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Europace (2002) 4, 215–218
doi:10.1053/eupc.2002.0250, available online at http://www.idealibrary.com on
AV-JUNCTIONAL ABLATION
Editorial
Between Scylla and Charybdis: a choice between equally
dreadful alternatives
On his long journey from Troy, Ulysses had to navigate
the Strait of Messina. On the Italian side was the rock
monster Scylla, on the Sicilian side was the whirlpool
Charybdis. To navigate between these obstacles in this
perilous passage, it was essential that Ulysses would
steer a steady course, lest he, his ship, and all his sailors
either be sucked to a watery grave by coming too close
to the whirlpool Charybdis or be devoured by the
monster Scylla.
His ablation or persistent conducted
arrhythmia?
The classic dilemma above often illustrates the situation of physicians who are forced to select between
treatment options for palliation of patients with
chronic long lasting diseases. In guarding against one
danger we often come close to, or succumb to,
another. The path of safety is seldom easily found.
Obviously, a similar analogy can be drawn by
choosing between options such as rate control and
rhythm control and/or drug therapy and nonpharmacological interventions when treating patients
with highly symptomatic atrial fibrillation.
Atrial fibrillation, which is the most common
supraventricular arrhythmia, can lead to cardiac dilatation and dysfunction[1]. Theoretically, restoration
of sinus rhythm should result in an improvement in
the patient’s symptoms as well as in cardiac function.
A comparable but not completely similar effect is
proposed to be obtained by a regular ventricular
paced rhythm[2]. This can be achieved by ablating the
atrio-ventricular (AV) junction followed by right ventricular (RV) apical pacing[3]. The reversibility of
Manuscript submitted 10 April 2002, and accepted 10 April 2002.
Correspondence: Luc Jordaens, MD, PhD, Department of Clinical
Electrophysiology, Thoraxcentre, Rotterdam, Dr Molewaterplein
40, 3015 GM, Rotterdam, The Netherlands. Tel: 31 10 463 3991;
Fax: 31 10 463 4420; E-mail: [email protected]
cardiac dysfunction after such an intervention was
one of the reasons that the concept of tachycardiomyopathy was introduced[4]. However, it is clear that
when atrial function is lost, the ventricular performance will suffer in the long term. Furthermore,
ablation does not influence the embolic risk and the
natural history, with respect to ischaemic stroke, is
not necessarily modified. On the other hand, AVjunctional ablation is an easy way to control ventricular rate and symptoms of patients referred with atrial
fibrillation[5]. Compared with more time consuming
approaches such as focal and/or linear ablations to
modify triggers and/or substrate, it is fast, and has a
high success rate, even in inexperienced hands. Therefore, it can be done in almost every intervention
laboratory (provided that an ECG machine with a
simple amplifier and an energy generator for radiofrequency generation are available). A real training
for electrophysiology (from a technical point of view)
is not necessary to complete this task, but in some
patients unexpected events may occur. After ablation,
pacemaker dependency is the rule requiring implantation of a VVIR system and orderly atrial electrical
activity is no longer thought to be present. This is a
disadvantage as it introduces device-related complications in to a patient’s life. This trade-off between
pacing and the original arrhythmia should be well
balanced.
Drugs or non-pharmacological intervention
for rate or rhythm control?
Inappropriately fast heart rates occur even during
minor exercise in patients with atrial fibrillation. This
is accompanied by depressed heart rate at peak
exercise in cases of left ventricular dysfunction.
Therefore, the aims of improving the patients’ functional ability can be reached by adequately controlling the rate. This attitude is supported by two recent
1099–5129/02/030215+04 $35.00/0 2002 The European Society of Cardiology. Published by Elsevier Science Ltd. All rights reserved.
216
Editorial
multicentre studies. These randomized trials presented at the Annual meeting of the American
College of Cardiology, Atlanta, 2002 suggest that
indeed rate control is equal to rhythm control in some
atrial fibrillation patients. The AFFIRM trial randomized patients to medical therapy either to restore
atrial rhythm or to control ventricular rate, whereas
the RACES trial compared rate control (achieved
by drugs) with rhythm control by electrical cardioversions. Basically, neither of these studies demonstrated any benefit for rhythm control. It, therefore,
can be believed that rate control alone is sufficient.
Patients often feel better in sinus rhythm. This is
certainly one of the reasons why novel nonpharmacological approaches were developed for
treating patients with atrial fibrillation. These interventions vary from ‘minor invasive’ approaches such
as implantation of an atrioverter, to complex, long
lasting interventional procedures such as pulmonary
vein and linear ablations. In the light of the results of
RACES and AFFIRM trials, however, it becomes
clearly more difficult to defend these interventions
unless the success rate will substantially rise. On the
other hand evidence has been presented that rhythm
control with antiarrhythmic drugs in heart failure has
disadvantages[6]. It seems therefore, that the above
mentioned complex interventions should be preserved
for patients who are highly symptomatic.
Survival or function: are the potential
advantages counterbalanced by increased
mortality?
The natural course of patients treated by AVjunctional ablation is still not known. Sudden death
has been reported in some subgroups of patients. It
was first attributed to the technique of DC shock
ablation[7], but, it was also observed after RF ablation[8]. In a meta-analysis of 21 studies with a total of
1181 patients, Wood et al. showed that the calculated
1-year mortality of ablation and pacing was comparable with medical therapy[5]. A considerable proportion of these deaths can be related to the acute effects
of AV-junctional ablation with QT prolongation and
slow pacing rate and/or unreliable escape rhythms[8,9].
Another subgroup of deaths was reported late after
AV-junctional ablation, mainly in patients with heart
failure[8]. The deterioration of pump function late
after AV-junctional ablation may play a role in this
mortality. Therefore, careful adjustment of the medical therapy for these patients with LV dysfunction is
very important including -blocker therapy, ACE
inhibitors, adjustment of electrolytes and avoidance
of antiarrhythmic therapy[7,10].
Europace, Vol. 4, July 2002
Symptoms and function: do we improve or
do we just palliate?
It is now generally accepted that supraventricular
incessant arrhythmias can lead to myocardial dysfunction and dilatation. Factors contributing to heart
failure when atrial arrhythmias are present are the
loss of an effective, well-timed atrial contraction and
the fast and irregular ventricular response. These
factors impair diastolic function and finally may lead
to tachycardiomyopathy. Although the advantage of
a regular ventricular response is important, RV apical
stimulation is not physiological because normal ventricular activation along the natural conduction system is not present or bypassed and the ventricles are
activated in an abnormal sequence. Despite these
theoretical disadvantages, several investigators
reported improvement in LV function after AVjunctional ablation in patients with permanent AF.
Interestingly enough this improvement was also seen
in patients without cardiomyopathy[11]. In contrast to
these findings, in recent studies left ventricular performance did not improve or deteriorated after this
treatment including the study by Bourke and colleagues[12,13]. Studies are convincingly showing that
quality of life indices significantly improved after
ablation of the atrio-ventricular junction. In the prospective multicentre randomized study of Brignole
and co-workers, a mixed population of patients with
atrial fibrillation and heart failure were recruited[14].
The ‘ablate and pace’ therapy was superior to drug
therapy in controlling symptoms, but the efficacy
appeared to be less than was observed in the
previously cited uncontrolled studies. Importantly,
objective cardiac performance did not show any
improvement with the treatment. This could be an
indication that different patients were investigated in
the above mentioned studies as left ventricular dysfunction could be a primary as well as a secondary
problem. Nevertheless, and this is important for
health care economy, less hospital admissions and
less doctor visits were necessary after ablation. So, it
seems that we do more than just palliation.
Do haemodynamics deteriorate or improve
after ablation?
That real tachycardiomyopathy will improve after
AV-junctional ablation in the short term is not a
surprise. That this improvement will be sustained for
several decades is still unproven. However, the
majority of patients treated by AV junctional ablation have no real tachycardiomyopathy, but long
standing or symptomatic atrial fibrillation. They will
Editorial
develop fibrotic tissue in the ventricles associated with
dilatation and it is not likely that they are going to
improve their function as the disease process is not
reversible. The evaluation of such deterioration is still
an issue, which should be clarified. Deterioration was
not shown by other investigators, as they measured
left ventricular function before ablation, and took
this as baseline, probably with serious technical limitations. In the study of Bourke et al., as well as in our
former study the LV ejection fraction (LVEF) was
measured several days after AV-junctional ablation
and was compared with a measurement taken months
later[12,13]. This approach allows measurements to be
performed under exactly the same conditions regarding heart rate and regularity. Furthermore, LVEF
measured by means of radionuclide ventriculography
(RNV) is more reproducible and has an error of less
than 3%. RNV seems less sensitive to the errors
caused by the deformed right ventricular geometry
during RV pacing because measurement is based on
planimetry.
Right ventricular apex or alternative pacing
sites?
The results showing the deleterious effect of right
ventricular apex pacing prompted the investigation of
alternative pacing sites, to preserve ventricular performance. Although the advantage of a regular ventricular response seems to be important[2], RV apical
stimulation is not physiological because normal ventricular activation along the natural conduction system is bypassed and the ventricles are activated in an
abnormal sequence. Chronic apical ventricular pacing
is associated with myocardial cellular changes and
leads to dysfunction of the left ventricle[15]. Diastolic
function improved in studies with right ventricular
outflow pacing, when the function was diminished at
baseline[16]. In contrast, Bourke and colleagues
demonstrated slight deterioration of diastolic function[13]. This suggests that not all patients will benefit
from this pacing modality. Theoretically, multisite,
or biventricular pacing may resynchronize the contraction pattern of the ventricles, in patients with
heart failure and ventricular dyssynchrony. Recoordination of the activation pattern can normalize
the so called functional mitral regurgitation and may
optimize left ventricular filling. Indeed, recent data
confirmed that patients in atrial fibrillation may
also benefit, but to achieve sufficient pacing time
catheter ablation of the atrioventricular node is often
required[17].
Although Ulysses survived one of the obstacles a
whirlpool called Charybdis, he came too close to
217
Scylla, a dreadful sea monster and lost six of his sailors
from the ship.
Since AV-junctional ablation is an alternative way of
rate control it still can be considered as a potential
treatment for symptomatic patients or for patients
when the primary aim is to improve quality of life as
addressed by the AIRCRAFT investigators[18]. However, it seems that cardiac function does not improve
or may decline in a considerable proportion of the
patients. Therefore, approaches, which may preselect
these patients or offer alternative pacing strategies for
preserving ventricular performance, would have a
role in their treatment. Until we understand how and
when to do this, we will certainly lose some of the
benefit for some of the patients.
LUC JORDAENS; TAMAS SZILI-TOROK
Department of Clinical Electrophysiology,
Thoraxcentre,
Erasmus Medical Centre Rotterdam,
The Netherlands
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