JACC: CARDIOVASCULAR IMAGING VOL. 3, NO.

11, 2010

© 2010 BY THE AMERICAN COLLEGE OF CARDIOLOGY FOUNDATION ISSN 1936-878X/$36.00

PUBLISHED BY ELSEVIER INC. DOI:10.1016/j.jcmg.2010.06.017

STATE-OF-THE-ART PAPER

Echocardiography-Guided Biventricular
Pacemaker Optimization
Tasneem Z. Naqvi, MD
Los Angeles, California

Optimization of atrioventricular delay (AVD) and interventricular delay (VVD) in patients with a biventricu-
lar (Biv) pacemaker has been associated with improvement in cardiac output acutely, a reduction in heart
failure symptoms, and improved exercise capacity. Several individual echocardiography (echo) Doppler
parameters have been used for pacemaker optimization. In this review, pacemaker optimization based on
echocardiographic evaluation of cardiac hemodynamics is presented. The goals of this paper are to discuss
studies in echo-guided pacemaker optimization, provide a systemic guide to pacemaker interrogation and
optimization in patients after Biv pacing who may have complex hemodynamic derangement, and finally,
to discuss studies in optimization with exercise or atrial pacing. Case examples highlighting hemodynamic
derangement in heart failure, tailoring of Biv pacemaker optimization to the underlying physiologic
derangement, and its improvement with optimization are presented. (J Am Coll Cardiol Img 2010;3:
1168 – 80) © 2010 by the American College of Cardiology Foundation

C
ardiac resynchronization therapy (CRT)
has become a new, effective treatment
modality in those with drug-resistant
advanced congestive heart failure.
Despite careful selection, as many as 30% to
40% of patients do not respond to CRT (1).
Echocardiography (echo) optimization of
atrioventricular delay (AVD) was included in
several randomized trials in CRT (1– 4). Ritter’s
method was used in the MIRACLE (Multi-
center InSync Randomized Clinical Evaluation)
study (1), iterative method in CARE-HF (Car-
diac Resynchronization-Heart Failure) study (3)
and a device-based algorithm was used in the
COMPANION (Comparison of Medical Ther-
apy, Pacing and Defibrillation in Chronic Heart
Failure) study (2). In clinical practice, however,
biventricular (Biv) pacemaker optimization is of-
ten overlooked (5), and AVD may be set empir-
ically at an out-of-box setting of 120 ms (6 – 8) or
programmed based on currently available electri-
cal algorithms (9). Currently available pacemak-
ers offer programmable AVD, interventricular
delays (VVD) (10), as well as rate-adaptive AVD
programming and rate-response features. The
purpose of this paper is to discuss the literature on
echo-guided optimization, discuss steps incorpo-
rating pacemaker interrogation, and demonstrate
utility of comprehensive echo to guide pacemaker
optimization. Multiple examples of hemody-
namic Doppler abnormalities in heart failure
are cited.
Studies in Echo-Guided Pacemaker
Optimization
Echo Doppler assessment of left ventricular
(LV) diastolic filling and LV ejection has been

From the Echocardiographic Laboratories, Keck School of Medicine, University of Southern California, Los Angeles,
California. Dr. Naqvi reports that she has research grants with Medtronic and St Jude and is a consultant for St Jude.
Manuscript received January 7, 2010; revised manuscript received May 24, 2010, accepted June 8, 2010.
JACC: CARDIOVASCULAR IMAGING, VOL. 3, NO. 11, 2010
NOVEMBER 2010:1168 – 80
the most commonly utilized method for pacemaker
optimization. Several studies from single centers
have shown improvement in cardiac output by
tailored echo Doppler-guided Biv pacemaker AVD
optimization (3,11–13). One single, blind, random-
ized trial that investigated the impact of AVD
optimization based on the aortic velocity time integral
(VTI) showed improvement in New York Heart
Association (NYHA) functional class in optimized
versus control patients (6). Similar to AVD optimiza-
tion, data from small, single-center studies demon-
strated that sequential Biv pacing after VVD optimi-
zation may acutely further improve LV stroke volume
(10,13,14), LV dP/dt (15), and LV dyssynchrony
(16); however, the incremental benefit of sequential
VVD remains inconclusive in multicenter studies.
Although sequence of AV versus VV optimization is
unclear, our own experience and other data (17)
suggest better results when AVD is optimized first.
This approach improves LV preload by ensuring
mitral valve closure immediately after completion of
atrial contraction, and in turn, cardiac output. Opti-
mal AVD changes over time; however, no consistent
trend in AVD changes has been observed (18 –20).
Echo Doppler Techniques in
Pacemaker Optimization
Doppler parameters used for echo-guided optimi-
zation include aortic VTI (21,22), diastolic mitral
flow pattern by Ritter’s method (23), iterative
method (24), diastolic filling time (3), VTI of mitral
inflow (25), Doppler-derived dP/dt (26), tissue
Doppler imaging (13,14), LV and right ventricular
(RV) pre-ejection delays, and myocardial perfor-
mance index (27). LV VTI has been shown to be
feasible and more reproducible compared with mi-
tral inflow VTI and filling time as well as measures
of dyssynchrony (22). LV ejection duration has also
been used instead of LV VTI or peak ejection
velocity (28) (Figs. 1 and 2). optimization using
Ritter’s method versus aortic VTI has yielded conflict-
ing results in the same patients (21). We have shown
the utility of comprehensive methods using multiple
echo Doppler parameters in improving cardiac output
acutely and NYHA functional class at 1 month
(29,30). A recent study showed that in nonresponders
to CRT, a multidisciplinary approach centered on Biv
pacemaker optimization in a heart failure program,
can reduce the adverse event rate, including death,
transplantation, and heart failure hospitalization (31).
Pacemaker optimization includes interrogation
of the pacemaker, evaluation of the baseline echo-
Naqvi 1169
Echocardiography in Pacemaker Optimization
cardiogram, AVD optimization, VVD optimiza-
tion, determination of rate-adaptive AVD, and
determination of appropriate sensitivity for rate
response.
The American Society of Echocardiography Ex-
pert Consensus Statement of 2008 (32) suggested a
simplified AVD optimization method. However,
due to variable results by individual Doppler param-
eters (21,22), we (29,30,33,34) and others (35,36)
have used a pacemaker optimization method utiliz-
ing individual patient hemodynamics. The reader is
referred to excellent reviews on pacemaker optimi-
zation using AVD (37) and VVD (38).
Pacemaker interrogation. Differences in Biv pace-
maker programming features in major pacemaker
devices are shown in Table 1. Pacemaker interro-
gation steps are listed in Table 2. Increasing atrial
or ventricular pulse width and/or amplitude may
enable atrial and/or Biv pacing. Increased
atrial pacing rate (to 70 to 85 beats/min) ABBREVIATIONS
may decrease or eliminate frequent atrial AND ACRONYMS
and/or ventricular premature beats (Fig.
3). Continuous atrial sensing or pacing AVD ⴝ atrioventricular delay
should be used during AVD optimization. Biv ⴝ biventricular
If a patient is intermittently sensing and CRT ⴝ cardiac resynchronization
pacing at heart rates between 60 and 70 therapy
beats/min, decreasing the backup atrial LV ⴝ left ventricle/ventricular
pacing rate to 50 to 55 beats/min may MR ⴝ mitral regurgitation
allow optimization during complete atrial NYHA ⴝ New York Heart
sensing, whereas increasing atrial pacing Association
to 65 to 70 beats/min may allow optimi- RV ⴝ right ventricle/ventricular
zation during complete atrial pacing when PW ⴝ pulsed wave
the intrinsic rate is less than 65 beats/min. VTI ⴝ velocity time integral
The “A-fib suppression” feature may have VVD ⴝ interventricular delay
to be turned OFF to prevent increased
paced atrial rate in those with atrial ectopy. Sleep
apnea may cause a large variation in pulsed wave
(PW) Doppler parameters during apneac versus
hyperpneac phase of respiratory cycle due to varia-
tion in heart rate: bradycardia and ventricular ec-
topy during apnea and tachycardia during hyper-
pnea, increase in mitral regurgitation (MR) during
bradypnea or apnea (Fig. 4), and marked interven-
tricular dependence due to extreme shifts in in-
trathoracic pressure during hyperpnea (33), hence
the recognition of sleep apnea is important before
optimization is attempted.
Baseline echocardiogram. A comprehensive evalua-
tion by a skilled sonographer, preferably with a
supervising cardiologist, of baseline echo Doppler
hemodynamics and filling pressures at the baseline
pacemaker settings (38,39) should be performed.
Appropriate Doppler filter, gain, scale, and sweep
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Echocardiography in Pacemaker Optimization NOVEMBER 2010:1168 – 80

Figure 1. Determination of Optimal AVD by the Ritter Method

Atrial truncation at a short atrioventricular delay (AVD) of 50 ms (A), E and A fusion at a long AVD of 250 ms (B), and optimal mitral
inflow at an AVD of 120 ms (C). A corresponding change in left ventricular (LV) velocity time integral (VTI) and ejection duration is seen
in D through F. Highest LV VTI of 18.8 cm is shown in F at optimal AVD. Ritter’s formula is shown at the bottom of the figure, where QA
is time from onset of QRS to end of mitral inflow A-wave. Note that diastolic mitral inflow filling time is longest (421 ms) at a short AVD
of 50 ms that is not optimal.

A B C

D E F

G H

I J

Figure 2. Determination of Optimal AVD by Iterative Method

Iterative method of AV optimization. An AVD of 50 ms (A) leads to premature closure of the mitral valve. Progressive increases in AVD
from 80 ms (B) to 170 ms (C) lead to progressive improvement in mitral inflow A-wave (white arrows, B and C) along with correspond-
ing improvement in LV VTI (D–F). AVD of 180 ms produces the best mitral inflow E and A combination (G), whereas 250 ms leads to
marked E and A approximation and reduction in diastolic filling time (H). LV VTI shows the highest value (15.62 cm) at AVD of 180 ms (I)
and deteriorates at 250 ms (J). Abbreviations as in Figure 1.
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Table 1. Differences in Major Manufacturer’s Devices

Medtronic St. Jude Boston Scientific

Model Consulta CRT-D Promote⫹RF (36) Cognis
Sensed AVD 30–350 ms 25; 30–325 ms 30–300 ms
Paced AVD 30–350 ms 25; 30–300 ms 30–300 ms
AVD increase ⬍200 ms 10 ms 10 ms 10 ms
AVD Increase ⬎200 ms 10 ms 25 ms 20 ms
VVD baseline LV first 4 ms LV first 10 ms LV first 5 ms
VVD programmable LV 0-80 ms 0–80 ms 0–100 ms
VVD programmable RV 0-80 ms 0–80 ms None
VVD increments 10 ms 5 ms* 10 ms, LV only
Effect of LV offset on LV AVD None None Shortens proportionately
Effect of LV offset on RV AVD Increases proportionately Increases proportionately None
Rate-adaptive AVD onset ⬎60 beats/min ⬎90 beats/min b/w LRL and UTR
Rate-adaptive AVD shortening Linear response b/w programmable rates Programmable 1-, 2-, or 3-ms Linear response b/w programmable rates
shortening per 1 beat/min
in rate (low, normal, high)
Rate-adaptive AVD manually programmable Yes No Yes
Rate-response sensing mechanism Accelerometer Electrical activity and Accelerometer
accelerometer
AVD ⫽ atrioventricular delay; b/w ⫽ between; LRL ⫽ lower rate limit; LV ⫽ left ventricular; RV ⫽ right ventricular; UTR ⫽ upper tracking rate; VVD ⫽ interventricular delay. *First available
programmable delay is 15 ms for LV first.

speed settings are critical in ensuring correct mea-
surements and for best temporal and spatial resolu-
tion. An optimized diastolic filling allows E and A
separation, making the end of mitral inflow A-wave
coincide with the R-wave of the electrocardiogram,
thus preventing atrial truncation (Fig. 1) and avoid-
ing diastolic MR. Presence of an abnormal relax-
ation pattern on mitral inflow Doppler usually
indicates adequate AVD programming (32,33), al-
though exceptions are not uncommon, whereas
pseudonormal or restrictive mitral inflow pattern,
Table 2. Pacemaker Interrogation
1. Percentage Biv pacing. If ⬍95%, consider significant atrial or
ventricular ectopy, atrial arrhythmia.
2. Percentage atrial pacing, VV offset, atrial and ventricular lead
sensing and pacing threshold, increased atrial or ventricular
lead thresholds, and programming of AVD at or above
intrinsic AVD.
3. Heart rate. Fixed heart rate on heart rate histogram may be
due to chronotropic incompetence or lack of use of rate-
response features or decreased sensitivity settings for rate
response or may indicate a significant limitation in physical
activity.
4. Intrinsic AVD. This determines range of AVDs available for
programming. A high intrinsic AVD due to poor AV
conduction allows a greater range of AVDs for programming.
5. Determine backup atrial pacing rate, turn it up to suppress
ectopy and down to physiological levels (60 beats/min) to
allow atrial sensing.
6. Determine heart rate variability, rate response, rate-response
sensitivity, lead thresholds.
7. Exclude presence of sleep apnea by using the respirometer
on the ultrasound system.
Biv ⫽ biventricular; VV ⫽ interventricular; other abbreviation as in Table 1.
truncation, or absence of A-wave (despite presence
of sinus rhythm), and E and A fusion suggest the
need to adjust AVD (32). Presence of prominent
pulmonary vein atrial reversal may indicate that the
AVD is too short (39) (Fig. 5). Presence of diastolic
MR by color Doppler gated to electrocardiogram
signal, and better by continuous wave Doppler, and
E and A fusion indicate that the AVD is too long
(Fig. 5). Decreased dP/dt, increased aortic pre-
ejection time, restrictive mitral and pulmonary vein
inflow pattern, presence of MR, and increased
pulmonary artery systolic pressure are nonspecific
markers of advanced LV dysfunction and/or in-
creased LV end diastolic and left atrial pressure, and
are a useful guide during pacemaker optimization
(29,30). Improvement in LV and RV dP/dt (Fig.
6), shortening of aortic pre-ejection delay, conver-
sion to a less restrictive mitral and/or pulmonary
inflow pattern (Fig. 6), reduction in RV–right atrial
gradient (Fig. 5), reduction in systolic MR (Fig. 7)
and tricuspid regurgitation, and elimination of di-
astolic MR or tricuspid regurgitation should be the
goal. Thus, in some patients, mitral inflow filling
time needs to be compromised by allowing some
atrial wave truncation to avoid diastolic MR. In
others, improvement in pulmonary vein filling pat-
tern to a less restrictive type dominates the choice of
optimal AVD or VVD setting (Fig. 6), whereas in
others, systolic MR (Fig. 7) or diastolic MR (Fig. 5)
guides optimization along with LV VTI and dia-
stolic filling evaluation. Improvement in most or all
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Figure 3. Effect of Atrial Pacing Rate and AVD LV Filling and Ejection

Effect of AVD optimization on diastolic function and LV ejection. To suppress ventricular ectopy, the atrial pacing rate was increased to 80 beats/min
at onset. Marked restrictive mitral inflow with tall E-wave, short deceleration time, and a small A-wave is shown at baseline at an AVD of 110 ms (A).
LV outflow pulsed wave (PW) Doppler shows decreased peak velocity of 0.5 m/s and pulsus alternans pattern (alternating increase and decrease in
peak velocity) indicating advanced LV dysfunction (B). At an optimal AVD of 170 ms, mitral inflow (C) became less restrictive. Pulsus alternans pat-
tern continued; however, LV ejection velocities increased to 0.6 m/s (D). Increased atrial pacing to 90 beats/min further improved mitral inflow (E)
and abolished pulsus alternans pattern on LV outflow Doppler (F). Abbreviations as in Figure 1.

of these aforementioned echo Doppler features
nearly always predicts a significant improvement in
the patient’s functional class after optimization (5).
Using this method, we have demonstrated an im-
provement, not only in diastolic filling parameters,
LV ejection duration, and VTI, but also in MR
grade, pulmonary artery pressure, as well as myo-
cardial performance index (29), and in functional
class at follow-up (30). Whether optimal mitral
inflow also provides optimal preload for RV has not
been evaluated and needs further study.
Pacemaker programming in resting conditions.
DETERMINATION OF OPTIMAL AVD. AVD optimi-
zation is generally performed before VVD optimi-
zation (Table 2). VV offset is turned OFF and
optimal AVD is determined by Ritter’s method
using mitral inflow PW Doppler (23) (Fig. 1). This
is done by using a combination of a short AVD and
the longest AVD that still provides complete Biv
capture. Start with 50 ms to 70 ms AVD and
progressively increase AVD in increments of 10 to
20 ms. The shortest AVD at which mitral inflow
A-wave is seen is considered the shortest AVD. A
long AVD, such as 250 ms, is then programmed. If
there is native AV conduction at this AVD (as
evident by change in surface QRS on the ultrasound
monitor [Fig. 8] and from intracardiac electro-
grams), AVD is decreased in 20-ms decrements
until fusion pattern and then complete Biv capture
occurs on surface and intracardiac electrograms.
Mitral inflow is then evaluated at this “long” AVD.
Not infrequently, AVD above 250 ms needs to be
tested. Review of QRS from the image stored at the
shortest AVD helps ensure that the QRS morphol-
ogy at highest AVD has resemblance to that at the
shortest AVD to confirm Biv pacing (Fig. 8).
Marking the transition in QRS morphology is
helpful (Fig. 8). Ritter calculation [(AVD long ⫹
QA short) ⫺ (AVD short ⫹ QA short) ⫹ AVD
short, where QA ⫽ time from onset of QRS to the
end of A-wave on mitral inflow] is made from the
mitral inflow at shortest and longest AVD (23).
Subtracting the time interval between end of trans-
mitral A-wave and onset of systolic MR from the
programmed AVD is another quick method of
determining optimal AVD (40). Occasionally, 30-
to 50-ms AVD is optimal and causes the best E
and A separation (Fig. 9). Not infrequently, AVD
(Fig. 2) of 300 ms is optimal. AVD above and
below the Ritter’s optimal AVD is tested until best
echo Doppler parameters are achieved. It is impor-
tant to ensure that optimal mitral inflow is associ-
ated with improved LV VTI, ejection duration, and
minimum isovolumic contraction time, MR, and
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Figure 4. Pulmonary Vein Atrial Reversal and Diastolic MR at Short and Long AVDs

Effect of a very short atrioventricular delay (AVD) on mitral inflow and pulmonary vein inflow is shown in A and B and that of long AVD
on mitral inflow and MR in C and D. A short AVD leads to absence of mitral inflow A-wave and marked pulmonary vein atrial reversal (B,
white arrow). Prolonged AVD causes E and A approximation (C), shortening of diastolic filling time (C), and appearance of diastolic
mitral regurgitation (MR) (white arrows, D). (E) Shows intermittent diastolic MR (white arrow) at an AVD of 130 ms with complete reso-
lution at an AVD of 80 ms (F). Diastolic tricuspid regurgitation is shown at an AVD of 200 ms (white arrows, G) with resolution at an
AVD of 80 ms (H) and a reduction in right ventricular–right atrial gradient in H compared with G.

pulmonary artery pressure. Evaluation of pulmonary
vein flow allows indirect assessment of left atrial
pressure. AVD that causes minimal atrial reversal, a
systolic dominant filling pattern, and lengthening of
pulmonary vein deceleration time should be used to
minimize left atrial pressure (29,30) (Figs. 4, 6, and 10).
In patients with mitral valve closure before pacemaker
spike at long AVDs, the iterative method may be used
whereby AVD is progressively increased in 10- to
25-ms increments from the shortest AVD (Fig. 2) or
progressively reduced in 10- to 25-ms decrements
from the longest AVD that provides Biv capture
without fusion until the optimal mitral inflow pattern
is obtained without atrial truncation or E and A
fusion. It is to be noted that the longest diastolic filling
time—often present at the shortest AVD—is not
always optimal (Fig. 1).
DETERMINATION OF OPTIMAL VVD. VVD only op-
timization has a role in patients in whom AVD
cannot be optimized such as those with atrial fibrilla-
tion. Small, single-center studies (13–16) including
our experience (29,30) demonstrate incremental ben-
efit of VVD optimization after AVD optimization.
Large, nonrandomized studies have shown acute ben-
efit of VVD optimization and improved follow-up
exercise capacity (10,14), whereas large, randomized
studies (41,42) have not found benefit of sequential
versus Biv pacing with nominal delay.
Prior studies have shown the utility of assessing
myocardial displacement using tissue Doppler (16)
as well as PW tissue Doppler (13). The range of
optimal VVD is relatively narrow and most com-
monly involves LV pre-excitation within 20 ms
(14). Automated color-coded velocity maps provide
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Figure 5. Effect of Cheyne-Stokes Respiration on Cardiac Hemodynamics

Effect of Cheyne-Stokes respiration on ventricular ectopy (A and B), heart rate (C and D), mitral inflow (E and F), and mitral regurgitation
(MR) (G and H) in 4 different patients. Respirograms are shown by green tracing above the electrocardiogram. Marked ventricular ectopy
is shown during hyperpnea (A) and apnea (B). O2 saturation varied between 79% in late apnea to 94% pre-apnea. Increased heart rate
(92 beats/min) is shown during hyperpnea (C), and bradycardia (60 beats/min) during apnea (D). E and A separation and increased dia-
stolic filling time is shown in E during bradycardia at an atrioventricular delay (AVD) of 210 ms, and E and A approximation is shown in
(F) during hyperpnea and increased heart rate at the same AVD. Hyperpnea is associated with moderate mitral regurgitation (MR) (G),
whereas hypopnea is associated with bradycardia and marked reduction in MR severity (H).

quick assessment of segmental LV and RV delays
and their change with VVD changes (32,33) (Fig.
11) or in myocardial displacement and function.
The majority of studies on VVD optimization have
used LV VTI (10,22), whereas other studies have
used myocardial performance index (20) and VVD
by PW Doppler of LV and RV outflow (27). Mitral
inflow is re-evaluated after optimal VV program-
ming and AVD readjusted if required. AVD ad-
justment is usually not required with Medtronic
(Minneapolis, Minnesota) or St. Jude’s (St. Jude
Medical, St. Paul, Minnesota) devices; however,
with a Boston Scientific (Natick, Massachusetts)
device, AVD needs to be increased by the amount
of LV offset and decreased by the amount of RV
offset (Table 1). With a Medtronic device, in-
creased LV pre-excitation may lead to fused rhythm
in RV. Current generation pacemakers do not allow
shortening of VVD, hence a large resting VVD at
lower heart rates may be excessive for a shorter RR
interval during exercise and may produce inter- and
intraventricular dyssynchrony at higher heart rates
or may even lead to loss of RV or LV capture due
to shortening of intrinsic AVD during exercise.
This may explain lack of beneficial effects of se-
quential VVD.
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A B C

E D

A S

D E F

S D D D
S D S S

Figure 6. Optimized Biv Pacing Improves Restrictive Diastolic Filling and LA Pressure

PW Doppler of mitral (A) pulmonary vein inflow (B) and continuous wave Doppler of the mitral regurgitation (MR) jet (C) during native rhythm in a
77-year-old woman with New York Heart Association (NYHA) functional class III. The pacemaker was programmed at a paced atrial rate of 80 ms,
paced AVD of 150 ms, and interventricular (VV) offset of 0 ms. Marked E and A fusion (A), restrictive pulmonary inflow pattern with S:D wave rever-
sal (B), and decreased LV dP/dt (blue bars at 1 m/s and 3 m/s of MR envelope) (C) is shown at native rhythm (AVD 250 ms). Premature ventricular
complexes (PVCs) are shown by a white arrow in B and C. Atrial rate was lowered to 65 beats/min, and an AVD of 50 ms produced a marked
improvement in diastolic filling pattern (D) and improvement in left atrial (LA) pressure as shown by pulmonary vein filling pattern (E). Improvement
in LV dP/dt during biventricular (Biv) pacing is shown (F). Note the increase in LV–LA gradient as shown by peak MR velocity of 4.9 m/s (96 mm Hg)
during Biv pacing (F) compared with 4 m/s (64 mm Hg) during native conduction (C), indicating lowering of left atrial pressure. Abbreviations as in
Figure 1.

Figure 7. Effect of Changes in AVD on MR

Effect of changes in AVD on MR in a patient with NYHA functional class II after cardiac resynchronization therapy (CRT). AVD was pro-
grammed at 350 ms by the primary care physician. Moderate to severe MR during native rhythm (AVD 350 ms) is shown (A). Biv pacing
at an AVD of 250 ms led to a reduction in MR severity (B). Further decrease in AVD to 130 ms led to a further reduction in MR severity
(C). Mild MR is seen at an optimal AVD of 160 ms (D). Significant improvement in symptoms occurred after optimization. Abbreviations
as in Figures 1, 2, 4, and 6.
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Figure 8. Evaluation of Surface QRS to Determine Biv Pacing

Surface QRS on the ultrasound monitor from lead III in response to atrioventricular delay (AVD) changes are shown. A was obtained dur-
ing transition from native rhythm at an AVD of 200 ms to a short AVD of 50 ms. Note the complete change in QRS pattern (A) during
biventricular (Biv) pacing (transition). (B) QRS at 140 ms shows morphology in-between native and Biv-paced rhythm representing fusion
complexes. C shows transition from an AVD of 130 ms to 80 ms (white arrow). The QRS morphology changes back to that shown in A,
indicating complete Biv pacing at an AVD of 80 ms. D shows transition from an AVD of 130 ms to 100 ms (white arrow) and QRS mor-
phology similar to that in A, suggesting complete Biv pacing.

Exercise and pacemaker optimization. Patients with at rest that is accentuated during exercise (43,44).
dilated cardiomyopathy have prolongation of LV In addition, abnormal shortening of LV diastolic
systole and an abnormal shortening of LV diastole time requires higher left atrial pressures to maintain

Figure 9. Effect of RV Pre-Excitation on LV AVD in Medtronic Device

Effect of interventricular delay on mitral inflow in a patient with a Medtronic Biv device at a paced atrial rate of 75 beats/min. A shows marked E
and A fusion at an AVD of 100 ms and LV pre-excitation of 20 ms at baseline, and B shows further E and A approximation with RV pre-excitation of
15 ms, because in Medtronic devices, RV pre-excitation causes a proportionate increase in LV AVD. Shortening of AVD to 60 ms led to no change in
mitral inflow (C). Shortening of AVD to 30 ms led to E and A separation (D). E and F were obtained at an increased paced atrial rate of 90 beats/min at an
AVD of 30 ms (E) and 50 ms (F). Note the E and A fusion in E and separation in F. This illustrates that occasionally, AVD may need to be increased at an
increased heart rate. Abbreviations as in Figures 1 and 4.
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Figure 10. Effect of Atrial Pacing on LV Filling and Ejection

Mitral inflow (A and B), pulmonary vein inflow (C and D), and LV outflow PW Doppler (E and F) at baseline (A-sensed AVD 120 ms: A, C,
and E) and optimal (A-paced 60 beats/min, AVD 300 ms: B, D, and F) pacemaker settings. An increase in A waves and decreased E/A ratio
occurred (B), and pulmonary vein pattern became S dominant with reduced D-wave deceleration time (D), indicating reduction in left atrial
pressure. An improvement in percentage LV ejection time also occurred (F). Abbreviations as in Figures 1 and 2.

LV filling during exercise, resulting in pulmonary However, current rate-adaptive AVD algorithms
congestion and exercise intolerance (45). Modern are based on data derived from patients with con-
pacemaker devices allow rate-response as well as duction abnormalities (45,46), who had otherwise
rate-adaptive AVD shortening during exercise. preserved RV and LV systolic function. Little is

Figure 11. Effect of Sequential Ventricular Pacing on Mechanical Asynchrony

Tissue synchronization images are shown in the apical 4-chamber view. Normal segments are coded in green, and delayed seg-
ments are coded in a progressive sequence of green, yellow, orange, and red. A is at a VV offset of 0 ms and optimal AV delay of
210 ms. Delay in systolic contraction is shown in the basal lateral wall, basal inferior interventricular septum, and RV free wall
(white arrows in A). Homogenous contraction in LV and RV is seen after LV pre-excitation of 30 ms (B). Effect of RV pre-excitation
on mechanical asynchrony is shown in another patient in C and D. Pacemaker was programmed at sensed AVD of 100 ms and LV
pre-excitation of 20 ms. Marked delay in the RV free wall and interventricular septum (white arrows in C) was present at baseline
settings. RV and septal delay decreased progressively as the VVD were changed to VV 0, right ventricular offset of 10, and then 15
ms (D). Abbreviations as in Figures 1, 4, and 6.
1178 Naqvi JACC: CARDIOVASCULAR IMAGING, VOL. 3, NO. 11, 2010

Echocardiography in Pacemaker Optimization NOVEMBER 2010:1168 – 80

Figure 12. Increased Atrial Pacing Rate Requires Progressive Shortening of AVD

Mitral inflow PW Doppler tracing at optimal AVD of 190 ms and LV offset of 0 ms (A). Atrial pacing rate was then increased to 70 beats/
min, and AVD was kept fixed at 190 ms. Marked E and A fusion developed (B). AVD was then progressively shortened to 120 ms until E
and A separation occurred (C). Paced atrial rate was then increased to 80 beats/min at the AVD of 120 ms. Marked E and A fusion devel-
oped again (D). Progressive shortening of AVD to 90 ms (E), and then 80 ms (F) caused mitral inflow E and A separation. Further short-
ening of AVD to 70 ms led to shortening of mitral inflow A-wave and premature closure of mitral valve. Hence, optimal AVD at a paced
atrial rate of 70 beats/min was 120 ms, and at 80 beats/min was 80 ms. Abbreviations as in Figures 1 and 2.

known about the magnitude of AVD shortening with
increased heart rate in heart failure patients and
whether AVD should be shortened, kept constant
(47,48), or prolonged (49) as heart rate increases.
Recent studies suggest that AVD changes during
exercise are variable (50). Another study found that
echocardiographic diastolic filling time and stroke
volume were better during exercise using shorter than
baseline AVD (Fig. 12) (51). The effect of optimiza-
tion at increased heart rate requires further studies.
Current Limitations of Pacemaker Programming
An evaluation of complex programming features
should be part of pacemaker optimization. Adjust-
ment of heart rate, atrial-pacing versus atrial-
sensing, and often times, evaluation of other Dopp-
ler parameters are required for pacemaker
optimization. Collaboration among heart failure,
electrophysiology, and echo specialists is needed for
successful heart failure programs incorporating
pacemaker optimization (31). The benefit of VVD
programming remains controversial and requires
further evaluation. Use of rate-response and rate-
adaptive AVD programming requires more in-
depth study. An anticipated increase in complexity
of pacemaker designs, including use of dual/
multiple LV and/or RV leads and/or electrodes and
need for reprogramming, is expected to make pace-
maker optimization more complex. Randomized
controlled trials comparing adjunct and alternate
techniques are needed, with long-term clinical end
points.
Reprint requests and correspondence: Tasneem Z. Naqvi,
1510 San Pablo Street, Suite 322, Division of Cardiology,
University of Southern California, Los Angeles, Califor-
nia 90033. E-mail: tnaqvi@usc.edu.

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Key Words: cardiac pacing y
Doppler y echocardiography y
pacemaker optimization.