachycardias have been as numerous as arrhythmias due
to classical muscular atrioventricular accessory pathways'181. This might suggest a community prevalence of
up to two per 1000 individuals. The electrophysiological
hallmark of the arrhythmia has been considered as
functional duality of AV nodal conduction, but this
feature has been found in a high proportion of individuals with no history of para AV nodal reentry119'201.
Unlike WPW syndrome, para AV nodal reentry tachycardia poses no immediate risk of death. Quality of life
is threatened by relatively frequent and what may be
persistent tachyarrhythmic events. These may be resistant to medical therapy, more so than WPW syndrome
arrhythmias, and in the past, relatively high doses of
digoxin with or without additional verapamil or betablockers have been advocated. With the realization that
para AV nodal reentry tachycardia uses a retrograde
slow pathway closely applied to the AV node'211 but
distinct from it has come the possibility of curative
radiofrequency ablation'221. When arrhythmias prove
medically intractable this approach should be pursued.
23
24 R. W. F. Campbell
••
§
3.6 | p
2.8 £
2.2 £
1.4 0
>70
<50
I
Age
Risk
of
AF
MI
Angina
ST/T
| BP
i
2.1 | 1
Stroke
3.0 ^
•
1 Decreased
1.3
Risk
imposed
byAF
Heart failure
Total mortality
Increased k
Figure 3 Mortality, heart failure and stroke risk correlated with atrial
fibrillation (Krahn et al.[rn).
Conclusions
For too long supraventricular tachycardias have been
dismissed as an occasional nuisance. Few who see
arrhythmia patients would categorize SVTs in this
way. Regardless of the underlying cardiovascular state,
supraventricular tachycardias produce serious symptoms and can dramatically impair quality of life. Apart
from the obvious haemodynamic and thromboembolic
risks already discussed, the psychological impact of SVT
should not be underestimated. Patients feel insecure
and vulnerable when their hearts inexplicably accelerate
and they become aware of an abnormal cardiac rhythm.
Whilst many will respond to reassurance, many
others do not. Many fear for their lives each time the
arrhythmia occurs.
Supraventricular
tachycardias
frequently
threaten the quality of life but only rarely threaten life
Eur Heart J, Vol. 17, Suppl C 1996
itself. In the one circumstance in which that
occurs — Wolff-Parkinson-White syndrome and atrial
fibrillation — an aggressive curative management
strategy is appropriate. Radiofrequency ablation is the
treatment of choice for high risk accessory pathways.
For all other supraventricular tachycardias, the aim of
management should be to abolish attacks or at the least
to minimize the impact of attacks. This latter may
be achieved by significant lengthening of the interval
between attacks'33' or by a significant reduction in attack
duration. Powerful 'new' antiarrhythmic drugs like
propafenone, flecainide and amiodarone have been
extensively investigated against SVTs and have shown
impressive efficacy. It is time to abandon older remedies
which are less effective and which have a less attractive
adverse affect profile. With judicious use of drugs and
ablation the nuisance and threat of supraventricular
tachycardia can be controlled.
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Figure 2 Prevalence of atrial fibrillation related to age and to features of cardiovascular
disease: myocardial infarction (MI), angina, ECG ischaemia (ST/T) and hypertension (|BP)
(Krahn et alF7*).
Supraventricular tachycardia
25
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