Paolo Terranova, MD
*,†; Barbara Severgnini, MD
†;
Paolo Valli, MD
†; Simonetta Dell'Orto, MD
†;
Enrico Maria Greco, MD
†
*U.O. Cardiologia e UTIC, Azienda Ospedaliera "S. Paolo"
- Polo Universitario, Department of Medicine, Surgery and Odontoiatry,
University of Milan, Italy.
†U. O. di Cardiologia, Presidio Ospedaliero "Causa Pia
Ospedaliera Uboldo", Cernusco sul Naviglio, Azienda Ospedaliera di
Melegnano, Milano, Italy.
Address for
correspondence: Dott. Paolo Terranova, MD, U. O. Cardiologia, A.
O. "S. Paolo", Dept. Medicine, Surgery and Odontoiatry
University of Milan, Italy. E Mail: Paolo.Terranova@unimi.it
Abstract
Pacing
prevention algorithms have been introduced in order to maximize the
benefits of atrial pacing in atrial fibrillation prevention. It has
been demonstrated that algorithms actually keep overdrive atrial
pacing, reduce atrial premature contractions, and prevent short-long
atrial cycle phenomenon, with good patient tolerance. However, clinical
studies showed inconsistent benefits on clinical endpoints such as
atrial fibrillation burden. Factors which may be responsible for
neutral results include an already high atrial pacing percentage in
conventional DDDR, non-optimal atrial pacing site and deleterious
effects of high percentages of apical ventricular pacing. Atrial
antitachycardia pacing (ATP) therapies are effective in treating
spontaneous atrial tachyarrhythmias, mainly when delivered early after
arrhythmia onset and/or on slower tachycardias. Effective ATP therapies
may reduce atrial fibrillation burden, but conflicting evidence does
exist as regards this issue, probably because current clinical studies
may be underpowered to detect such an efficacy. Wide application of
atrial ATP may reduce the need for hospitalizations and electrical
cardioversions and favorably impact on quality of life. Consistent
monitoring of atrial and ventricular rhythm as well as that of ATP
effectiveness may be extremely useful for optimizing device programming
and pharmacological therapy.
Key Words: Antitachycardia;
Atrial fibrillation; Pacing; Prevention algorithms.
Introduction
Atrial fibrillation is surely the most common arrhythmia in clinical
practice and nowadays its incidence is increasing mainly due to the
progressive ageing of population. Atrial fibrillation represents also
the cardiac rhythm disorder that causes the highest number of
hospitalizations
1 and is
associated with higher mortality
2,
major clinical complications such as heart failure, acute myocardial
infarction, stroke
3, and
impaired quality of life
4.
Atrial fibrillation is frequently associated with ventricular
tachyarrhythmias. It has been calculated that 20% of the patients with
conventional indication for cardioverter defibrillator implantation had
atrial fibrillation before implant and that during the lifespan of the
device more than 50% may develop atrial fibrillation
5,6. Antiarrhythmic drugs
have been widely used for cardioversion and maintenance of sinus
rhythm, but they showed a limited and usually temporary efficacy
7. As a consequence, several
non-pharmacological therapies, including physiological pacing, pacing
prevention algorithms, anti-tachycardia pacing therapies and low-energy
internal cardioversion have been introduced to treat drug refractory
patients and have been implemented in multifunction implantable devices
8.
Pacing prevention algorithms
Antiarrhythmic
benefits of atrial and dual-chamber pacing versus single-chamber
ventricular pacing in reducing atrial fibrillation recurrences and in
preventing progression to permanent atrial fibrillation have been
clearly demonstrated in large prospective trials enrolling either sinus
node disease patients or unselected patients candidate for pacemaker
implantation
9-11.
It has also been suggested that availability of rate responsiveness may
maximize the effect of physiological pacing
12.
Pacing prevention algorithms have been introduced in order to maximize
the preventive benefits of atrial pacing. Specific mechanisms involved
in atrial fibrillation prevention by pacing algorithms include
premature atrial contraction suppression or conditioning, with fewer
chances to initiate atrial fibrillation, short-long atrial cycle
prevention and maintenance of a high degree of exit block from all
natural subsidiary atrial pacemakers. Several algorithms have been
introduced by the different manufacturers during the last years. To
summarize, they may be classified as follows: 1) dynamic sinus rhythm
overdrive, 2) premature atrial beat reaction (short-long cycle
prevention and ectopy overdrive), 3) post-tachycardia overdrive to
prevent early recurrence of atrial fibrillation, and 4) prevention of
inappropriate rate fall after exercise. The atrial pacing preference
algorithm was the first evaluated, before being implemented in market
released devices, as a temporary software, named "consistent atrial
pacing", which could be downloaded into a conventional dual-chamber
pacemaker via telemetry using a custom research telemetry device. It
included a diagnostic which could be interpreted by a special Microsoft
Excel spreadsheet. Diagnostic data were available also when the
algorithm was switched off (suspended). The reliability and
effectiveness of such algorithm was evaluated in a prospective
randomized pilot study in which 61 patients with brady-tachy syndrome
were enrolled and implanted with a rate responsive dual-chamber
pacemaker
13. After
downloading of the algorithm, patients were randomly assigned to
algorithm programming "on" or "suspended", with crossover after 1
month. Consistent atrial pacing induced an increase in atrial pacing
percentage from 77 to 96%, and was associated with an 80% reduction of
premature atrial contractions' number. Atrial fibrillation recurrences
were not reduced in the overall population, but they significantly
decreased by 42% when considering the patients in whom the atrial
pacing percentage was < 90% during the algorithm "suspended" period.
Algorithm tolerance was good with no severe adverse events. The atrial
rate stabilization algorithm has been evaluated (alone or combined with
consistent atrial pacing) in 16 patients with brady-tachy syndrome
14. With regard to the effects on atrial
fibrillation burden, 11 patients (69%) were found to benefit
significantly from the consistent atrial pacing or atrial rate
stabilization algorithms (reduction > 50% of atrial fibrillation
burden). In detail, 7 patients were responders to both algorithms, 2 to
consistent atrial pacing only, and 2 to atrial rate stabilization only.
The ability of
the post-mode switching overdrive algorithm to stabilize the atrial
rate after termination of treated atrial arrhythmias has been studied
in 15 patients with structural heart disease and documented atrial and
ventricular arrhythmias, receiving a Jewel AF device
15. The algorithm was active in 41% of
600 spontaneous atrial tachyarrhythmia episodes. It was capable of
driving and stabilizing the atrial rhythm in the presence of slow
spontaneous atrial rhythm or premature atrial beats with normal
atrioventricular conduction. In case of premature atrial beats with any
degree of atrioventricular block, the algorithm stabilized the
ventricular rate. The authors concluded that the algorithm is reliable
and might be of benefit for atrial arrhythmia treatment.
Efficacy of
preventive pacing algorithms has been confirmed by the preliminary
results of the AF Therapy Study
16.
In 97 patients with a history of paroxysmal atrial fibrillation of at
least 1 year, who had experienced at least three episodes during the
last 3 months and were refractory to drug therapy, activation of four
different preventive algorithms was associated with a significant
improvement in all pre-selected endpoints: atrial fibrillation burden,
average sinus rhythm duration, mean time in-between atrial arrhythmia
episodes and number of patients free of atrial arrhythmias lasting >
1 min. All benefits were observed either in patients with or without
conventional indication for pacing. Similarly, in the ADOPT trial
17, in which 320 patients were enrolled
in a parallel design with randomization to algorithms on vs. off,
symptomatic atrial fibrillation burden was reduced by 25% in the
treatment group. On the contrary, atrial fibrillation episode number,
quality of life and hospitalizations did not differ between the two
randomization arms. An important criticism of ADOPT trial was that only
symptomatic AF was used as an end-point.
Also, a
retrospective analysis by the ADOPT investigators presented in Heart
Rhythm 2004 suggested that less ventricular pacing is associated
with less AF recurrence (although the results did not reach statistical
significance). Concern about the actual effectiveness of prevention
algorithms in improving clinical outcome has been raised by the
conflicting results
18,19
of the most recently published studies in which arrhythmia burden was
usually selected as the main endpoint. To explain that, the interaction
with other critical factors has been claimed, first of all the atrial
pacing site. It is well known that atrial pacing from the right atrial
appendage is associated with a prolonged P wave duration with
unfavorable effects on atrial conduction and refractoriness. Clinical
studies suggest that combining prevention algorithms with interatrial
septal pacing may lead to better clinical outcome
20. Furthermore, the hemodynamic negative
effects of unnecessary ventricular pacing in dual-chamber pacing
systems may counterbalance the preventive role of pacing algorithms.
Blanc et al.
21 demonstrated
that pacing algorithms could reduce the atrial arrhythmia burden only
in patients with ventricular pacing percentage < 70%. In the MOST
study
22, in patients with
sinus node disease, atrial fibrillation recurrences had reverse
relationship with ventricular pacing percentage. Moreover, the OASES
trial
23 showed that the AF
Suppression algorithm was even more effective when the atrial lead was
implanted in the low atrial septum. In patients with right atrial
appendage leads, the algorithm reduced AF burden as measured by
mode-switches by 49%, whilst in patients with low atrial septal leads,
the AF burden was reduced by 70%. However, whereas the ADOPT and OASES
trials showed that this AF suppression algorithm reduces AF, trials
testing other algorithms have not shown a similar efficacy. The ATTEST
trial
24 evaluated the
efficacy of overdrive pacing, and high-rate pacing algorithms in
patients with AF and an indication for pacing. There were no
statistically significant differences in recurrence of symptomatic AF
or in AF burden. ATP terminated 54% of atrial tachycardia episodes, but
high-frequency pacing could not terminate AF. Another subsequent trial,
quite similar to OASES one, the ASPECT
25,
showed that pacing from the atrial septum resynchronizes the atrium and
provides an antiarrhythmic effect that enhances the efficacy of the
suppression algorithms.
It is very
important to recognize the differences between these trials. The ADOPT
17 and OASES trials
23 tested the efficacy of a single
algorithm to prevent AF, whereas ATTEST
24
tested the efficacy of 3 preventive pacing algorithms and 2 pacing
algorithms designed to terminate atrial tachyarrhythmias. Moreover, the
follow-up in ATTEST trial was 3 and not 6 months. Another matter with
the OASES and the ASPECT trials was the crossover design. Because the
beneficial effect of atrial pacing may persist, this design may have
limited the observed efficacy of the pacing algorithms. Thus the
difference in results between these trials may reflect differences in
study design or differences in the efficacy of the algorithms
used. Finally, due to high variability of atrial fibrillation
recurrence patterns
26,
published studies may be underpowered to demonstrate the true benefits
of prevention algorithms.
In summary, 2
trials have shown that AF suppression algorithms enhances the
antiarrhythmic effects of atrial pacing in patients with AF and an
indication for pacing. Thus, minimizing ventricular pacing and placing
the atrial lead in the septum may probably enhance the efficacy of
these algorithms.
Atrial antitachycardia pacing to
treat atrial tachyarrhythmias
It has been
demonstrated that rapid atrial pacing delivered for treating atrial
tachycardia or atrial flutter may be effective in restoring sinus
rhythm in 60-90% of patients
27.
Maximal effectiveness can be usually obtained by delivering
antitachycardia pacing at a rate that is slightly greater than the
atrial arrhythmia rate. Delivering of some extrastimuli following a
rapid pacing train may be more efficacious than overdrive atrial pacing
at the same pacing cycle length in terminating atrial flutter
28. High-frequency pacing may change
atrial tachycardia in transient atrial fibrillation with later sinus
rhythm restoration. Appropriate detection of atrial tachyarrhythmias
and efficacy of pacing therapies in patients receiving a dual
defibrillator have been evaluated in large series. Adler et al.
29 reported on 537 patients with
ventricular arrhythmia implanted with the Medtronic 7250 dual
defibrillator (Medtronic Inc., Minneapolis, MN, USA) who were enrolled
in the Worldwide Jewel AF Study and followed on average for 1 year.
Seventy-four percent had a documented history of prior atrial
tachyarrhythmias. Seventy-one percent of the patients had atrial
therapies enabled at some time during the follow up, allowing
collection and analysis of 3500 atrial episodes from 167 patients. In
the 7250 Dual Defibrillator Italian Registry
30,
105 patients were enrolled. Implant indication was represented by
combination of ventricular and atrial tachyarrhythmias in 52% of
patients, ventricular tachyarrhythmias only in 33%, and atrial
tachyarrhythmias only in 14%. During a mean follow-up of 6 months, 863
treated atrial episodes were collected and analyzed. Gold et al.
31, on behalf of the Worldwide Jewel
AF-Only Investigators, studied 146 patients with recurrent drug
refractory atrial fibrillation without prior ventricular
tachyarrhythmias, who were implanted with a dual defibrillator and were
followed on average for 1 year. During the follow-up 4913 treated
episodes were available for stored electrogram analysis and therapy
efficacy evaluation. Atrial tachyarrhythmia detection was very good in
all the studies with a positive predictive value of atrial detection
ranging from 91 to 99%. The most common reasons of inappropriate
detection were represented by far-field R-wave oversensing during sinus
rhythm or cluster of premature atrial contractions. Reprogramming of
atrial sensitivity allowed in some case avoidance of inappropriate
detection due to far-field R-wave oversensing. Sensitivity of atrial
tachycardia and fibrillation detection and validation of continuous
detection of atrial tachyarrhythmias have been specifically addressed
by Swerdlow et al.
42 who
performed 80 Holter recordings with telemetered atrial electrograms in
58 patients, implanted because of combination of atrial and ventricular
arrhythmias. Continuous detection of atrial tachyarrhythmia could be
demonstrated in 96% of patients with spontaneous episodes. Atrial
sensitivity for arrhythmia detection was 100%. It is worthwhile to
stress that the atrial arrhythmia detected at very early onset was very
commonly a well organized atrial tachycardia. Among 2380 episodes in
the worldwide series, 63% were classified as atrial tachycardia (mean
atrial cycle 278 ± 56 ms) and 37% as atrial fibrillation (mean
cycle 204 ± 35 ms). In the Italian Registry, among 863 atrial
episodes, 53% were automatically classified by the device as atrial
tachycardia and 47% as atrial fibrillation. After revision of the
stored data, among 843 appropriately detected episodes, 55% were
clinically classified as atrial fibrillation and 45% as atrial
tachycardia. In the AF-Only group, among 3116 episodes treated by
antitachycardia pacing, 67% were classified as atrial tachycardia.
Efficacy of
antitachycardia pacing therapy in the three series is reported in
Table 129-31. The efficacy was estimated in two
ways: 1) crude estimate, defined as the proportion of successful
terminations out of the total number of treated episodes; 2) adjusted
estimate, using the generalized estimate equation method
30 which allows adjusting estimate for
multiple episodes within a patient through a correlation structure
between episodes and patients.
Table 1: Efficacy of antitachycardia
pacing on spontaneous atrial tachyarrhythmias (AE = Adjusted Estimate;
CE = Crude Estimate; CI = Confidence Interval).
In the
worldwide study
29-31,
a subanalysis performed to compare the efficacy of burst+ vs. ramp
therapy for atrial tachycardia did not find any significant difference
between the two therapies. An history of atrial flutter was the only
independent predictor of pacing efficacy for atrial tachycardia, while
no independent predictors could be identified for atrial fibrillation.
No comparison was feasible between burst+ or ramp and high-frequency
burst because the last was usually applied after unsuccessful delivery
of burst+ or ramp therapy.
Pooling all
antitachycardia pacing therapies (burst+, ramp and 50 Hz burst), their
efficacy consistently increased as far as atrial arrhythmia cycle
lengthened. As a matter of fact, in the Italian Registry, while the
relationship between efficacy of atrial burst+ and ramp vs. atrial
cycle length was very high (r2 = 0.85, p < 0.001), the relationship
between efficacy of 50 Hz burst and atrial cycle length was very poor,
with a trend toward a reverse correlation (r2 = 0.31, p < 0.05).
Such a difference could be explained by taking into account the
mechanisms of action of different antitachycardia pacing techniques.
During overdrive pacing, the wavefront of pacing stimulus enters the
reentrant pathway in the antidromic and orthodromic direction. The
antidromic wavefront blocks by collision the arrhythmia wavefront,
while the orthodromic wavefront may either reset the tachycardia or
stop it, when early enough to be blocked in a refractory area. Slower
tachycardias, due to a wider excitable gap, may be more easily
terminated in this way. Termination of atrial tachyarrhythmias by
high-frequency pacing is typically preceded by tachycardia
acceleration, which becomes unable to be sustained, hence resulting in
arrhythmia termination and sinus rhythm restoration. It has been
hypothesized that high-frequency pacing induces a new faster reentrant
circuit which is unable to sustain itself
34.
This mechanism looks independent of the arrhythmia cycle.
Looking at
individual patients, random and wide distribution of median atrial
cycles at onset during the follow-up was observed in the majority of
them. A subgroup showed a narrow Gaussian distribution along either a
fast (200 ms) or a slow band (250 ms). Antiarrhythmic drugs have been
demonstrated to be capable of modifying atrial cycle profile.
Antiarrhythmics may modify the electrophysiological properties of the
atria and the arrhythmia organization pattern by lengthening the mean
atrial arrhythmia cycle and by widening the temporal excitable gap
35-37. Dijkman and
Wellens
38 demonstrated that
atrial arrhythmias in defibrillator patients with structural heart
disease, receiving class III antiarrhythmic drugs, frequently had
longer cycle lengths than atrial fibrillation. In fact, among 600
spontaneous episodes, atrial fibrillation was diagnosed in 19%, fast
polymorphic atrial tachycardia in 20%, fast monomorphic atrial
tachycardia in 57%, and slow atrial tachycardia in 4%. Drug-induced
atrial cycle length changes may impact on atrial antitachycardia pacing
therapy efficacy. In spite of that, in the AF-Only series there were no
drugs that were independent predictors of therapy efficacy.
Finally,
increasing the delay from arrhythmia detection to therapy delivery was
associated with a significant reduction in efficacy. Optimal delay has
been identified in less than 5 min in the Worldwide Study and in less
than 1 min in the Italian Registry. That was probably due to the fact
that the majority of atrial tachyarrhythmias accelerated in few minutes
after onset. Considering that slower arrhythmias can be more easily
treated by pacing techniques, a short delay in therapy delivery should
be recommended. The efficacy of 50 Hz burst on atrial fibrillation may
be a matter of debate. Wide local capture of atrial fibrillation has
been documented
39. Data
from canine studies suggested that high-frequency pacing could
accelerate the local atrial fibrillation cycle length and destabilize
the reentrant rhythm so that destabilized atrial fibrillation could be
converted to sinus rhythm in some cases. Anyway, in humans termination
of persistent atrial fibrillation by high-frequency pacing could never
be demonstrated
40-41.
High-frequency pacing may terminate induced atrial fibrillation during
electrophysiological study with a 33% efficacy rate
34 and atypical atrial flutter with a 60%
efficacy rate
41. In
selected cases, local capture of new-onset atrial fibrillation and
entrainment of a relatively large area of the atria
42 could have destabilized the arrhythmia
by reducing the number of wavelets of the random reentry, hence
preventing arrhythmia sustenance. Anyway, considering that
arrhythmia classification is based on atrial activity at atrial lead
site, misclassification of atrial tachycardia as atrial fibrillation
cannot not be excluded. Furthermore, some episodes may have terminated
spontaneously after therapy delivery
43.
The ASPEN-ICD
and ASSIST trials will probably give more data about these new
perspectives. They will test the algorithm in patients with ICDs.
The former will determine if the first episodes of AF can be prevented
by the algorithm, whereas the latter will test if this algorithm
prevents AF in patients who have a history of atrial arrhythmia.
Safety of
antitachycardia pacing therapy was excellent since no ventricular
arrhythmia induction was observed in any case after antitachycardia
pacing delivery. These data suggest that, on a large scale, these
algorithms would presumably be safe, and that it would be necessary to
better determine how effective atrial ATP is, and whether it would
reduce hispitalizations and/or electrical or pharmacological
cardioversions and thereby improve quality-of-life.
Conclusions
As stated in
the discussed trials, pacing prevention algorithms should probably be
better and further evaluated, before having a definitive and
comprehensive answer on their utility. Clinical studies showed
inconsistent clinical benefits of the algorithms, although they reduce
atrial fibrillation triggers such as premature atrial complexes, thus
preventing short-long cycle phenomenon. Factors which may be
responsible for neutral results include: 1) high atrial pacing
percentage in conventional DDDR, 2) non-optimal atrial pacing site, 3)
deleterious effects of high percentages of ventricular pacing, and 4)
inappropriate study design and endpoint selection. Variability of
atrial arrhythmia recurrence patterns and onset mechanisms suggest
individual programming of prevention algorithms by using data stored in
the device memory. Atrial antitachycardia pacing is an effective tool
to treat atrial tachyarrhythmias and it may stop nearly 50% of
arrhythmia episodes. In particular, all previously described data are
more related to atrial tachycardia reduction than to atrial
fibrillation decrease. Delivery of atrial therapies early after
arrhythmia onset and on more organized arrhythmias may improve success
rate. Associated use of antiarrhythmic drugs, mainly propafenone and
flecainide, may further increase effectiveness by lengthening atrial
arrhythmia cycle.
Effective
antitachycardia pacing therapies may reduce atrial fibrillation burden,
but conflicting evidence does exist as regards this issue, probably
because current clinical studies may be underpowered to detect such an
efficacy. Consistent monitoring of atrial and ventricular rhythm as
well as that of antitachycardia pacing effectiveness may be extremely
useful for optimizing device programming and pharmacological therapy.
At present the efficacy of pacing algorithms to prevent AF is by no
means something that has been proved beyond reasonable doubt, so that
more large-scale prospective trials are needed to answer this question.
Our information is currently based on small trials and any attempt to
extrapolate these data to the general population will probably produce
inaccurate results. Clinical endpoints should be further
investigated in future studies.
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