CLINICAL RESEARCH
Europace (2010) 12, 1262–1269
doi:10.1093/europace/euq167
Pacing and CRT
Can optimization of pacing settings compensate
for a non-optimal left ventricular pacing site?
Margot D. Bogaard *, Pieter A. Doevendans, Geert E. Leenders, Peter Loh,
Richard N.W. Hauer, Harry van Wessel, and Mathias Meine
Department of Cardiology, University Medical Center Utrecht, Heidelberglaan 100, Q05.2.314, 3584 CX Utrecht, The Netherlands
Received 8 January 2010; accepted after revision 28 April 2010; online publish-ahead-of-print 18 June 2010
Aims
Optimal left ventricular (LV) lead position improves the response to cardiac resynchronization therapy (CRT).
However, in some patients it is not possible to position the LV lead at an optimal pacing site. The aim of this
study was to determine whether optimization of the pacing settings atrioventricular delay (AVD) and interventricular
delay (VVD) can compensate for a non-optimal LV pacing site.
.....................................................................................................................................................................................
Methods
In 16 patients with heart failure [New York Heart Association class III (13) or IV (3), median QRS duration of 172 ms
and results
and median LV ejection fraction of 20%] the acute haemodynamic effect of biventricular pacing was assessed at ≥2
pacing sites by the increase in maximum rate of LV pressure rise (%dP/dtmax). At each site the AVD and VVD were
optimized. Biventricular pacing with nominal settings at a non-optimal LV pacing site improved dP/dtmax by 12.8%
(20.5 to 23.2%). This could be further improved by 6.5 percentage points (1.2– 13.9) by optimization of pacing settings (P ¼ 0.001) and by 9.9 percentage points (3.7– 13.3, P ¼ 0.004) by optimization of pacing site. Optimization of
the LV pacing site and pacing settings together improved %dP/dtmax by 16.2 per cent points (10.0–21.8, P , 0.001).
.....................................................................................................................................................................................
Conclusion
Optimization of the AVD and VVD can partly compensate for a non-optimal LV pacing site. However, a
combination of an optimal LV pacing site and optimized pacing settings gives the best acute haemodynamic
response.
----------------------------------------------------------------------------------------------------------------------------------------------------------Keywords
Cardiac resynchronization therapy † Interventricular delay † Atrioventricular delay † Left ventricular lead site †
Optimization † dP/dtmax
Introduction
In symptomatic patients with chronic congestive heart failure, a
wide QRS complex and an impaired left ventricular (LV) ejection
fraction, cardiac resynchronization therapy (CRT) improves morbidity and mortality of heart failure.1,2 However, since a substantial
percentage of these patients does not respond,3 there is still need
for improvement.
The main rationale for CRT is based upon the observation that
the presence of ventricular dyssynchrony can induce systolic and
diastolic dysfunction and thereby worsen heart failure. By continuously pacing both ventricles after atrial pacing or sensing, achievement of optimal inter- and intraventricular synchrony as well as
atrioventricular synchrony is pursued.
Optimizing the delay between atrial pacing or sensing and biventricular pacing (atrioventricular delay, AVD) influences both
diastolic and systolic function and has shown to improve clinical
outcome at intermediate follow-up.4 Optimizing the delay
between left and right ventricular (RV) pacing (interventricular
delay, VVD) has shown to be effective in improving acute and
intermediate follow-up variables in several non-randomized
studies,5 – 7 although randomized studies have yet failed to demonstrate a significant effect on outcome.8,9
Optimal LV lead position improves the response to CRT.10,11
However, due to individual variations in anatomy and local
pacing and sensing characteristics, the LV lead cannot always be
positioned at the optimal site. The aim of this study was therefore
to determine the acute haemodynamic response to optimization
of the AVD and VVD at two or more LV pacing sites during
device implantation, and to determine whether optimization of
these pacing settings can compensate for a non-optimal LV
pacing site.
* Corresponding author. Tel: +3188 755 9447; fax: +31 88 755 5479, Email: [email protected]
Published on behalf of the European Society of Cardiology. All rights reserved. & The Author 2010. For permissions please email: [email protected].
1263
Compensating a non-optimal LV pacing site
Methods
Study population
All patients met the indication criteria of the current international
guidelines for CRT, including chronic heart failure in New York
Heart Association (NYHA) functional class III or IV despite optimal
pharmacological therapy, LV ejection fraction of ≤35% and QRS
duration of ≥120 ms on 12-lead surface electrocardiogram. All CRT
devices were implanted in the University Medical Center Utrecht,
The Netherlands. As part of the standard implantation procedure,
pacing settings and LV pacing site were optimized. Patients were
included in this retrospective analysis if the acute haemodynamic
effect of VVD optimization was evaluated at multiple LV pacing sites
and a baseline dP/dtmax measurement was repeated at all pacing
sites. Patients were excluded from dP/dtmax measurement if they had
LV thrombus, aorta prosthesis, mechanical aortic valve replacement
or severe aortic valve stenosis.
Implantation procedure
Before lead implantation, a pressure wire (PressureWirew 5, St. Jude
Medical, Inc., St. Paul, MN, USA) was placed in the left ventricle by
femoral arterial access, supported by a 4-F multi-purpose catheter
that was subsequently pulled back into the distal aortic arch. Via the
cephalic or subclavian vein, the RV lead was positioned in the apex
and the atrial lead was implanted in the right atrial appendage. A
guiding catheter was placed into the coronary sinus and a retrograde
venogram of the coronary sinus and its tributaries was obtained by
direct balloon-occlusive angiography in two directions [right anterior
oblique (RAO) 308 and left anterior oblique (LAO) 408]. The implanting physician temporarily placed the LV lead at two or more sites overlying the anterolateral, lateral or posterolateral LV free-wall via the
tributaries of the coronary sinus. Only sites that could be a potential
final pacing site were tested. These were sites with a stable lead position, acceptable sensing and pacing functions and no phrenic nerve
stimulation. After optimization of the pacing settings, the LV lead
was finally positioned at the site with the best acute haemodynamic
effect.
Pacing site determination
At every evaluated LV pacing site, biplane fluoroscopy was performed
in LAO 408 and RAO 308 projections and used to determine the anatomic position of the LV lead tip. In the RAO 308 projection, the heart
contour was divided into three equal parts from base to apex. In the
LAO 408 projection the heart contour was divided into five equal
parts of 408 from anterior to posterior. The great cardiac vein
thereby mainly covered the anterior LV segment and the mid-cardiac
vein mainly the posterior segment. The other tributaries covered
their equally named LV segments, although sub-branches may crossover to adjacent segments (Figure 1).
Optimization of pacing settings and LV
pacing site
The acute haemodynamic effect of pacing was reflected by the
maximum rate of pressure rise (dP/dtmax) in the LV. The dP/dtmax
was automatically derived from the continuous invasive LV pressure
measurements (Radi Analyzer Physio Monitor v1.0 beta4, St. Jude
Medical, Inc., St. Paul, MN, USA) with a sample rate of 100 Hz. The
average dP/dtmax was derived from 10 consecutive paced beats, starting
from the third beat after a new pacing mode was applied. Premature
ventricular beats and the first following beat were manually deleted
from the analysis. Every pacing mode was separated by 10 s of baseline
pacing. Baseline pacing consisted of atrial overdrive pacing in patients
with sinus rhythm or RV pacing in patients with atrial fibrillation.
The effect of biventricular pacing could therefore be compared with
baseline pacing at a similar rate of 5 – 10 beats per min above the intrinsic heart rate. To compare the effect of biventricular pacing between
different pacing settings (AVD and VVD) and between multiple
pacing sites, the relative increase of dP/dtmax compared with baseline
(%dP/dtmax) was used. Average baseline dP/dtmax was derived from
10 consecutive beats at the end of the optimization sequence at
each LV pacing site.
At each LV pacing site, consecutive optimization of the AVD and
VVD was performed. In four patients with atrial fibrillation, only optimization of the VVD was performed. In patients with sinus rhythm the
optimization procedure started with shortening of the AVD from
240 – 80 ms in steps of 20 ms during atrial synchronous simultaneous
biventricular pacing. The optimal AVD was defined as the AVD that
showed the highest %dP/dtmax. Next, VVD optimization was performed starting with LV pacing preceding RV pacing by 80 ms (indicated by a negative VVD) and reducing the VVD in steps of 20 ms
until the RV was paced 80 ms before the LV (indicated by a positive
VVD). During this procedure, the previously determined optimal
AVD was programmed and kept constant for the timing of LV
pacing. The optimal VVD was defined as the VVD with the highest
%dP/dtmax. In patients with atrial fibrillation, the VVD was optimized
during biventricular VVI pacing. In every patient the effect of pacing
with nominal pacing settings was also evaluated. Nominal settings
were defined as an AVD of 120 ms (if applicable, in sinus rhythm
patients) and simultaneous ventricular pacing (VVD of 0 ms).
The optimal and non-optimal LV pacing sites were defined as the
site with the highest and lowest %dP/dtmax, respectively, during biventricular pacing with optimal pacing settings.
To define the acute haemodynamic response to CRT, %dP/dtmax
responses of all patients were pooled and divided into tertiles. The
%dP/dtmax responses at nominal settings, optimal AVD, and optimal
AVD and VVD, both at the optimal and non-optimal site, were
pooled. Based on these tertiles, a moderate acute haemodynamic
CRT responder was defined by %dP/dtmax ≥14 and ,31, a high
responder was defined by %dP/dtmax ≥31 and a low responder by
%dP/dtmax ,14.
Statistical analysis
Continuous variables were expressed as median with interquartile
range (IQR) and were compared with the Wilcoxon signed rank test
for paired observations or the Mann– Whitney test for independent
observations. A P-value of 0.05 was considered significant. Data analysis was performed with SPSS 15.0 (SPSS, Inc., Chicago, Illinois).
Results
Study population
Sixteen patients were included in this analysis. All patients were in
the NYHA class III (n ¼ 13) or IV (n ¼ 3) despite optimal pharmacological therapy, had a median LV ejection fraction of 20%
(17 –22) and a left bundle branch block with a median QRS duration of 172 ms (165 –174) on the 12-lead surface electrocardiogram. The median PQ interval on the surface electrocardiogram
was 203 ms (164 –234). Ten patients were male and the median
age was 68 years (62–75). Nine patients had a previous myocardial
infarction (Table 1).
1264
M.D. Bogaard et al.
Figure 1 Localization of the left ventricular lead tip in a coronary sinus tributary. Left panels: right anterior oblique 308 and left anterior
oblique 408 projections. Right panels: relative number of times an evaluated segment was the optimal LV pacing site (red bar: optimal site;
blue bar: evaluated, not optimal site). A, anterior; AL, anterolateral; L, lateral; P, posterior; PL, posterolateral.
Implantation
Optimal vs. non-optimal pacing sites
One CRT-pacemaker and 15 CRT-defibrillator devices were
implanted: Atlas II HF, St. Jude Medical, Inc. (n ¼ 1); Livian (n ¼
1), Cognis 100-D (n ¼ 4), Boston Scientific Corporation; Contak
Renewal 4 AVT HE (n ¼ 3), 4 RF HE (n ¼ 4), 4 RF (n ¼ 2), TR
CRT-P (n ¼ 1), Guidant Corporation. The following LV leads
were implanted: Acuity Steerable (n ¼ 5), Easytrak 2 (n ¼ 9),
Guidant; QuickSite 1056T, St. Jude Medical (n ¼ 1); Attain 4196,
Medtronic (n ¼ 1). In five patients, the LV lead was not implanted
at the optimal site as determined by %dP/dtmax. This was due to
phrenic nerve stimulation (n ¼ 2), unacceptable pacing thresholds
(n ¼ 1) or an unstable position (n ¼ 2). There were no
procedure-related complications.
Pacing at an optimal site instead of a non-optimal site relatively
improved the acute haemodynamic response with 52% (18–
222%) during biventricular pacing with optimal settings (P ,
0.001, Figure 2). The effect of biventricular pacing with nominal settings or with an optimal AVD was also significantly improved by
replacing the LV lead to an optimal site (Figure 2). Optimization
of the LV pacing site therefore improved the number of acute
responders (Figure 3). The acute haemodynamic response to
site-optimization in individual patients with and without previous
infarction can be seen in Table 1.
Pacing sites
The AVD was optimized in 12 patients with sinus rhythm. AVD optimization relatively improved the %dP/dtmax increase with 28% (9–
122%) at optimal sites and 47% (19–191%) at non-optimal sites,
respectively (both P ¼ 0.003) (Figure 2). Additional VVD optimization
in these patients relatively increased %dP/dtmax with 18% (4–29%) at
On average, four coronary sinus tributaries were identified per
patient. Optimization was performed at 44 sites in total and 2–6
sites per patient. The number of times a certain segment was evaluated or was defined as the optimal site is shown in Figure 1.
Optimization of the AVD and VVD at
optimal and non-optimal sites
1265
Compensating a non-optimal LV pacing site
Table 1 Individual patient characteristics
AF/SR
QRS (ms)
LVEF (%)
NYHA
class
Infarction
Non-optimal
site
Optimal site
Response
..........................................
Non-optimal site
Optimal site
...............................................................................................................................................................................
1
AF
172
19a
3
Mid L
Distal L
Low
Low
2
AF
186
20b
4
Mid A
Basal AL
Low
Moderate
3
4
AF
SR
182
172
20a
19a
3
4
Inferiorc
Apicald
Mid L
Basal L
Basal AL
Mid L
Low
Moderate
Moderate
High
5
SR
142
24a
3
Anteroseptalc
a
Distal PL
Basal L
Low
Low
6
SR
198
10
3
Distal L
Distal PL
Moderate
High
7
8
SR
SR
164
156
17b
17b
3
3
Mid L
Mid A
Mid L
Mid AL
High
High
High
High
9
SR
174
28b
3
Inferiorc
Mid AL
Distal AL
Moderate
Moderate
b
Mid L
Mid L
Mid PL
Mid PL
Low
Low
High
Moderate
10
11
SR
SR
172
168
18
22b
4
3
Anteriorc
12
SR
146
22b
3
Posterolaterale
Mid L
Mid AL
Low
Moderate
172
166
b
27
21b
3
3
Inferiorc
Distal PL
Distal L
Mid L
Mid AL
High
High
High
High
174
b
3
Inferoseptald
Mid PL
Mid L
High
High
b
3
Inferoposterolaterald
Distal PL
Mid AL
Moderate
High
13
14
15
16
SR
SR
SR
AF
174
21
8
A, anterior; AL, anterolateral; AF, atrial fibrillation; L, lateral; LVEF, LV ejection fraction; PL, posterolateral; SR, sinus rhythm.
a
LVEF was derived from bi-plane echocardiography.
b
LVEF was derived from radionuclide blood pool imaging.
c
Infarct localization was derived from echocardiography.
d
Infarct localization was derived from radionuclide scintigraphy.
e
Infarct localization was derived from magnetic resonance imaging.
Figure 3 Number of acute haemodynamic responders. Low
responders, %dP/dtmax , 14;
moderate
responders, %dP/
dtmax ≥ 14 and ,31; high responders, %dP/dtmax ≥ 31.
Figure 2 Acute haemodynamic response at optimal and nonoptimal pacing sites at various pacing settings. Relative increase
in dP/dtmax during biventricular pacing, compared with baseline
pacing (atrial overdrive pacing in patients with sinus rhythm, or
RV pacing in patients with atrial fibrillation). Data shown are
median, IQR and P-values. Biv nom, biventricular pacing with
nominal AVD and nominal VVD; Biv AV opt, biventricular
pacing with optimal AVD and nominal VVD; Biv AV VV opt,
biventricular pacing with optimal AVD and optimal VVD.
*P , 0.001 compared to non-optimal site; †P ¼ 0.021 compared
to non-optimal site, ‡P ¼ 0.004 compared to non-optimal site.
the optimal sites (P ¼ 0.01) and 16% (8–45%) at the non-optimal sites
(P ¼ n.s.) (Figure 2). In the complete group of 16 patients, optimization
of the AVD (if applicable) and VVD together resulted in a relative
increase in %dP/dtmax of 32% (14–133%) compared with biventricular
pacing with nominal settings at the optimal sites and 57% (16–127%)
at the non-optimal sites (P ¼ n.s. between sites). Optimization of
pacing settings improved patients from low-to-moderate or from
moderate-to-high acute responder in five cases at the non-optimal
sites (Figure 3) and in eight cases at the optimal sites.
The optimal AVD was 180 ms (160–200 ms) at the non-optimal
site and 180 ms (130–215 ms) at the optimal site. In four patients
1266
M.D. Bogaard et al.
Figure 4 Illustrative case: acute haemodynamic response to AVD and VVD optimization at an optimal and non-optimal site. *Optimal setting.
the optimal AVD did not change between the sites; in other patients
it changed up to 60 ms. The optimal AVD, to the first pacing ventricular lead, represented 88% (70–99) of the PQ interval.
The optimal VVD was 230 ms (260 to 5 ms) and 220 ms
(240 to 0 ms) at non-optimal and optimal sites, respectively.
Comparing the non-optimal and optimal site, pacing the LV first
was optimal in 11 and 12 patients, simultaneous pacing in 4 and
2 patients, and RV first pacing in 1 and 2 patients, respectively. In
all but two patients the optimal VVD changed between sites.
Optimization of settings compared with
optimization of LV pacing site
Optimization of pacing settings at a non-optimal LV pacing site
improved %dP/dtmax by 6.5 percentage points (1.2 –13.9, P ¼
0.001), compared with an improvement in %dP/dtmax by 9.9
percentage points (3.7– 13.3, P ¼ 0.004) by optimization of the
LV pacing site. Settings- and site optimization together improved
%dP/dtmax by 16.2 percentage points (10.0– 21.8, P , 0.001). An
illustrative case of settings- and site optimization is shown in
Figure 4. The number of moderate and high acute responders
increased by optimization of pacing settings at a non-optimal site,
however optimization of both pacing site and pacing settings
further increased the number of high acute responders to nine,
and reduced the number of acute low-responders to two
(Figure 3).
Discussion
The present study showed that optimization of pacing settings
could partly compensate for a non-optimal pacing site, however,
combined optimization of LV pacing site and pacing settings led
to the best acute haemodynamic response.
Optimal vs. non-optimal pacing sites
Although all tested pacing sites were located at the LV free wall, we
observed significant differences in acute haemodynamic response
between the LV pacing sites. The optimal site was distributed
fairly uniformly between segments, although a slight predisposition
for the anterolateral segment seemed to exist. In clinical practice
the LV lead is often pragmatically aimed at the lateral or posterolateral LV wall. Previously, other groups defined the optimal LV
lead site by the area of maximal mechanical dyssynchrony on echocardiogram,12 – 18 which showed a heterogeneous distribution of
the optimal sites. In 53–69% of patients a site other than lateral
was defined optimal. The inter-individual heterogeneity in
optimal LV pacing sites might be explained by variations in left
bundle branch block, i.e. where the fascicles lie anatomically and
which fascicle is mainly involved,19,20 by areas of slow conduction
within the LV21,22 and by scar tissue from previous myocardial
infarctions.23,24 The mild predisposition for an anterolaterally
located optimal LV pacing site in this study can be explained by
these inter-individual variations. Also, there is a variation in classification of segments. The border area between the anterolateral
and lateral segments, as defined by our classification (Figure 1),
may be classified as a lateral segment by others.10
Physicians placing the LV lead at the site with maximal mechanical
delay confirmed the importance of pacing at an optimal LV pacing
site for echocardiographic and clinical outcome.10,12 – 18 Pressure
volume loop-guided studies showed that an optimal LV stimulation
site improves stroke work.10,25 Additionally, the LV dP/dtmax and
pulse pressure could significantly differ within the same tributary.11
The LV lead electrical delay26 was shown to be positively correlated with dP/dtmax increase. Our data confirm previous studies
showing that one anatomic LV pacing site is not consistently
superior to another LV pacing site, which emphasizes the need
for individualized optimization of the LV pacing site.
Optimization of the AVD at optimal and
non-optimal sites
Optimization of the AVD significantly increased the acute haemodynamic effect of CRT, irrespective of the LV free-wall pacing site.
The authors are not aware of any previous publication on the
effect of optimization of the AVD at multiple LV free-wall pacing
sites within patients. The optimal AVD varied up to 100 ms
Compensating a non-optimal LV pacing site
between different pacing sites within individual patients. The LV lead
location might influence the optimal AVD and VVD by changing the
route and duration of the paced LV depolarization front, and thereby
the interaction with the right depolarization fronts. The cooperation
between intrinsic and paced ventricular depolarization fronts can be
roughly estimated by dividing the AVD by the intrinsic PQ interval.
Since in this patient group, the optimal AVD to first pacing ventricle
represented 88% of the PQ interval, it seems that fusion of intrinsic
conduction via the right bundle branch and the paced ventricular
wavefronts was established.
Optimization of the VVD at optimal and
non-optimal sites
Since a desirable LV pacing location cannot always be established, it
is a clinically relevant question to ask whether pacing at a nonoptimal LV pacing site can be compensated for by adjusting
another parameter. Because the VVD indicates the time delay
between LV and RV pacing, it has been hypothesized that individual
optimization of the VVD could accomplish this.
Optimization of the VVD did not significantly improve %dP/dtmax
at non-optimal sites, although it did improve the acute haemodynamic benefit at optimal LV pacing sites. Previously, Lane
et al.27 found that VVD optimization significantly increased the
ejection fraction at both lateral and inferior sites in 10 patients.
Lane et al. compared sites based on anatomy (lateral vs. inferior)
and therefore could have pooled optimal and non-optimal pacing
sites in one category. The lack of a significant improvement by
VVD optimization at non-optimal sites in our patient group
could partly be due to the small number of patients. It could
also be explained by a limitation of the VVD to compensate for
certain non-optimal sites. VVD optimization influences ventricular
dyssynchrony by changing the relative timing of the paced LV front
compared with the paced RV front. Optimal fusion of the left and
right depolarization fronts improves inter- and intraventricular synchrony. Synchronized activation of the lateral LV wall and the interventricular septum reduces systolic myocardial stretch and
improves contractility.26 – 29 However, if the paced LV front originates from a non-optimal site, the starting point, direction and
possibly also the velocity of the LV front are non-optimal21 and
the LV segment with latest activation might still be reached relatively late during LV activation, despite an ‘optimal’ VVD. This
could explain why optimizing the VVD further improved acute haemodynamics when the LV lead was placed optimally but not when
it was placed at a non-optimal site. For superior synchronization,
an optimal LV pacing site is mandatory, as reflected by the
superior %dP/dtmax increase when a patient was paced with
optimal settings at an optimal LV site.
This limited effect of VVD optimization at non-optimal LV pacing
sites may play a role in the disappointing results of randomized
studies, failing to demonstrate a significant effect of VVD optimization on long-term outcome in CRT patients.
Limitations
This is a retrospective study with concurrent limitations. However,
baseline characteristics correspond to data from large CRT trials1,2
1267
and outcome bias was overcome by using dP/dtmax as an objective
outcome measure.
The sample size was small but nevertheless a significant
improvement in dP/dtmax was observed by both optimization of
LV pacing site and pacing settings. The effect of AVD and VVD
optimization at more than one LV pacing site was not reported
before, by knowledge of the authors. These results can therefore
be seen as a stimulation to aim at optimal CRT during the implantation procedure, and to do further research in this field.
The acute haemodynamic response was defined by relative
increase in dP/dtmax and divided in tertiles with cut-offs of 14
and 31%. Arbitrarily set binary cut-offs of 1010,30,31 or 25%32
were previously used, but these values were never validated.
The cut-offs of 14 and 31% were not validated either, but they
were based on observed distribution of dP/dtmax responses. Furthermore, instead of a binary discrimination (response yes/no), a
group with moderate response was created, which gave the opportunity to detect additional improvements in patients with a moderate response at baseline. The influence of acute dP/dtmax increase
on long-term clinical outcome was not assessed. When we
compare acute dP/dtmax increase to another acute haemodynamic
parameter such as acute increase in stroke work, this reveals a
concordant response (.10% increase) in 53%30 and concordant
optimal LV lead position in 69%.10 Of both acute haemodynamic
parameters, the relationship to long-term clinical outcome is yet
unknown.
Although LV dP/dtmax is considered a fair surrogate for contractility, it is also influenced by preload.33 Preload can vary due to
medication, fluid administration or breathing. All measurements
were performed at the end of the implantation procedure under
stable conditions without administration of medication or fluids
to the patient, and averaged over 10 consecutive beats, thereby
including several breathing cycles. Therefore, influence of preload
on the results of this study can be considered minimal.
The baseline dP/dtmax can vary during the optimization procedure. In this study, the effect of a shifting baseline was minimized
by several measures. First, to limit the influence of heart rate on LV
dP/dtmax, the baseline dP/dtmax was measured at the same heart
rate as during biventricular pacing. Second, to avoid a possible
effect of prolonged pacing on dP/dtmax, baseline pacing was
applied between each evaluated pacing setting. Third, the optimal
pacing site and settings were defined by the relative increase in
dP/dtmax compared with a baseline, instead of the absolute dP/
dtmax. The variation in the baseline dP/dtmax within patients was
not statistically significant.
Not all available coronary sinus tributaries were tested in all
patients. This was due to either an inability to reach this tributary
with the LV lead or because the implantation time had to be
limited. Nevertheless a significant difference between the optimal
and non-optimal sites would only be expected to become more
significant if more sites were tested. The sites where the best
result was expected (anterolateral, lateral, posterolateral) were
always included if possible.
Information about regional mechanical delays was not available
in these patients. A strategy of aiming the LV lead at the site of
maximal mechanical delay is not always feasible because of
anatomy or pacing characteristics. However, the method proposed
1268
in this article can be applied to all patients. The dP/dtmax is an
objective parameter without the issue of intra- or inter-observer
variability and it explores the global and not the regional LV
function.
The benefit of optimization of pacing site and settings may be
different in patients with previous myocardial infarction compared
with patients without previous myocardial infarction. Although no
significant difference in acute haemodynamic response was
observed between these groups in this study, the numbers of
patients were too small to rule out a different response with
certainty.
Clinical relevance
The results of this study suggest that implanting cardiologists have
to search for the optimal LV lead site and for the optimal pacing
settings in all individual patients, and not accept less due to anatomic difficulties or a possible increase in implantation time. If circumstances necessitate implanting the LV lead at an apparently
non-optimal site, it is still profitable to optimize the AVD;
however, the effect of VVD optimization seems to be limited.
Whether the acute haemodynamic benefit, as assessed by LV dP/
dtmax, will translate into a better long-term outcome was not
determined in this study.
Conclusion
Previously it has been shown that the localization of the LV pacing
site can influence the response to CRT. This study showed that
optimization of pacing settings has an additional positive effect
on the acute haemodynamic response irrespective of the LV
pacing site. Optimizing the AVD and VVD can partly compensate
for a non-optimal LV pacing site, however the acute haemodynamic response is significantly better when both the LV pacing
site and the pacing settings are individually optimized.
Conflict of interest: M.M. has received speaker’s honoraria from
St. Jude Medical and Boston Scientific Corp. and is a consultant for
Boston Scientific Corp. All other authors state that they have no
conflicting interests to declare.
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doi:10.1093/europace/euq165
Online publish-ahead-of-print 1 June 2010
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Atrioventricular nodal reentrant tachycardia with varying atrio-ventricular
conduction and QRS morphology
Jacek Pawel Majewski * and Jacek Lelakowski
Department of Electrocardiology, John Paul II Hospital, ul. Pradnicka 80, Krakow, Poland
* Corresponding author. Tel: +48 501 362 792, Email: [email protected]
A 42-year-old male was referred to us for radiofrequency ablation of typical atrioventricular nodal reentrant tachycardia (AVNRT).
During the electrophysiological testing, we documented the AVNRT with 2:1 atrio-ventricular block. The ventricular premature
beat (VPB) with right bundle branch block morphology (fourth QRS) resulted in prolongation of cycle length, allowing recovery of
His bundle conduction. The VPB caused initially slight conduction delay in the left bundle with subsequent aberration to left
bundle branch block during 1:1 atrio-ventricular conduction. The case shows that AVNRT may produce various ECG patterns in
the same patient due to functional fluctuations in conduction system.
Conflict of interest: none declared.
Published on behalf of the European Society of Cardiology. All rights reserved. & The Author 2010. For permissions please email: [email protected].