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New Approaches to Evaluate Dyssynchrony
Review
Acta Cardiol Sin 2010;26:142-50
New Approaches to Evaluate Mechanical
Dyssynchrony - Potential Usefulness in
Predicting Response to Cardiac
Resynchronization Therapy
Chun-Li Wang,1,2 Chia-Tung Wu,1 Yung-Hsin Yeh,1 Lung-Sheng Wu1 and Chi-Tai Kuo1,2
Cardiac resynchronization therapy (CRT) is an established therapy for patients with advanced heart failure and wide
QRS intervals. Numerous single-center studies indicated that the assessment of mechanical dyssynchrony helps
predict response to CRT. However, two multi-center studies disprove the idea that the conventional assessment of
mechanical dyssynchrony is useful for CRT patient selection. The purpose of this review is to provide an overview
of the conventional methods as well as three novel approaches (cross-correlation analysis, Fourier analysis of strain
uniformity, and discoordination analysis) for dyssynchrony assessments and their potential usefulness in predicting
response to CRT.
Key Words:
Cardiac resynchronization therapy · Dyssynchrony · Echocardiography
INTRODUCTION
Mechanical dyssynchrony assessment:
conventional steps and its limitations
Mechanical dyssynchrony, the difference in regional
contraction timing, is usually a consequence of electrical
dyssynchrony due to ventricular conduction delay or
right ventricular pacing. 8-15 Data from single-center
studies suggests that numerous parameters of mechanical dyssynchrony can improve patient selection for CRT
on the top of a wide QRS duration.8-10,12-14 These parameters include the septal-to-posteior wall motion delay
on M-mode echocardiography (> 130 ms), anteroseptalto-posterior wall delay using speckle tracking radial
strain (> 130 ms) and several indices based on tissue
Doppler imaging (TDI), such as septal to lateral delay
(SLD) in apical 4-chamber view (> 60 ms), maximum
difference in opposing wall delay (MD) in apical 4chamber or long-axis views (> 65 ms) and the standard
deviation of 12 sites (TsSD) using longitudinal tissue
Doppler velocities (> 34 ms).8-10,12,16-19
However, recent two multi-center prospective studies disprove the idea that the assessment of mechanical
dyssynchrony is useful for CRT patient selection. The
Cardiac resynchronization therapy (CRT) is an established treatment for patients with advanced heart failure (HF) and wide QRS intervals (> 0.12 sec).1,2 CRT
improves cardiac function and clinical symptoms and
reduces mortality. 3-8 However, despite its overall efficacy, 30% to 40% patients receiving CRT do not benefit from the therapy, and one concern is that patient selection, which has been based on a wide QRS duration,
inadequately identifies mechanical dyssynchrony.8-12 It
has been proposed that mechanical dyssynchrony rather
than electrical dyssynchrony better predicts response to
CRT.8-10,12-14
Received: October 19, 2009 Accepted: November 24, 2009
1
First Division of Cardiovascular Department, Chang Gung Memorial
Hospital, Linkou Branch; 2College of Medicine, Chang Gung
University, Taoyuan, Taiwan.
Address correspondence and reprint requests to: Dr. Chi-Tai Kuo,
First Division of Cardiovascular Department, Chang Gung Memorial
Hospital, Linkou Branch, Taoyuan, Taiwan. Tel: 886-3-328-1200,
ext. 8162; Fax: 886-3-327-1192; E-mail: [email protected]
Acta Cardiol Sin 2010;26:142-50
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New Approaches to Evaluate Dyssynchrony
the adverse consequences of asynchronous activation by
stimulating the right ventricle and left ventricle simultaneously or pacing the left ventricle only.
The conventional steps for quantifying mechanical
dyssynchrony are as follows. First, curves to depict the
motion or deformation of ³ 2 segments of the left ventricle (velocity, strain or strain rate) are determined from
TDI or speckle tracking echocardiography. Second, the
time from a reference point on electrocardiogram to a
peak of velocity or strain is measured for each curve. Finally, mechanical dyssynchrony is quantified from the
dispersion of the time-to-peak values (the difference or
the standard deviation). Although fast and easy to measure, time-to-peak analysis that uses only a single data
point of the velocity or strain curve is methodologically
simplistic and likely susceptible to noise and technical
factors. Recent studies including the PROSPECT trial
have shown that time-to-peak analysis is highly observer-dependent and poorly reproducible, even in normal controls.20,27 Peak systolic velocities from TDI are
often difficult to locate in cases of multiple peaks, a flat
velocity contour, marked beat-to-beat variations and no
positive velocity during systole.28 Another issue is that
TDI measures motion relative to the transducer, whether
active or passive. The failing heart may show a rocking
movement that is difficult to interpret the data and that
the measured value may not really represent asynchronous contraction.29
Most of mechanical dyssynchrony analyses only assess the time differences of mechanical activity in different regions and do not consider the magnitude of regional contraction. Therefore, such analysis is unable to
clarify whether the measured value truly reflects a temporal delay in mechanical contraction due to asynchronous activation or the heterogeneity of LV contraction in
the wall. The former is a likely target for CRT, whereas
for the latter, the role of CRT is not clear.25
Predictors of Response to CRT (PROSPECT) trial prospectively evaluated the value of 12 echocardiographic
metrics of mechanical dyssynchrony to predict response
to CRT, based on both conventional and TDI-based
methods, in 426 patients with HF and a standard indication for CRT from 53 medical centers.20 Given the modest sensitivity and specificity in this trial, no echocardiographic measure of dyssynchrony could be recommended to improve patient selection for CRT beyond
current guidelines. Likewise, the Resynchornization
Therapy in Patients with HF and Narrow QRS (RethinQ)
trial showed that patients with a QRS duration < 130 ms
and evidence of mechanical dyssynchrony, primarily
based on TDI measures, did not benefit from CRT.21
In view of the two negative studies of mechanical
dyssynchrony, we are faced with a paradox. On one side,
numerous single-center studies indicated that the assessment of mechanical dyssynchrony helps predict response
to CRT. On the other side, randomized multi-center trials
showed contradictory results. Although many studies
have been done to quantify mechanical dyssynchrony in
hopes of refining patient selection, there is still no ideal
dyssynchrony parameter that can be used to recommend
whether a patient should undergo CRT. Many experts
believe that techniques to quantify mechanical dyssynchrony need to be refined, not abandoned, and will
play a role in selecting patients for CRT in the future.22-26
To realize the limitations of mechanical dyssynchrony, it is necessary to know why mechanical dyssynchrony might occur and how we measure it. In normal subjects, the left ventricle is activated almost simultaneously through the rapid conduction system, and this
is followed by synchronous contraction. Patients who
have left bundle branch block or other ventricular conduction disturbances have a markedly different activation sequence. In patients with left bundle branch block,
the inter-ventricular septum and right ventricle are activated early, whereas the posterior and lateral left ventricular (LV) walls are activated late. The time difference in activation leads to early septal and late posterior-lateral contraction. Early septal contraction causes
posterior-lateral thinning or stretching, followed by late
posterior-lateral contraction causing septal thinning or
stretching. This asynchronous contraction generates
heterogeneous strain and stress in the left ventricle and
results in inefficient LV performance. CRT can reverse
Cross-correlation analysis of dyssynchrony
Fornwalt et al. developed a new parameter, crosscorrelation delay (XCD), to measure dyssynchrony throughout the cardiac cycles.30,31 XCD uses a signal processing method called a cross-correlation analysis that
utilizes all velocity data from 3 consecutive beats. The
analysis is computed between two tissue velocity curves
by shifting one curve in relation to the other along the
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Acta Cardiol Sin 2010;26:142-50
Chun-Li Wang et al.
ing mechanical dyssynchrony by XCD or XCA may be
useful for expanding the benefits of CRT to potential
subjects who do not fulfill the current CRT criteria.
time axis and computing the correlation coefficient between the two curves for each time shift. A cross-correlation coefficient value of 1 indicates that the two curves
are completely synchronous in time, whereas a value of
0 indicates that there is no correlation between the two
curves. The time shift that results in the maximum correlation coefficient is the temporal delay (Figure 1). The
advantage of XCD is that the analysis does not require
identification of ejection phase or manual selection of
peak systolic velocities.
Fornwalt et al. compared the ability of XCD with the
conventional dyssynchrony parameters SLD, MD and
TsSD to discriminate between normal controls and CRT
responders.31 XCD performed better than conventional
parameters in discriminating responders from normal
controls. XCD was also the only one that showed a decrease after CRT in responders. However, it is important
to note that the temporal delay derived from the crosscorrelation analysis may be inaccurate when the correlation is weak (e.g., correlation coefficient < 0.5).31 This
concern may become important when using cross-correlation analysis to distinguish between CRT responders
and non-responders.
In a recent study, Olsen et al showed that XCD was
unable to distinguish between non-responders and responders.32 They used acceleration data instead of velocity data for cross-correlation analysis. Myocardial
acceleration was computed from the differentiation of
velocity data and was tentatively more close to contractility than velocity. The investigators evaluated the ability of cross-correlation analysis of systolic myocardial
acceleration (XCA) with SLD and TsSD to discriminate
between control groups (with narrow QRS) and CRT responders and between responders and non-responders.32
Similar to XCD, XCA discriminated CRT responders
from control groups with a significantly higher area under curve (AUC) than SLD and TsSD (0.95 vs. 0.59 and
0.75, respectively). XCA also discriminated responders
from non-responders (AUC = 0.66) but not significantly
better than SLD (AUC = 0.55) and TsSD (AUC = 0.58).
With XCA, dyssynchrony in control subjects was
found to be rare, whereas with conventional measures,
dyssynchrony was found in > 30 % of control subjects.
This finding suggests that conventional dyssynchrony
metrics are less specific and overestimate the prevalence
of mechanical dyssynchrony. Better specificity at detectActa Cardiol Sin 2010;26:142-50
Fourier analysis for strain uniformity
Mechanical dyssynchrony can be quantified by the
Fourier decomposition of myocardial strain. 33-35 The
Fourier analysis of each component of the strain is determined over time and space. The zero-order component
S0 of the Fourier decomposition is constant and represents perfectly synchronous contraction, whereas the
first-order component, S1, is sinusoidal and represents
completely asynchronous contraction. The temporal uniformity of strain (TUS) or circumferential uniformity
ratio estimate (CURE) index is calculated as the ratio of
the sum of the synchronous segments (S0) and the sum
of the both S1 and S0 over time.33-35 For a perfectly synchronous motion, TUS or CURE index provides a value
of 1, whereas for a completely asynchronous motion, it
is equal to 0 (Figure 2).
Byrne et al. used the magnetic resonance imaging
and CURE index to compare mechanical dyssynchrony
and the impact of CRT on dyssynchrony between failing
hearts with a right bundle branch block versus left bundle branch block. 33 They found that mechanical dyssynchrony was less in right bundle branch block and
CRT had less effect on failing hearts with right bundle
branch block than those with left bundle branch block.
Bertola et al. calculated the TUS index from speckletracking strain data.35 They found that radial TUS predicted response to CRT (AUC = 0.65), whereas dyssynchrony measure (TsSD strain ) did not (AUC = 0.54)
and was the only one that predicted LV ejection fraction
improvement after CRT.
Fourier analysis of strain uniformity is a more sophisticated quantitative method as compared to conventional dyssynchrony assessment. The TUS (or CURE)
index takes a geographic dispersion of strain into account and may differentiate temporal delays in contraction due to heterogeneity of a failing heart from temporal
delays due to asynchronous activation. However, the analysis assumes a sine wave spatial variation in strain which
may be not true in some patients. In addition, TUS are not
very reproducible. From the Bland-Altman plots shown in
the study of Bertola et al., the 95% limits of agreement
are almost the same as the mean values of TUS.22,35
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New Approaches to Evaluate Dyssynchrony
A
B
C
Figure 1. Myocardial velocity traces and cross-correlation analysis of myocardial velocity. Arrows mark peak systolic velocities in velocity traces
and temporal delay (TD) as well as maximum cross-correlation coefficients (XCC) in cross-correlation analysis plots. (A) Despite a large difference
in time-to-peak systolic velocity (151 ms) in a normal subject, cross-correlation analysis reveals a high degree of synchrony: TD = 9 ms and XCC =
0.88. (B) Baseline date of a CRT responder. Velocity analysis shows significantly delayed peak of the posterior wall (98 ms). Cross-correlation
analysis reveals a significant delay (TD = 162 ms). (C) Six-month follow-up data of a CRT responder. Velocity analysis shows a delayed peak of the
posterior wall (63 ms) but cross-correlation analysis indicates a high degree of synchrony: TD = 0 ms and XCC = 0.9. AVO, aortic valve opening;
AVC, aortic valve closure.
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Chun-Li Wang et al.
A
B
C
Figure 2. Three-dimensional plot of radial strain in a normal subject (A) and a CRT responder before (B) and 6 months after CRT (C) arranged
according to time and ventricular location (left panels); temporal uniformity of strain (TUS) in the same subject evaluated by means of Fourier
analysis (right panels). (A) TUS was 0.998, suggesting synchronous thickening around the ventricle. (B) Baseline TUS was 0.652, suggesting
dyssynchrony. (C) TUS improved from 0.652 to 0.959, indicating resynchronization after 6 months of CRT.
tients with a wide QRS duration.22,25 A more comprehensive assessment of regional myocardial mechanics may
be achieved from indices describing mechanical discoordination, i.e. the amount and distribution of lengthening/shortening or thinning/thickening within the LV
Analysis of mechanical discoordination
The poor performance of mechanical dyssynchrony
metrics in the multi-center studies may be that time differences in onset or peak velocity or strain only partially
reveal the mechanical disturbance of left ventricle in paActa Cardiol Sin 2010;26:142-50
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New Approaches to Evaluate Dyssynchrony
wall. 36 Kirn et al. developed a novel discoordination
measure, called internal stretch fraction (ISF), to quantify the relative circumferential lengthening (internal
stretch) versus circumferential shortening during the
ejection phase by tagging magnetic resonance imaging.36
The amount of stretch (or shortening) was calculated as
the product of the number of regions with stretch (or
shortening) and their average amount of stretch (or
shortening), integrated over the ejection phase (Figure
3). They compared the new index with dyssynchrony
metrics and found that only ISF could differentiate responders from non-responders.
It will be highly valuable to quantify ISF by echocardiography that makes its application and post-CRT
A
B
C
Figure 3. Radial strain rate plots and discoordination analysis (ISF) in a normal subject (A) and a CRT responder before (B) and 6 months after
CRT (C). Tracings of strain rate of 6 mid-ventricular segments are represented as gray lines. The time course of the average thickening [ep(t)] and
average thinning [en(t)] are represented as blue line and red line, respectively. The amount of myocardial thickening (ep) and thinning (en) during the
ejection phase are represented with the area below curve ep(t) and above curve en(t), respectively. Internal stretch fraction (ISF) was calculated as
-(en/ep) ´ 100%. (A) ISF was 0, suggesting no discoordination. (B) Baseline ISF was 118%, suggesting marked discoordination. (C) ISF decreased
from 118% to 10%, indicating recoordination after 6 months of CRT. AVO, aortic valve opening; AVC, aortic valve closure.
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Chun-Li Wang et al.
times with potentially different heart rates and loading
conditions from when the mid-ventricular images were
acquired, so that the marking of ejection phase adds a
source of potential error to the quantification of ISF.
In the above sections, we describe the commonly
used conventional dyssynchrony parameters and three
new approaches for assessing mechanical dyssynchrony.
Advantages and disadvantages of each echocardiographic method for the quantification of mechanical
dyssynchrony are summarized in Table 1. Although the
presence of LV dyssynchrony appears to play an important role in determining the response to CRT, many factors are associated with the outcome of CRT-treated
patients. Comprehensive assessments of mechanical
dyssynchrony, myocardial scar burden, the site of latest
mechanical activation, and venous anatomy pre-operatively may help to identify those who will not derive any
benefit or be potentially worsened.40,41
follow-up more practical and cheaper, and lessens the
burden for patients with heart failure. From our initial
experience, mechanical discoordination could be quantified using speckle-tracking echocardiography. 37 We
found less discoordination in normal subjects and most
CRT non-responders. An acute reduction in discoordination (recoordination) rather than resynchronization
predicted LV reverse remodeling after CRT.37
ISF is conceptually related to internal flow fraction,
which can be measured by conductance catheter or magnetic resonance imaging and has been shown to decrease
significantly after CRT.38,39 When there are alternating regions of myocardial expansion and contraction, blood will
be sequestered in the heart rather than ejected to the systemic circulation. The internal flow fraction or ISF measures the overall inefficiency of the heart by comparing
the amount of effective contraction with the amount of
internal energy wasting.36-39 The advantage of ISF over
conventional metrics is that it takes into account regional
dispersion of strain during the ejection period, rather
than at a single time point in a strain signal. The limitation of ISF is its dependency on timing of aortic opening
and closure. The timing must be collected at different
CONCLUSION
Whenever a novel method develops that will open a
Table 1. Advantages and disadvantages of echocardiographic methods for the assessment of mechanical dyssynchrony
Methods
17,18
Advantages
Disadvantages
M-mode
No specific echocardiographic machine is
needed
Easy to perform
Difficult to determine the timing of peak inward
motion if the wall is akinetic or has complex
motion
A high degree of variability
Color-coded tissue Doppler
velocity8-10,16,19
High temporal resolution
Allows simultaneous comparison of multiple
segments
Susceptible to translational motion or tethering
effect
A high degree of variability
Radial strain by speckle
tracking12,14
Less affected by translational motion and
tethering effect
Less variability
Require specific software
Less temporal resolution
Cross-correlation analysis31,32 Nearly automated analysis
Less variability
Rare dyssynchrony detected in normal subjects
The calculated time delay may be inaccurate if the
velocity correlation is weak
Fourier analysis of strain
uniformity33-35
Nearly automated analysis
Allows assessment of geographic strain
dispersion
Sophisticated method
Based on the assumption of a sine wave variation
in strain
Discoordination analysis36,37
Nearly automated analysis
Allows assessment of the amount of internal
stretch (energy wasting)
Requires identification of ejection phase
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New Approaches to Evaluate Dyssynchrony
new window into the heart function and disclose things
that we have not appreciated previously. Advances in
analysis and better understanding of dyssynchrony and
discoordination will help us find an accurate, reliable
and practical parameter for selecting CRT patients in the
future. Until then, patient selection must use the parameter previously validated in landmark clinical studies: the
QRS duration.
8.
9.
10.
ACKNOWLEDGEMENT
This study was supported by research grant CMRPG
381221 from the Chang Gung Memorial Hospial, Linkou branch, Taiwan.
11.
12.
REFERENCES
13.
1. Epstein AE, DiMarco JP, Ellenbogen KA, et al. ACC/AHA/HRS
2008 Guidelines for Device-Based Therapy of Cardiac Rhythm
Abnormalities: a report of the American College of Cardiology/
American Heart Association Task Force on Practice Guidelines
(Writing Committee to Revise the ACC/AHA/NASPE 2002
Guideline Update for Implantation of Cardiac Pacemakers and
Antiarrhythmia Devices): developed in collaboration with the
American Association for Thoracic Surgery and Society of
Thoracic Surgeons. Circulation 2008;117:e350-408.
2. Hunt SA, Abraham WT, Chin MH, et al. 2009 focused update incorporated into the ACC/AHA 2005 Guidelines for the Diagnosis
and Management of Heart Failure in Adults: a report of the
American College of Cardiology Foundation/American Heart
Association Task Force on Practice Guidelines: developed in collaboration with the International Society for Heart and Lung
Transplantation. Circulation 2009;119:e391-479.
3. Cazeau S, Leclercq C, Lavergne T, et al. Effects of multisite
biventricular pacing in patients with heart failure and intraventricular conduction delay. N Engl J Med 2001;344:873-80.
4. Auricchio A, Stellbrink C, Sack S, et al. Long-term clinical effect
of hemodynamically optimized cardiac resynchronization therapy in patients with heart failure and ventricular conduction delay.
J Am Coll Cardiol 2002;39:2026-33.
5. Breithardt OA, Stellbrink C, Franke A, et al. Acute effects of cardiac resynchronization therapy on left ventricular Doppler indices
in patients with congestive heart failure. Am Heart J 2002;143:
34-44.
6. Abraham WT. Cardiac resynchronization therapy for the management of chronic heart failure. Am Heart Hosp J 2003;1:55-61.
7. Breithardt OA, Stellbrink C, Herbots L, et al. Cardiac resynchronization therapy can reverse abnormal myocardial strain dis-
14.
15.
16.
17.
18.
19.
20.
21.
22.
149
tribution in patients with heart failure and left bundle branch
block. J Am Coll Cardiol 2003;42:486-94.
Bax JJ, Bleeker GB, Marwick TH, et al. Left ventricular dyssynchrony predicts response and prognosis after cardiac resynchronization therapy. J Am Coll Cardiol 2004;44:1834-40.
Penicka M, Bartunek J, De Bruyne B, et al. Improvement of left
ventricular function after cardiac resynchronization therapy is
predicted by tissue Doppler imaging echocardiography. Circulation 2004;109:978-83.
Yu CM, Fung JW, Zhang Q, et al. Tissue Doppler imaging is
superior to strain rate imaging and postsystolic shortening on the
prediction of reverse remodeling in both ischemic and nonischemic heart failure after cardiac resynchronization therapy. Circulation 2004;110:66-73.
Hawkins NM, Petrie MC, Macdonald MR, et al. QRS duration
alone to select patients for cardiac resynchronization therapy: flying in the face of the evidence? Eur Heart J 2006;27:3074-5.
Suffoletto MS, Dohi K, Cannesson M, et al. Novel speckle-tracking radial strain from routine black-and-white echocardiographic
images to quantify dyssynchrony and predict response to cardiac
resynchronization therapy. Circulation 2006;113:960-8.
Yu CM, Fung WH, Zhang Q, et al. Understanding nonresponders
of cardiac resynchronization therapy -- current and future perspectives. J Cardiovasc Electrophysiol 2005;16:1117-24.
Gorcsan J 3rd, Tanabe M, Bleeker GB, et al. Combined longitudinal and radial dyssynchrony predicts ventricular response
after resynchronization therapy. J Am Coll Cardiol 2007;50:
1476-83.
Wu CT, Kuo CT, Luqman N, et al. Three-dimensional automated
contour detection for global systolic dyssynchrony index measurements. Acta Cardiol Sin 2008;24:136-43.
Soliman OI, Theuns DA, Geleijnse ML, et al. Spectral pulsedwave tissue Doppler imaging lateral-to-septal delay fails to predict clinical or echocardiographic outcome after cardiac resynchronization therapy. Europace 2007;9:113-8.
Pitzalis MV, Iacoviello M, Romito R, et al. Ventricular asynchrony predicts a better outcome in patients with chronic heart
failure receiving cardiac resynchronization therapy. J Am Coll
Cardiol 2005;45:65-9.
Pitzalis MV, Iacoviello M, Romito R, et al. Cardiac resynchronization therapy tailored by echocardiographic evaluation of
ventricular asynchrony. J Am Coll Cardiol 2002;40:1615-22.
Yu CM, Fung WH, Lin H, et al. Predictors of left ventricular reverse remodeling after cardiac resynchronization therapy for
heart failure secondary to idiopathic dilated or ischemic cardiomyopathy. Am J Cardiol 2003;91:684-8.
Chung ES, Leon AR, Tavazzi L, et al. Results of the Predictors
of Response to CRT (PROSPECT) trial. Circulation 2008;117:
2608-16.
Beshai JF, Grimm RA, Nagueh SF, et al. Cardiac-resynchronization therapy in heart failure with narrow QRS complexes. N
Engl J Med 2007;357:2461-71.
Fornwalt BK, Delfino JG, Sprague WW, et al. It’s time for a paraActa Cardiol Sin 2010;26:142-50
Chun-Li Wang et al.
23.
24.
25.
26.
27.
28.
29.
30.
31.
32.
digm shift in the quantitative evaluation of left ventricular dyssynchrony. J Am Soc Echocardiogr 2009;22:672-6.
Rademakers LM, de Boeck BW, Maessen JG, et al. Development
of strategies for guiding cardiac resynchronization therapy. Heart
Fail Clin 2008;4:333-45.
Marwick TH. Hype and hope in the use of echocardiography for
selection for cardiac resynchronization therapy: the Tower of
Babel revisited. Circulation 2008;117:2573-6.
Kass DA. An epidemic of dyssynchrony: but what does it mean?
J Am Coll Cardiol 2008;51:12-7.
Gorcsan J 3rd, Abraham T, Agler DA, et al. Echocardiography for
cardiac resynchronization therapy: recommendations for performance and reporting - a report from the American Society of
Echocardiography Dyssynchrony Writing Group endorsed by the
Heart Rhythm Society. J Am Soc Echocardiogr 2008;21:191-213.
Conca C, Faletra FF, Miyazaki C, et al. Echocardiographic
parameters of mechanical synchrony in healthy individuals. Am J
Cardiol 2009;103:136-42.
Anderson LJ, Miyazaki C, Sutherland GR, et al. Patient selection
and echocardiographic assessment of dyssynchrony in cardiac
resynchronization therapy. Circulation 2008;117:2009-23.
Marwick TH, Starling RC. The riddle of determining cardiac
resynchronization therapy response a physiologic approach to
dyssynchrony therapy. J Am Coll Cardiol 2008;52:1410-2.
Delfino JG, Fornwalt BK, Eisner RL, et al. Cross-correlation
delay to quantify myocardial dyssynchrony from phase contrast
magnetic resonance (PCMR) velocity data. J Magn Reson Imaging 2008;28:1086-91.
Fornwalt BK, Arita T, Bhasin M, et al. Cross-correlation quantification of dyssynchrony: a new method for quantifying the synchrony of contraction and relaxation in the heart. J Am Soc
Echocardiogr 2007;20:1330-7.
Olsen NT, Mogelvang R, Jons C, et al. Predicting response to cardiac resynchronization therapy with cross-correlation analysis of
myocardial systolic acceleration: a new approach to echocardiographic dyssynchrony evaluation. J Am Soc Echocardiogr 2009;
Acta Cardiol Sin 2010;26:142-50
22:657-64.
33. Byrne MJ, Helm RH, Daya S, et al. Diminished left ventricular
dyssynchrony and impact of resynchronization in failing hearts
with right versus left bundle branch block. J Am Coll Cardiol
2007;50:1484-90.
34. Helm RH, Leclercq C, Faris OP, et al. Cardiac dyssynchrony
analysis using circumferential versus longitudinal strain: implications for assessing cardiac resynchronization. Circulation
2005;111:2760-7.
35. Bertola B, Rondano E, Sulis M, et al. Cardiac dyssynchrony
quantitated by time-to-peak or temporal uniformity of strain at
longitudinal, circumferential, and radial level: implications for
resynchronization therapy. J Am Soc Echocardiogr 2009;22:
665-71.
36. Kirn B, Jansen A, Bracke F, et al. Mechanical discoordination
rather than dyssynchrony predicts reverse remodeling upon cardiac resynchronization. Am J Physiol Heart Circ Physiol 2008;
295:H640-6.
37. Wang CL, Wu CT, Yeh YH, et al. Recoordination rather than
resynchronization predicts reverse remodeling after cardiac resynchronization therapy. J Am Soc Echocardiogr 2010;23:611-20.
38. Fornwalt BK, Gonzales PC, Delfino JG, et al. Quantification of
left ventricular internal flow from cardiac magnetic resonance
images in patients with dyssynchronous heart failure. J Magn
Reson Imaging 2008;28:375-81.
39. Steendijk P, Tulner SA, Schreuder JJ, et al. Quantification of left
ventricular mechanical dyssynchrony by conductance catheter in
heart failure patients. Am J Physiol Heart Circ Physiol 2004;
286:H723-30.
40. Nazar L., Wang CL, Sung RJ, Kuo CT. Emerging role of cardiac
resynchronization therapy in heart failure. Acta Cardiol Sin
2008;24:1-14.
41. Sanderson JE. Echocardiography for cardiac resynchronization
therapy selection. Fatally flawed or misjudged? J Am Coll
Cardiol 2009;53:1960-4.
150