Download Conventional and biventricular pacing in patients with first

REVIEW
Europace (2012) 14, 1414–1419
doi:10.1093/europace/eus089
Conventional and biventricular pacing in patients
with first-degree atrioventricular block
S. Serge Barold* and Bengt Herweg
Florida Heart Rhythm Institute, Tampa, FL, USA
Received 23 December 2011; accepted after revision 14 March 2012; online publish-ahead-of-print 19 April 2012
Recent reports suggest that first-degree atrioventricular block is not benign. However, there is no evidence that shortening of the PR interval
can improve outcome except for symptomatic patients with a very long PR interval ≥0.3 s. Because these patients require continual forced
pacing, biventricular pacing should be used according to accepted guidelines for third-degree AV block. Functional atrial undersensing may
occur in patients with conventional dual-chamber pacing and first-degree AV block because the sinus P-wave tends to be displaced into the
post-ventricular atrial refractory period (PVARP) an arrangement that may cause a pacemaker syndrome. Prevention requires programming a
shorter AV and PVARP that is feasible because retrograde conduction is rare in first-degree AV block patients. A relatively new pacing mode
to minimize right ventricular stimulation has been designed by eliminating the traditional AV interval but with dual-chamber backup. This
pacing mode permits the establishment of very long AV intervals that may cause pacemaker syndrome. About 50% of patients undergoing
cardiac resynchronization therapy (CRT) have a PR interval ≥200 ms. The CRT patients with first-degree AV block are prone to develop
electrical desynchronization more easily than those with a normal PR interval. The duration of desynchronization after exceeding the upper
rate on exercise is also more pronounced. AV junctional ablation is rarely necessary in patients with first-degree AV block but should be
considered for symptomatic functional atrial undersensing or when the disturbances caused by first-degree AV block during CRT cannot
be managed by programming.
----------------------------------------------------------------------------------------------------------------------------------------------------------Keywords
Cardiac pacing † Biventricular pacing † Pacemaker syndrome † Cardiac resynchronization † First-degree
atrioventricular block † Long PR interval
The PR interval represents the time needed for an electrical
impulse from the sinoatrial node to conduct through the atria,
the atrioventricular node (AVN), the bundle of His, the bundle
branches, and the Purkinje fibres. Thus, PR interval prolongation
or first-degree AV block may be due to conduction delay within
the right atrium, the AVN, the His–Purkinje system, or a combination of these. A long PR interval is much more commonly caused
by dysfunction of the AVN than by conduction impairment in the
His– Purkinje system. If the QRS complex is of normal duration and
configuration, then the conduction delay is almost always at the
level of the AVN. Occasionally, the conduction delay can be the
result of an intra-atrial conduction defect. PR prolongation is
common in patients receiving cardiac resynchronization therapy
(CRT). In the Comparison of Medical Therapy, Pacing, and Defibrillation in Heart Failure (COMPANION) trial, a study of patients
in whom resynchronization was considered necessary, about 50%
of patients had PR intervals ≥ 200 ms.1
Prognosis of first-degree
atrioventricular block
Epidemiological data from the Framingham Study have shown that
first-degree AV block (PR intervals .200 ms, the electrocardiographic (ECG) equivalent of AV prolongation) is associated with
increased risk of all-cause mortality in the general population.2
The PR prolongation .200 ms (excluding AV nodal blocking
drugs) increased the risk of atrial fibrillation two-fold and pacemaker implantation three-fold.2 However, the prognostic effects
of first-degree AV block were not evaluated in patients with established coronary artery disease (CAD). A recently published study
demonstrated that over a follow-up of 5 years, patients with
stable CAD and PR ≥ 220 ms had a significantly higher risk of
reaching the combined end point of heart failure (HF) or cardiovascular death.3 First-degree heart block itself causes no symptoms
and generally needs no treatment and it is likely that it is simply
* Corresponding author. Tel: +1 813 891 1922; fax: +1 813 891 1908, Email: [email protected]
Published on behalf of the European Society of Cardiology. All rights reserved. & The Author 2012. For permissions please email: [email protected].
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Conventional and biventricular pacing
associated with more severe disease. These new findings challenge
previously held assumptions that PR prolongation or first-degree
AV block has a benign prognosis. These data, however, do not
suggest that shortening the PR interval could improve outcomes
or that a prolonged (unless the prolongation is marked or
.0.30 s in selected patients4) PR interval causes serious adverse
haemodynamic consequences per se.
Conventional pacing
Although there is little evidence to suggest that pacemakers
improve survival in patients with isolated first-degree AV block,
it is now recognized that marked (PR ≥ 0. 30 s) first-degree AV
block can cause symptoms similar to those in the pacemaker syndrome even in the absence of higher degrees of AV block.4 – 6 Uncontrolled trials have shown that symptoms of many patients with
a PR interval ≥0.30 s can be improved with dual-chamber pacing
regardless of left ventricular (LV) function but especially in patients
with normal LV function.
In the setting of a very long PR interval, one must remember that
some patients with inter-atrial conduction delay may already be
haemodynamically compensated because delayed conduction to
the left atrium may be associated with an appropriately timed
mechanical left AV synchrony, a situation where a pacingcontrolled AV delay would not be expected to produce further
haemodynamic improvement.7
Implantation of a conventional dual-chamber pacemaker may
improve cardiac performance on a short-term basis in a minority of patients with severe HF, first-degree AV block, and a
narrow QRS complex.4 Conventional DDD pacing abolishes
pre-systolic mitral regurgitation and increases the time for
forward flow. However, elimination of diastolic mitral regurgitation plays as yet an undefined but probably small role in the
overall haemodynamic benefit but it may result in more
optimal haemodynamic performance because of a lower-left
atrial pressure and higher LV preload at the onset of systole.4
However, DDD pacing with right ventricular (RV) stimulation
in patients with a PR interval ≥300 ms may induce long-term
deterioration of LV function, because the device is committed
to forced RV pacing 100% of the time. Long-term deterioration
of LV function during DDD or DDDR pacing may eventually necessitate an upgrade to biventricular pacing. It would therefore
seem prudent at the outset to consider the implantation of a
biventricular DDD or DDDR device even with a narrow QRS
complex in patients with an LV ejection fraction ≤ 35% by
using the recommendations for complete AV block where
pacing is also expected for a high percentage of the time
(New York Heart Association, NYHA, class I in the American
guidelines and NYHA class II in the European guidelines).5,6
There is a need to study the impact of biventricular pacing in
patients with HF due to diastolic dysfunction with a normal
LV ejection fraction and narrow QRS.
Functional atrial undersensing
The combination of a relatively fast sinus rate and long PR interval
with a suboptimally programmed pacemaker provides the
appropriate setting for the development of functional atrial undersensing [by pushing the P-wave into the post-ventricular atrial refractory
period (PVARP) and also into the post-ventricular atrial blanking
period].8 – 17 This situation may cause symptoms similar to the pacemaker syndrome. Bode et al. 8 who studied 255 pacemaker patients
with Holter recordings found 9 patients with atrial undersensing
despite an adequate atrial signal. All nine patients exhibited substantial
delay of spontaneous AV conduction (284 + 61 ms, range 230–
410 ms). In these patients, the P-waves fell continually within the
PVARP of 276 + 26 ms (no PVARPs functioned with automatic extension in response to ventricular extrasystoles). When functional
atrial undersensing occurs, the ECG shows sinus rhythm, a long spontaneous PR interval and conducted QRS complexes but no pacemaker stimuli. The conducted QRS complexes activate the
ventricle while the P-waves remain trapped in the PVARP. The pacemaker itself acts as a ‘bystander’ in that it can initiate the pacemakerlike syndrome but the ECG then shows no pacemaker activity. Bode
et al.8 also observed that functional atrial undersensing could be
initiated and terminated by appropriately timed atrial and ventricular
extrasystoles. Functional atrial undersensing should theoretically continue indefinitely as long as the atrial rate remains relatively fast and
constant. It will, however, terminate when slowing of the sinus rate
produces a PP interval longer than the implied total atrial refractory
period (TARP) which is the sum of the intrinsic PR interval (not the
programmed AV delay) and the programmed PVARP. Programming a
shorter PVARP (using no extension after a ventricular premature
beat and avoiding algorithms for the automatic termination
of pacemaker-mediated tachycardia by PVARP extension) and a
shorter AV delay may prevent functional undersensing. A relatively
short PVARP involves little risk of pacemaker-mediated tachycardia
because patients with a prolonged PR interval are much less likely
to demonstrate retrograde VA conduction.18,19 One should avoid
sensor-varied and auto-PVARP functions because they function
with a relatively long PVARP at rest that shortens with activity.
Functional atrial undersensing may respond to noncompetitive
atrial pacing which is a programmable function that promotes AV
resynchronization by delivering a premature but appropriately
delayed atrial stimulus 300 ms after atrial activity is detected in the
PVARP.
Ablation of the atrioventricular junction
Ablation of the AV junction with resultant complete AV block
should be considered in difficult situations as a last resort
therapy where the symptomatic disturbances by first-degree
AV block cannot be eliminated by reprogramming the
pacemaker.20
Right atrial pacing
Atrial pacing should be performed from the low atrial septal region
near the coronary sinus where the paced P-wave and the PR interval are shorter than with right atrial pacing.21 A low atrial pacing
site would also target an associated inter-atrial conduction delay.
A shorter PR interval during atrial pacing may even make functional
AAI pacing feasible in some patients.
1416
First-degree atrioventricular block
with pacemakers designed to
minimize or prevent right
ventricular stimulation
The concern about the impact of long-term RV pacing on LV function, has fostered the development of a new class of pacemaker
characterized by elimination (rather than prolongation) of the traditional AV interval in favour of atrial pacing with dual-chamber
backup in the case of AV block.22 – 29 In the Medtronic Managed
Ventricular Pacing (MVP) system during the AAI(R) mode, the
device permits the establishment of very long PR intervals
without the emission of a ventricular output (VP). The very long
AV or PR intervals (AP– VS or AS –VS) will persist as long as a
sensed ventricular event (VS) occurs before the sensed atrial
event (AS) or the expected atrial stimulus (AP). The AV uncoupling with such long AV delays may degrade pump function in
patients with LV dysfunction.27 The Sorin AAISafeR pacing mode
works the same way as the Medtronic device except that it activates dual-chamber pacing after a number of very long AV intervals
within a programmable range (upper duration ¼ 450 ms).28,29 Such
a pacemaker response to a long PR interval is not available in the
Medtronic design.
Sweeney et al. 30 recently reported the results of a large study in
ICD recipients in whom two groups of patients were compared:
pacing in the DDD mode with MVP (rate 60) vs. VVI mode (rate
40). There were 101 patients with a PR interval .230 ms (mean
255–260) with a follow-up mostly for 2 years. The patients with a
long PR interval and MVP revealed a 2.8× increased risk of combined end point of death + HF hospitalizations/HF urgent care compared with the long PR patients in the VVI 40 group (P ¼ 0.019).
There was no direct comparison of regular DDD vs. DDD MVP
pacing. The findings suggest that a long PR interval is a marker for
worse heart disease (aggravated by RV pacing in the study) rather
than a detrimental consequence of the MVP algorithm.
The AAI(R) pacing with a very long PR interval is a well-known
cause of pacemaker syndrome.31 This form of pacemaker syndrome has resurfaced recently during the MVP or the AAISafeR
mode when AS or AP initiates a very long AV or PR intervals.26
These pacing modes are contraindicated in patients with marked
first-degree AV block and those with any form of second- or thirddegree AV block likely to switch to first-degree AV block by the
influence of catecholamine stimulation during exercise.
Cardiac resynchronization
Several reports have suggested that patients with first-degree AV
block have a poorer outcome with CRT compared with patients
with a normal PR interval. In a study based on the Multicenter
InSync Randomized Clinical Evaluation (MIRACLE) trial, Pires
et al. 32 found that the absence of first-degree AV block was associated with a better response to CRT (P ¼ 0.005). Tedrow et al. 33
found that patients with first-degree AV block tended to have a
poorer outcome than patients with a normal PR interval though
the data were not quite statistically significant (hazard ratio ¼
S.S. Barold and B. Herweg
1.01, P ¼ 0.0650). Two other large studies have shown that a prolonged baseline PR interval is associated with an unfavourable CRT
outcome.34,35 The predictive value of baseline and 3-month ECG
variables were evaluated in the Cardiac Resynchronization in
Heart Failure (CARE-HF) trial where HF patients were randomized
to medical therapy (n ¼ 409) vs. medical therapy (n ¼ 404).34 The
primary end point was a composite of death from any cause or
hospitalization for HF. At baseline PR . 200 ms was present in
31% of the patients in the CRT arm and 21% in the medical
therapy arm. A prolonger PR interval at baseline and at 3
months predicted unfavourable outcome. Those patients who
developed shorter PR intervals during the first 3 months after randomization had a favourable outcome.34
The reason why CRT patients with first-degree AV block do not
fare as well as patients with normal AV conduction may involve
several mechanisms. (i)The long PR interval may be a marker of
more advanced myocardial disease before CRT initiation.1 The
recent study of Olshansky et al. 1 has reinforced this contention. It
is possible but as yet unproven that there may be a higher incidence
of inter- and intra-atrial conduction delay and left atrial dysfunction
in patients with marked first-degree AV block. (ii) Fusion with intrinsic activation or ‘concealed resynchronization’. Ventricular activation
in patients with a normal PR interval may have resulted in fusion of
wavefronts coming from the right bundle branch and the impulse
from LV pacing thereby avoiding potentially deleterious RV apical
stimulation.36 The recent study of Olshansky et al. 1 challenges this
concept. These investigators showed that patients with prolonged
PR intervals were, indeed, a higher-risk group with poorer outcomes
(judging from the comparison of the control groups assigned to
optimal medical therapy alone). The excessive risk of the long PR
group was eliminated by CRT pacing. Patients with longer PR intervals had the same outcomes after CRT compared to those with
normal PR intervals who also underwent CRT. As the patients
with long PR intervals were sicker to start with the proportional
degree of improvement by CRT was higher in this group compared
with the group with normal PR intervals.
Emergence from upper rate limitation
After exceeding the programmed upper rate, a CRT device may
not resume 1 : 1 atrial tracking when the sinus rate drops immediately below the programmed maximum tracking rate (MTR)37 – 41
(Figure 1). The reason is that the AR–VS interval (spontaneous
AV conduction) . programmed AS – VP interval, where AR is an
atrial event detected in the PVARP (where atrial tracking cannot
occur), VS is a ventricular-sensed event, and VP is a ventricularpaced event. Therefore, the implied TARP during desynchronized
activity or AR– VS operation is equal to [(AR –VS) interval +
PVARP] and must be longer than the programmed TARP which
is equal to [(AS –VP) interval + PVARP]. The pacemaker will continue to operate with desynchronized AR –VS cycles below the
maximum tracking rate (MTR) until the sinus interval (PP interval)
drops below the duration of the implied TARP or [(AR –VS)
interval + PVARP] interval. At this point the sinus P can escape
out of the PVARP. In patients with a long PR interval resynchronization will occur at a slower atrial rate than in patients with a
normal PR interval. Let us examine an example in a CRT patient
with a PR interval of 300 ms and a device with a sensed AV
1417
Conventional and biventricular pacing
Figure 1 Diagram showing an upper rate response with the
P-wave falling within the PVARP in the setting of normal AV conduction. Ventricular resynchronization occurs with AS– VP
sequences (as programmed) when the sinus rate is below the
MTR. When the atrial rate exceeds the MTR at point 1, the
P-wave falls within the PVARP (detected in the atrial refractory
period and depicted on an AR marker) and ventricular resynchronization is lost. The spontaneous rhythm takes over with AR –VS
sequences and AR conducting to the ventricle (depicted by VS).
When the sinus rate falls below the MTR at point 2, ventricular
resynchronization does not occur immediately because the
timing cycles of the device force the continuation of AR– VS
sequences. Failure of ventricular resynchronization at this stage
results from the longer ‘intrinsic TARP’ which is equal to
[(AR – VS) + PVARP] which is longer than the programmed
TARP ¼ [(AS – VP) + PVARP] simply because AR– VS . AS– VP.
Ventricular resynchronization with AS– VP sequences is restored
at point 3 when the sinus or atrial interval (P– P) . [(AR – VS) +
PVARP], at a sinus rate substantially lower than the MTR.
AS, atrial-sensed event; VS, ventricular-sensed event; VP,
biventricular-paced event; AR, atrial event detected in the atrial
refractory period of the pacemaker where tracking cannot
occur; AV, atrioventricular; MTR, maximum tracking rate;
PVARP, post-ventricular atrial refractory period; CRT, cardiac
resynchronization theraphy; TARP, total atrial refractory period
(Reproduced with permission from ref. 37).
delay of 100 ms, a PVARP of 250 ms, and an MTR of 150 ppm.
Assume that the patient exceeds the programmed MTR during activity. Loss of CRT will occur when the atrial rate exceeds
150 bpm. When the atrial rate drops below the MTR of
150 bpm, AV synchrony cannot return immediately. Cardiac resynchronization therapy with AV synchrony will be reestablished only
when the PP (sinus) interval becomes longer than the implied
TARP (PR interval + PVARP) or (300 + 250) ¼ 550 ms corresponding to a sinus rate of 109 –110 ppm. Loss of CRT in this situation may be important haemodynamically and symptomatically
(Figure 1).
Loss of resynchronization without
attaining the programmed upper rate
Desynchronization sequences (AR–VS, AR –VS, . . ..) containing
trapped or locked P-waves within the PVARP can also occur unrelated to a fast atrial rate . the programmed upper rate. There are
many causes of electrical desynchronization starting at rates slower
than the programmed MTR.39 Ventricular premature complexes
are commonly responsible for the initiation of desynchronization.
Desynchronization starts by shifting pacemaker timing so that the
succeeding undisturbed sinus P-waves now fall in the PVARP.
The alteration in pacemaker timing will tend to keep sinus
P-waves trapped in the PVARP as long as the P –P interval ,
implied TARP or [(AR –VS) + PVARP]. The presence of firstdegree AV block strongly favours the initiation and perpetuation
of electrical ‘desynchronization’ especially in association with a
relatively fast atrial rate and a relatively long PVARP. Such AR –
VS sequences may be symptomatic. They may also produce a reduction of CRT ‘dose’. Special programmable algorithms become
active whenever a CRT device detects AR –VS, AR– VS, . . .
sequences suggestive of ventricular desynchronization. The algorithms automatically shorten the PVARP for one cycle or only a
few cycles thereby allowing exit of the P-wave from the PVARP
and restoration of 1:1 atrial tracking.40,41 A different system in Biotronik CRT devices utilizes an AV Control window which is not an
algorithm that ‘unlocks’ P-waves ‘trapped’ in the PVARP.42 It has
been designed to prevent P-waves from becoming ‘trapped’ in
the PVARP: a ventricular-sensed event occurring within the AV
Control interval (that starts with an atrial event) does not start a
PVARP (zero PVARP) so that P locking in the PVARP cannot
occur when the AV conduction time is shorter than the AV
Control interval. ‘Locking’ of the P-wave into the PVARP may
also be prevented by slowing down the sinus rate with drugs
such as beta-blockers as CRT permits the use of larger doses
than before device therapy.
Ablation of the atrioventricular junction
Refractory cases (usually associated with marked first-degree AV
block) can be treated by AV junctional ablation to ensure continual
biventricular pacing. Also if there is inter-atrial conduction delay
with a long PR interval, it may be impossible to prolong the AV
delay sufficiently to adjust for the delayed left atrial activation
because the atrial impulse reaches the AV junction relatively
early and gives rise to a spontaneous QRS complex which is not
wanted in CRT. In this situation AV junctional ablation may be
beneficial.
Conclusion
Functional atrial undersensing may occur in patients with conventional dual-chamber pacing and first-degree AV block because the
sinus P-wave tends to be displaced into the PVARP, an arrangement that may cause a pacemaker syndrome. Prevention of atrial
undersensing requires programming a shorter AV and PVARP
(and turning off all algorithms dependent on temporary PVARP
prolongation). A shorter PVARP carries little risk of pacemakermediated tachycardia because patients with a prolonged PR interval are much less likely to demonstrate retrograde ventriculoatrial
conduction. Relatively new pacing algorithms to minimize RV
stimulation, function without a traditional AV interval and permit
the establishment of very long AV intervals that may cause pacemaker syndrome. Patients with first-degree AV block undergoing
cardiac resynchronization are more susceptible to develop
1418
electrical desynchronization (with P-waves trapped in the PVARP)
from a variety of causes. In this situation AV synchrony can be
restored by algorithms that automatically and temporarily
shorten the PVARP upon detection of desynchronized sequences
or prevented by eliminating the PVARP of ventricular-sensed
beats. Ablation of the AV junction is rarely required but should
be considered in patients who remain symptomatic despite
timing adjustments of device function (short PVARP and elimination of algorithms involving a long PVARP) and avoidance of
sinus tachycardia with larger doses of beta-blocker therapy.
Conflict of interest: none declared.
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EP CASE EXPRESS
doi:10.1093/europace/eus094
Online publish-ahead-of-print 15 May 2012
.............................................................................................................................................................................
Dormant conduction revealed by adenosine to guide electrical isolation
of the superior vena cava
Juan F. Viles-Gonzalez, Marc A. Miller, and Andre d’Avila*
Helmsley Electrophysiology Center, Mount Sinai School of Medicine, New York City, NY, USA
* Corresponding author. Helmsley Electrophysiology Center, Mount Sinai Hospital and School of Medicine, One Gustave L. Levy Place, PO Box 1030, New York City,
NY 10029, USA. Tel: +1 212 241-7114; fax: +1 646 537 9691, Email: andre.d’[email protected]
The restoration of electrical conduction in injured, pulmonary vein (PV) tissue (dormant
conduction) via adenosine-mediated hyperpolarization has been utilized to guide the
need for additional ablation. The superior vena cava (SVC) and PVs have similar cardiac muscular extensions. We present a patient with recurrent paroxysmal atrial fibrillation after pulmonary vein isolation. All PVs were found to be electrically isolated, before and after the
infusion of isoproterenol and adenosine. Two challenges of isoproterenol failed to demonstrate extra PV triggers or atrial arrhythmias. A decision was made to isolate the SVC
despite the absence of non-PV triggers. Phrenic nerve location was defined by high-output
pacing (orange dots). The SVC ablation was initiated in the postero-septal aspect of the
SVC–right atrium (RA) junction towards the most anterior portion of the vein. The SVC
isolation was achieved during RF delivery on the most septal portion of the right atrial appendage (white dots). Four more RF lesions were delivered anterior to this area to extend
the lesion set. Adenosine was then administered demonstrating transient reconnection
between the SVC and the RA. Additional RF applications were required on the anterior
aspect of the SVC closer to the area where the phrenic nerve was located (green dots).
Despite this, repeat administration of adenosine resulted in transient reconnection once again and additional lesions were given on
the same area of breakthrough (red dots), which resulted in permanent SVC isolation. This report of dormant electrical conduction
between the SVC and the RA illustrates the potential role for adenosine injection in our current ablation strategy during SVC isolation.
The full-length version of this report can be viewed at: http://www.escardio.org/communities/EHRA/publications/ep-case-reports/
Documents/dormant-conduction-adenosine.pdf
Funding
A.d’A. has received consulting fees and grant support from St Jude Medical, the manufacturer of the electroanatomic mapping system, and
Biosense Webster the manufacturer of the ablation catheter used in this series.
Published on behalf of the European Society of Cardiology. All rights reserved. & The Author 2012. For permissions please email: [email protected].