Circulation. 2008;117:2009-2023
doi: 10.1161/CIRCULATIONAHA.107.721332
(Circulation. 2008;117:2009-2023.)
© 2008 American Heart Association, Inc.
Contemporary Reviews in Cardiovascular Medicine |
Patient Selection and Echocardiographic Assessment of Dyssynchrony in Cardiac Resynchronization Therapy
Lisa J. Anderson, MD;
Chinami Miyazaki, MD;
George R. Sutherland, MD, PhD;
Jae K. Oh, MD
From the Department of Cardiology, St. George’s Hospital, London, United Kingdom (L.J.A., G.R.S.); and Division of Cardiovascular Diseases, Mayo Clinic, Rochester, Minn (C.M., J.K.O.).
Correspondence to Jae K. Oh, MD, Division of Cardiovascular Diseases, Mayo Clinic College of Medicine, 200 First St SW, Rochester, MN 55905. E-mail oh.jae{at}mayo.edu
Key Words: echocardiography • heart failure • pacemakers • pacing
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Introduction
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Appropriate cardiac resynchronization therapy (CRT) enhances
quality of life and improves survival in patients with refractory
heart failure due to systolic dysfunction and mechanical dyssynchrony.
On the assumption that the main therapeutic mechanism of CRT
is the correction of dyssynchronous myocardial contraction,
imaging-based measures of dyssynchrony have been intensely investigated
with the aim of predicting response to therapy. Numerous echocardiographic
dyssynchrony parameters have been proposed, but no large prospective
trial have been published to prove the clinical utility of any
of these indexes. Moreover, the methodology to derive the proposed
dyssynchrony indexes has not been standardized. Therefore, the
purpose of this article is to critically review the current
status of proposed dyssynchrony indexes by echocardiography
for patient selection and to recommend future investigations
in this area.
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CRT: From Origins to Routine Clinical Practice
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The adverse effects of dyssychronous activation
1 and the ability
to correct these abnormalities with biventricular stimulation
2 were described long ago, but the potential therapeutic application
was not realized until an unprecedented study in 1990 reported
recovery from intractable heart failure in 16 patients implanted
with conventional dual-chamber pacemakers programmed to a short
atrioventricular (AV) delay.
3 Although these results could not
be reproduced in prospective studies
4,5 and improvements could
only be demonstrated short-term in highly selected patients,
6 the race to find a pacing therapy for heart failure had begun.
On the hypothesis that the disappointing results of dual-chamber pacing in prospective studies were due to cancelling or overcoming the beneficial effects of AV synchronisation by the adverse effect of RV pacing-induced dyssynchrony,7,8 Cazeau and colleagues proposed a 4-chamber pacing mode and reported the first successful permanent implant in 1994.9 Early randomized controlled trials confirmed short-term improvements in functional capacity and quality of life for patients.10–13 However it was the Comparison of Medical Therapy, Pacing, and Defibrillation in Heart Failure (COMPANION; n=1520 patients) and the Cardiac Resynchronisation in Heart Failure (CARE-HF; n=804 patients) trials that firmly established the role of CRT in contemporary heart failure therapy by demonstrating a significant reduction in combined all-cause mortality and hospital admissions.14,15
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Selection of Candidates in CRT Clinical trials
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The prerequisites of refractory cardiac failure (New York Heart
Association class 3 or 4 and optimal medical therapy) and severe
left ventricular (LV) impairment were apparent and have not
varied between trials. The requirement of sinus rhythm to combine
both AV and ventricular resynchronization was stipulated in
all the randomized controlled trials with the exception of a
substudy of 39 patients in the Multisite Stimulation in Cardiomyopathy
(MUSTIC) trial.
16 However, the choice of a surrogate marker
for LV electromechanical dyssynchrony was more problematic and
varied between the acknowledged "empirical choice" of a QRS
>150 ms in MUSTIC, to inclusion of all patients with QRS
>120 ms in COMPANION, to combined ECG and echo inclusion
criteria in CARE-HF (QRS >150 ms or QRS >120 ms plus 2
out of 3 of aortic preejection delay >140 ms, interventricular
delay >40 ms, and maximal contraction of the posterolateral
wall occurring after the onset of LV filling).
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Defining Response to Therapy
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The best measure for defining response to CRT has not been established.
However, nonresponse to CRT was recognized early on,
12,17,18 spawning a plethora of small nonrandomized echocardiographic
studies aiming to predict response to CRT. "Response" was usually
defined by echocardiographic rather than clinical parameters,
and cutoffs for response differed, resulting in varying proportions
of "nonresponders." Furthermore, dyssynchrony indexes did not
predict clinical response so well as reverse remodeling.
19,20 However, Yu and colleagues justified the use of echocardiographic
parameters by reporting that reverse remodeling (reduction in
LV end-systolic volume
10%) predicted 1-year survival but that
clinical parameters (New York Heart Association class and 6-minute
walk and quality of life scores) were unrelated to survival
in these heart failure patients. A recent study comparing clinical
and echocardiographic responses to CRT demonstrated clinical
improvement in 70% but reverse remodeling, defined as reduction
in LV end-systolic volume
15%, in only 56%. Interestingly, when
change in LV end-systolic volume was subdivided into quintiles
of response, a clear relationship was seen between the percentage
of clinical responders and degree of reverse remodeling, suggesting
a spectrum rather than an absolute response/nonresponse to CRT.
21
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Current Recommended Selection Criteria for CRT
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As successive publications each proposed a new dyssynchrony
measure to reliably predict outcome, the clinician was presented
with a bewildering array of echo determinants on which to base
his or her selection. The publication of almost identical European
22 and American Heart Association/American College of Cardiology
(AHA/ACC)
23 guidelines for CRT in 2005 that omitted any reference
to echocardiographic measures of dyssynchrony was therefore
met with relief by heart failure specialists and electrophysiologists
alike. However, recent UK National Institute for Health and
Clinical Excellence (NICE) guidelines
24 may be interpreted as
a retrograde step by some. Echocardiographic measures of "mechanical
dyssynchrony" are required for patients with QRS of 120 ms to
150 ms, with no guidance on how best to measure this dyssynchrony,
the cutoffs to use, or indeed whether AV, interventricular or
LV dyssynchrony is required.
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Proposed Echocardiographic Dyssynchrony Parameters
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In the following section, we describe the currently proposed
echocardiographic intra- and interventricular dyssynchrony parameters,
their technical pros and cons, and existing prognostic data
for each technique, which are not all consistent. Key features
and findings of published reports of echocardiographic intraventricular
dyssynchrony parameters for the prediction of response to CRT
are summarized in
Table 1
. Disadvantages and advantages of each
echocardiographic method for the quantification of intraventricular
mechanical dyssynchrony are listed in
Table 2.
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Table 2. Technical Advantages and Disadvantages of Echocardiographic Methods for the Assessment of Mechanical Dyssynchrony
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Intraventricular Dyssynchrony
M-Mode Echocardiography
Septal-posterior wall motion delay, the time difference between peak inward motion of the ventricular septum and the posterior wall, is obtained from parasternal short axis M-mode images. An initial report showed septal-posterior wall motion delay 130 ms to predict reduction in LV end-systolic volume index >15% with a sensitivity of 100% and a specificity of 63% in 20 patients at 1 month25 and later to predict improvement in LV ejection fraction (LVEF) >5% and better prognosis at 6 months after CRT.26 However, such a delay could only be quantified in regions that were perpendicular to the ultrasound beam and was feasible in only half of patients.27,37 M-mode of color tissue Doppler imaging enhances timing measurements (Figure 1) but is still limited to assessments of the septum and the posterior wall. In 3 subsequent reports, septal-posterior wall motion delay did not predict outcome after CRT.27,28,37
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Figure 1. M-mode echocardiography with color-coded tissue velocity. a, Timing of ventricular septal (VS) wall motion is difficult to define because of its severe hypokinesis and the lack of distinct peaks. b, Color coding of tissue velocity helps to identify the exact wall motion timing as transition point of blue to red color for septal wall (arrows) and red to blue color for posterior wall (arrowheads) (right). LV indicates left ventricle; PW, posterior wall; and SPWMD, septal-posterior wall motion delay.
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Tissue Velocity
Tissue Doppler imaging (TDI) allows measurement of either longitudinal tissue velocity or deformation (strain) of myocardium, both of which have been used to measure mechanical dyssynchrony. Most publications have employed tissue velocity dyssynchrony measurements, but its methods have not been standardized in following areas:
- Both pulsed-wave TDI and color-coded TDI have been used to identify peak systolic velocity.
- Both time to peak velocity and time to onset of systolic velocity have been measured to calculate dyssynchrony index.
- The number (2, 6, or 12) and location of segments sampled to obtain dyssynchrony index have varied.
- Both the standard deviation and the maximum difference of timing intervals have been used to calculate a dyssynchrony index.
- Velocity peaks were measured during the ejection period only or in both the ejection and the postejection period.
The advantage of pulsed-wave TDI is that it does not require high-end equipment, specific software, or offline analysis, and its drawback is that it requires sampling of multiple regions from different cardiac cycles, which is time consuming and renders tissue velocity peaks more difficult to identify. A sum of dyssynchrony index measured from the time to onset of tissue velocity in each of the basal septal, lateral, inferolateral, and right ventricular free walls showed a sensitivity of 96% and specificity of 77% to predict increase in LVEF >25% after CRT.31 However more recently, no significant difference in septal–lateral delay in time to onset of systolic velocity using pulsed-wave TDI was found between responders and nonresponders.34 Furthermore, neither septal–lateral delay in time to peak nor onset of systolic velocity predicted clinical improvement or reverse remodeling.33
Most published data on mechanical dyssynchrony have used color-coded TDI, which allows simultaneous processing of multiple sample points on the same image for a more comprehensive assessment of dyssynchrony. Bax and colleagues reported that basal septal–lateral delay >60 ms in time to peak systolic velocity predicted a short-term improvement in EF,35 and similar dyssynchrony index (maximum difference in opposing basal segment delay in the apical 4-chamber or 2-chamber view) >65 ms predicted reverse remodeling at 6 months after CRT.19 Yu and colleagues proposed a dyssynchrony index of standard deviation in time to peak systolic velocity among 12 basal and mid segments (Ts-SD) (Figures 2 and 3). Ts-SD >32.6 ms predicted reverse remodeling 3 months after CRT with a sensitivity and specificity of 100% in the initial 30 patients39 and Ts-SD >31.4 ms with a sensitivity of 96% and specificity of 78% in a subsequent 54 patients.40 Yu and colleagues also showed that correlation with reverse remodeling after CRT was better with Ts-SD than any other tissue Doppler parameters, including 2-segment delay, 6–basal segment delay, and maximum difference in 12 segments.40 On the other hand, the Resynchronization Therapy in Normal QRS (RethinQ) study recently found no benefit to CRT in patients with heart failure with a narrow QRS interval (<130 ms) when study entry was determined by a delay of at least 65 ms between 2 opposing walls using color-coded tissue velocity technique.51
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Figure 2. Color-coded tissue velocity recordings from 12 LV segments before (a) and after (b) CRT in 65-year–old patient with nonischemic cardiomyopathy whose LVEF improved by 17% at 6 months after CRT. Apical 4-chamber (left), long-axis (middle), and 2-chamber (right) views are shown. Difference in time to peak velocity during ejection period (arrows) were markedly reduced after CRT.
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Figure 3. Color-coded tissue velocity recordings from 12 LV segments before (a) and after (b) CRT in 71-year–old patient with ischemic cardiomyopathy whose LVEF improved by 19% at 6 months after CRT. Apical 4-chamber (left), long-axis (middle), and 2-chamber (right) views are shown. Before CRT (a), marked difference in time to peak systolic velocity was noted among multiple segments (arrows). b, Six months after CRT, no improvement had occurred in the difference in time to peak systolic velocity.
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Why is there this discrepancy? Determining which "peak" to measure may be a part of the problem. Difficulty in identifying a correct peak to measure is illustrated by several examples in Figure 4. Two distinct peaks of tissue velocity during the ejection period are not uncommon from the free wall even in normal subjects52 (Figures 4 and 5). Such double peaks often show beat-to-beat variability in velocities (Figure 4). Besides, patients with conduction delay and impaired systolic function often show more prominent positive velocities during isovolumic contraction or in the postsystolic period than in the ejection period and sometimes do not show a distinct peak during the ejection period (Figure 4). Therefore, considerable variations in measurements may arise depending on which peak is selected.
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Figure 4. Examples of tissue velocity waveforms. a, Double peaks (arrows) in anterolateral wall in normal subject. b, One of the double peaks (arrows) is located at the time of aortic valve opening in anterior wall in LBBB patient. c, Beat-to-beat variability in velocity of 2 peaks (arrows) during ejection period. d, Postsystolic peak (*) is higher than systolic velocity (arrow) in the inferoseptal segment in LBBB patient. e, Positive deflection at aortic valve opening at downslope shoulder of presystolic velocity (arrow) is the highest peak during ejection period. f, No positive velocity was found during ejection period and prominent presystolic (arrowhead) and postsystolic wave (*) were observed in inferoseptal wall.
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Figure 5. Tissue velocity waveforms in a normal subject from 4-chamber (left), apical long-axis (middle), and 2-chamber views (right). Substantial difference in time to peak systolic velocity was observed among segments (Basal septal-lateral wall motion difference: 100 ms, standard deviation in time to peak systolic velocity: 55 ms).
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The aforementioned studies19,35,39,40 of tissue velocity–derived dyssynchrony indexes used peaks only within the ejection period. However, it is also known that dyssynchronous motion in electrical activation delay is characterized by early septal motion frequently seen in the isovolumic contraction period and delayed lateral motion during the postsystolic period.53 Assessments of myocardial motion that include pre- or postejection periods, or both, may have more value for dyssynchrony measurement than those that focus on motion solely during the ejection period. When postsystolic peak velocities were included, an anteroseptal-posterior delay >65 ms predicted improvement in stroke volume >15% with a specificity of 92%.38 On the other hand, the maximum difference in time to peak velocity predicted reverse remodeling with a poor specificity of 55% three months after CRT when postsystolic peaks were included.20 Yu and colleagues reported a similar detrimental effect for predicting response to CRT when postsystolic peaks were included.40,41 In another study, the percentage of segments showing delayed longitudinal contraction after aortic valve closure correlated with response to CRT.46
Dependence of tissue velocity dyssynchrony parameters on longitudinal motion to represent regional contraction in this population may also be problematic. In hearts with left bundle branch block (LBBB) and reduced LV contraction, long-axis forces are frequently unbalanced, both in their timing and magnitude of contraction. In such "rocking" hearts, overall rotational motion may be greater than any local velocity induced by regional contraction, and thus the local long-axis velocity curve may no longer reflect the timing and magnitude of regional contraction, and the timing of radial motion may better reflect regional contraction as it is less dependent on long-axis rotation.
Strain Imaging
Strain can be measured by TDI or by 2-dimensional speckle tracking and, as it is less affected by tethering or translation induced by unbalanced rocking motion, would theoretically be a more reliable measure of regional myocardial contraction. Tissue Doppler–derived strain is highly angle dependent and may be difficult to measure in patients with a spherical dilated heart and highly angulated basal segments. 2-dimensional speckle tracking based on speckle pattern recognition in B-mode echocardiography may prove to be superior because it is angle independent, allowing assessment of radial, circumferential, and longitudinal strain in all segments. The theoretical disadvantage of speckle tracking is its temporal resolution, which is lower than in tissue velocity–derived strain, especially in dilated hearts requiring large sector size for the imaging.
Using TDI, an abnormal strain pattern (premature early systolic shortening of the septum accompanied by lateral prestretch and followed by postsystolic lateral wall shortening) and its reversal immediately after CRT has been described in patients with left bundle branch block (Figure 6).54 A delay >130 ms in time to peak radial strain in the anteroseptal and inferolateral walls predicted a short-term increase in stroke volume,47 and the standard deviation in time to peak longitudinal strain among 12 basal and mid segments predicted reverse remodeling 6 months after CRT.49 Using 2-dimensional speckle tracking, a delay >130 ms in time to peak systolic radial strain among 6 mid segments in the parasternal short-axis view (Figure 7) predicted increase in LVEF >15% with a sensitivity of 89% and a specificity of 83% at 8 months after CRT.48
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Figure 6. Tissue Doppler–derived longitudinal strain waveforms in 12 mid (aqua) and basal (yellow) segments before (a) and 6 months after (b) CRT in the patient with dilated cardiomyopathy and LBBB who achieved reverse remodeling after CRT. a, Peak strain was marked with arrows. Basal inferoseptal (left upper), anteroseptal (mid upper), and inferior (right upper) segments show early longitudinal shortening occurring during the preejection period. b, Strain waveforms at 6 months after CRT show that early shortening occurring in the preejection period diminished in inferoseptal, anteroseptal, and inferior walls (upper panels).
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Figure 7. Radial strain curves from short-axis view of speckle tracking echocardiography. Significant timing difference was found among time to peak radial strain before CRT (a), and it was reduced after CRT (b).
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In contrast to these positive results, Yu and colleagues reported that standard deviation in time to peak systolic TDI-derived strain in 12 segments did not predict the response to CRT in 2 studies (a first study in 55 patients42 and a second in 256 patients43). Another study also showed dyssynchrony indexes derived from speckle tracking and tissue Doppler strain did not correlate with reverse remodeling 6 months after CRT.44
Three-Dimensional Echocardiography
Three-dimensional echocardiography enables the measurement of dyssynchrony indexes derived from the difference in minimal segmental volume and the standard deviation in time to minimal volume among 16 segments. Short-term improvement in 3-dimensional dyssynchrony index is seen after CRT.55,56 To date, no published study has assessed whether 3-dimensional echocardiography predicts response to CRT.
Poor temporal resolution compared with 2-dimensional or tissue Doppler echocardiography prevents precise measurement of timing and may result in failure to detect the brief early abnormal septal motion typical of left bundle branch block. Moreover, 3-dimensional full-volume image acquisition requires several consecutive beats with regular R-R intervals, limiting its application in patients with atrial fibrillation or frequent ectopic beats.
Interventricular Dyssynchrony
The preejection period difference between pulsed-wave Doppler flow in the aorta and pulmonary artery is used to represent interventricular dyssynchrony, correlates with QRS duration, and typically exceeds 40 ms in patients with QRS >150 ms.57 Although initially overlooked,25,58 the predictive value of preejection period difference was recently highlighted in 2 multicenter prospective trials. The Selection of Candidates for CRT (SCART) group reported that interventricular dyssynchrony >44 ms and smaller end-systolic diameter were the only independent predictors for combined clinical and echocardiographic response,34 and the CARE-HF group found that a cutoff value of 49.2 ms separated event-free curves after CRT.59
The tissue velocity delay between RV and LV free walls has also been used to represent interventricular dyssynchrony. However, contrary to the positive results from large prospective studies using pulsed-wave Doppler, interventricular dyssynchrony measured from tissue velocity either using time to peak19,40 or onset34 was not predictive for the effect of CRT.
Cardiac Time Intervals
Delayed electrical activation results in slow pressure development within the LV with delay in aortic valve opening and closure.60 Isovolumic relaxation can be prolonged because of continuing depolarization in late-activated segments and elastic recoil in early-activated segments after passive stretch by later-activated segments. The filling period shortens and is accentuated by concomitant AV delay. Isovolumic periods are prolonged at the expense of both ejection and filling period. Shortening of isovolumic contraction and prolongation of filling time are seen acutely after CRT and persist at follow-up, suggesting that these changes are related to an immediate change in electrical activation rather than subsequent reverse remodeling.61 Simple measurements of cardiac time intervals using pulsed-wave Doppler have been proposed as indirect measures of dyssynchrony and predictors of response to CRT. Total isovolumic time (sum of isovolumic contraction and relaxation times) correlated with the improvement of exercise capacity and cardiac output after CRT.62,63
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Current Role of Echocardiography Before and After CRT
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High-quality echocardiography imaging is vital in the work-up
of patients before beginning CRT. In addition to assessing ejection
fraction for standard inclusion criteria, echocardiography plays
a key role in determining pathogenesis, provides information
on the extent of viable myocardium, which is relevant for extent
of response to CRT, and is also essential for ruling out treatable
valvular and ischemic pathologies. Echocardiography is also
important after CRT for optimization of pacemaker AV delay.
The defining CRT trials aimed to synchronize both atrioventricular
and ventricular dyssynchrony (hence the inclusion requirement
of sinus rhythm), and protocols required AV optimization (using
either echocardiographic or intracardiac electrical delay method)
in all patients. However, at present, most publications in this
field are small nonrandomized studies. Clear guidance on the
requirement for routine AV optimization or agreement on the
"best method" is lacking, and as a result wide variations in
practice exist. Larger randomized trials are required therefore
to establish (1) the relative additional effect of AV delay
optimization and (2) the best (echocardiographic or intracardiac
electrical delay) method to use. In an ideal scenario, echocardiographic
dyssynchrony measurements would guide the electrophysiologist
in obtaining the ideal lead position. However, in practice this
is often determined by venous anatomy and there may be more
potential for echocardiographic lead position guidance during
surgical epicardial lead placement. Currently, a major limitation
of echocardiography, as well as of other studies, is not being
able to identify nonresponders with a very high accuracy. Although
some centers may select patients for CRT on the basis of echocardiography
measurement of dyssychrony,
64 we do not yet have an echocardiography
parameter with a very high specificity or negative predictive
value, on the basis of which CRT could be denied to patients
who meet conventional selection criteria.
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Conclusion and Recommendations
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Despite the huge output of publications in this field, we do
not presently advise incorporating echocardiographic dyssynchrony
parameters for the selection of candidates for CRT for the following
reasons: First, no large published clinical trials exist to
demonstrate benefit with a particular dyssynchrony index. Second,
conflicting results are emerging on the predictive value of
dyssynchrony indexes. Third, all the parameters described to
date have either technical or theoretical limitations. A practical
parameter or index for selection of appropriate patients for
CRT should be simple and preferably should not require offline
analysis. Clinically, it will be more important to identify
nonresponders to CRT using various clinical, laboratory, and
echocardiographic data with a very high accuracy. This ideal
parameter has not been found.
Echocardiography also has an ongoing role in helping us to understand how CRT actually works. It is possible that response or nonresponse to CRT involves multiple interrelated mechanisms (myocardial viability within the paced area, underlying myocardial conditions such as fibrosis and hypertrophy, and location of the pacing lead) rather than a single mechanism of LV dyssynchrony. Before we hastily exclude potential candidates on the basis of indexes that are not yet validated in large clinical trials, we should try to better comprehend the pathophysiological mechanisms underlying response and nonresponse to therapy. Prospective randomized trials incorporating echocardiography are likely to play an important role in establishing extended indications for CRT. It may require several parameters, which could be used in a stepwise fashion, different parameters for different groups of patients (for example, ischemic versus nonischemic patients), or a combination of these methods, to select or exclude patients for CRT. Until we have a clinically reliable and practical parameter, inclusion criteria based on the major randomized trials should be employed to provide CRT to all deserving patients.
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Appendix: Current ACC/AHA/NASPE 2005 Guideline Update
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Patients with LVEF
35%, sinus rhythm, and New York Heart Association
functional class III or ambulatory class IV symptoms despite
recommended optimal medical therapy and who have cardiac dyssynchrony,
which is currently defined as a QRS duration >120 ms, should
receive CRT unless contraindicated (
Class: I, Level of Evidence: A).
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Acknowledgments
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Disclosures
Dr Miyazaki reports grants from Medtronic, Guidant, and St Jude. Dr Sutherland reports the loan of Vingmed System 7 Ultrasound Machine and honoraria from GE. Dr Anderson and Dr Oh report no conflicts.
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References
|
|---|
- Wiggers CJ. The muscular reactions of the mammalian ventricles to artificial surface stimuli. Am J Physiol. 1925; 73: 346.[Free Full Text]
- Gibson DG, Chamberlain DA, Coltart DJ, Mercer J. Effect of changes in ventricular activation on cardiac haemodynamics in man. Comparison of right ventricular, left ventricular, and simultaneous pacing of both ventricles. Br Heart J. 1971; 33: 397–400.[Free Full Text]
- Hochleitner M, Hörtnagl H, Ng CK, Hörtnagl H, Gschnitzer F, Zechmann W. Usefulness of physiologic dual-chamber pacing in drug-resistant idiopathic dilated cardiomyopathy. Am J Cardiol. 1990; 66: 198–202.[CrossRef][Medline]
[Order article via Infotrieve]
- Linde C, Gadler F, Edner M, Nordlander R, Rosenqvist M, Rydén L. Results of atrioventricular synchronous pacing with optimized delay in patients with severe congestive heart failure. Am J Cardiol. 1995; 75: 919–923.[CrossRef][Medline]
[Order article via Infotrieve]
- Gold MR, Feliciano Z, Gottlieb SS, Fisher ML. Dual-chamber pacing with a short atrioventricular delay in congestive heart failure: a randomized study. J Am Coll Cardiol. 1995; 26: 967–973.[Abstract]
- Brecker SJ, Xiao HB, Sparrow J, Gibson DG. Effects of dual-chamber pacing with short atrioventricular delay in dilated cardiomyopathy. Lancet. 1992; 340: 1308–1312.[CrossRef][Medline]
[Order article via Infotrieve]
- Askenazi J, Alexander JH, Koenigsberg DI, Belic N, Lesch M. Alteration of left ventricular performance by left bundle branch block simulated with atrioventricular sequential pacing. Am J Cardiol. 1984; 53: 99–104.[CrossRef][Medline]
[Order article via Infotrieve]
- Rosenqvist M, Issaz K, Botvinick EH, Dae MW, Cockrell J, Abbott JA, Schiller NB, Griffin JC. Relative importance of activation sequence compared to atrioventricular synchrony in left ventricular function. Am J Cardiol. 1991; 67: 148–156.[CrossRef][Medline]
[Order article via Infotrieve]
- Cazeau S, Ritter P, Bakdach S, Lazarus A, Limousin M, Henao L, Mundler O, Daubert JC, Mugica J. Four chamber pacing in dilated cardiomyopathy. Pacing Clin Electrophysiol. 1994; 17: 1974–1979.[CrossRef][Medline]
[Order article via Infotrieve]
- Cazeau S, Leclercq C, Lavergne T, Walker S, Varma C, Linde C, Garrigue S, Kappenberger L, Haywood GA, Santini M, Bailleul C, Daubert JC; Multisite Stimulation in Cardiomyopathies (MUSTIC) Study Investigators. Effects of multisite biventricular pacing in patients with heart failure and intraventricular conduction delay. N Engl J Med. 2001; 344: 873–880.[Abstract/Free Full Text]
- Auricchio A, Stellbrink C, Sack S, Block M, Vogt J, Bakker P, Huth C, Schöndube F, Wolfhard U, Böcker D, Krahnefeld O, Kirkels H; Pacing Therapies in Congestive Heart Failure (PATH-CHF) Study Group. 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: 2026–2033.[Abstract/Free Full Text]
- Abraham WT, Fisher WG, Smith AL, Delurgio DB, Leon AR, Loh E, Kocovic DZ, Packer M, Clavell AL, Hayes DL, Ellestad M, Trupp RJ, Underwood J, Pickering F, Truex C, McAtee P, Messenger J; MIRACLE Study Group. Multicenter InSync Randomized Clinical Evaluation. Cardiac resynchronization in chronic heart failure. N Engl J Med. 2002; 346: 1845–1853.[Abstract/Free Full Text]
- Higgins SL, Hummel JD, Niazi IK, Giudici MC, Worley SJ, Saxon LA, Boehmer JP, Higginbotham MB, De Marco T, Foster E, Yong PG. Cardiac resynchronization therapy for the treatment of heart failure in patients with intraventricular conduction delay and malignant ventricular tachyarrhythmias. J Am Coll Cardiol. 2003; 42: 1454–1459.[Abstract/Free Full Text]
- Bristow MR, Saxon LA, Boehmer J, Krueger S, Kass DA, De Marco T, Carson P, DiCarlo L, DeMets D, White BG, DeVries DW, Feldman AM; Comparison of Medical Therapy, Pacing, and Defibrillation in Heart Failure (COMPANION) Investigators. Cardiac-resynchronization therapy with or without an implantable defibrillator in advanced chronic heart failure. N Engl J Med. 2004; 350: 2140–2150.[Abstract/Free Full Text]
- Cleland JG, Daubert JC, Erdmann E, Freemantle N, Gras D, Kappenberger L, Tavazzi L; Cardiac Resynchronization-Heart Failure (CARE-HF) Study Investigators. The effect of cardiac resynchronization on morbidity and mortality in heart failure. N Engl J Med. 2005; 352: 1539–1549.[Abstract/Free Full Text]
- Leclercq C, Walker S, Linde C, Clementy J, Marshall AJ, Ritter P, Djiane P, Mabo P, Levy T, Gadler F, Bailleul C, Daubert JC. Comparative effects of permanent biventricular and right-univentricular pacing in heart failure patients with chronic atrial fibrillation. Eur Heart J. 2002; 23: 1780–1787.[Abstract/Free Full Text]
- Leclercq C, Cazeau S, Le Breton H, Ritter P, Mabo P, Gras D, Pavin D, Lazarus A, Daubert JC. Acute hemodynamic effects of biventricular DDD pacing in patients with end-stage heart failure. J Am Coll Cardiol. 1998; 32: 1825–1831.[Abstract/Free Full Text]
- Auricchio A, Stellbrink C, Block M, Sack S, Vogt J, Bakker P, Klein H, Kramer A, Ding J, Salo R, Tockman B, Pochet T, Spinelli J. Effect of pacing chamber and atrioventricular delay on acute systolic function of paced patients with congestive heart failure. The Pacing Therapies for Congestive Heart Failure Study Group. The Guidant Congestive Heart Failure Research Group. Circulation. 1999; 99: 2993–3001.[Abstract/Free Full Text]
- Bax JJ, Bleeker GB, Marwick TH, Molhoek SG, Boersma E, Steendijk P, van der Wall EE, Schalij MJ. Left ventricular dyssynchrony predicts response and prognosis after cardiac resynchronization therapy. J Am Coll Cardiol. 2004; 44: 1834–1840.[Abstract/Free Full Text]
- Notabartolo D, Merlino JD, Smith AL, DeLurgio DB, Vera FV, Easley KA, Martin RP, León AR. Usefulness of the peak velocity difference by tissue Doppler imaging technique as an effective predictor of response to cardiac resynchronization therapy. Am J Cardiol. 2004; 94: 817–820.[CrossRef][Medline]
[Order article via Infotrieve]
- Bleeker GB, Bax JJ, Fung JW, van der Wall EE, Zhang Q, Schalij MJ, Chan JY, Yu CM. Clinical versus echocardiographic parameters to assess response to cardiac resynchronization therapy. Am J Cardiol. 2006; 97: 260–263.[CrossRef][Medline]
[Order article via Infotrieve]
- Swedberg K, Cleland J, Dargie H, Drexler H, Follath F, Komajda M, Tavazzi L, Smiseth OA, Gavazzi A, Haverich A, Hoes A, Jaarsma T, Korewicki J, Lévy S, Linde C, Lopez-Sendon JL, Nieminen MS, Piérard L, Remme WJ; Task Force for the Diagnosis and Treatment of Chronic Heart Failure of the European Society of Cardiology. Guidelines for the diagnosis and treatment of chronic heart failure: executive summary (update 2005): The Task Force for the Diagnosis and Treatment of Chronic Heart Failure of the European Society of Cardiology. Eur Heart J. 2005; 26: 1115–1140.[Free Full Text]
- Hunt SA, Abraham WT, Chin MH, Feldman AM, Francis GS, Ganiats TG, Jessup M, Konstam MA, Mancini DM, Michl K, Oates JA, Rahko PS, Silver MA, Stevenson LW, Yancy CW, Antman EM, Smith SC Jr, Adams CD, Anderson JL, Faxon DP, Fuster V, Halperin JL, Hiratzka LF, Jacobs AK, Nishimura R, Ornato JP, Page RL, Riegel B; American College of Cardiology; American Heart Association Task Force on Practice Guidelines; American College of Chest Physicians; International Society for Heart and Lung Transplantation; Heart Rhythm Society. ACC/AHA 2005 guideline update for the diagnosis and management of chronic heart failure in the adult: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Update the 2001 Guidelines for the Evaluation and Management of Heart Failure): developed in collaboration with the American College of Chest Physicians and the International Society for Heart and Lung Transplantation: endorsed by the Heart Rhythm Society. Circulation. 2005; 112: e154–e235.[Free Full Text]
- Final Appraisal Determination: Cardiac Resynchronization Therapy for the Treatment of Heart Failure. London, UK: National Institute for Health and Clinical Excellence; 2007.
- Pitzalis MV, Iacoviello M, Romito R, Massari F, Rizzon B, Luzzi G, Guida P, Andriani A, Mastropasqua F, Rizzon P. Cardiac resynchronization therapy tailored by echocardiographic evaluation of ventricular asynchrony. J Am Coll Cardiol. 2002; 40: 1615–1622.[Abstract/Free Full Text]
- Pitzalis MV, Iacoviello M, Romito R, Guida P, De Tommasi E, Luzzi G, Anaclerio M, Forleo C, Rizzon P. Ventricular asynchrony predicts a better outcome in patients with chronic heart failure receiving cardiac resynchronization therapy. J Am Coll Cardiol. 2005; 45: 65–69.[Abstract/Free Full Text]
- Marcus GM, Rose E, Viloria EM, Schafer J, De Marco T, Saxon LA, Foster E; VENTAK CHF/CONTAK-CD Biventricular Pacing Study Investigators. Septal to posterior wall motion delay fails to predict reverse remodeling or clinical improvement in patients undergoing cardiac resynchronization therapy. J Am Coll Cardiol. 2005; 46: 2208–2214.[Abstract/Free Full Text]
- Díaz-Infante E, Sitges M, Vidal B, Mont L, Delgado V, Marigliano A, Macias A, Tolosana JM, Tamborero D, Azqueta M, Roig E, Paré C, Brugada J. Usefulness of ventricular dyssynchrony measured using M-mode echocardiography to predict response to resynchronization therapy. Am J Cardiol. 2007; 100: 84–89.[CrossRef][Medline]
[Order article via Infotrieve]
- Sassone B, Capecchi A, Boggian G, Gabrieli L, Saccà S, Vandelli R, Petracci E, Mele D. Value of baseline left lateral wall postsystolic displacement assessed by M-mode to predict reverse remodeling by cardiac resynchronization therapy. Am J Cardiol. 2007; 100: 470–475.[CrossRef][Medline]
[Order article via Infotrieve]
- Jansen AH, van Dantzig J, Bracke F, Meijer A, Peels KH, van den Brink RB, Cheriex EC, Delemarre BJ, van der Wouw PA, Korsten HH, van Hemel NM. Qualitative observation of left ventricular multiphase septal motion and septal-to-lateral apical shuffle predicts left ventricular reverse remodeling after cardiac resynchronization therapy. Am J Cardiol. 2007; 99: 966–969.[CrossRef][Medline]
[Order article via Infotrieve]
- Penicka M, Bartunek J, De Bruyne B, Vanderheyden M, Goethals M, De Zutter M, Brugada P, Geelen P. Improvement of left ventricular function after cardiac resynchronization therapy is predicted by tissue Doppler imaging echocardiography. Circulation. 2004; 109: 978–983.[Abstract/Free Full Text]
- Jansen AH, Bracke F, van Dantzig JM, Meijer A, Korsten EH, Peels KH, van Hemel NM. Optimization of pulsed wave tissue Doppler to predict left ventricular reverse remodeling after cardiac resynchronization therapy. J Am Soc Echocardiogr. 2006; 19: 185–191.[CrossRef][Medline]
[Order article via Infotrieve]
- Soliman OI, Theuns DA, Geleijnse ML, Anwar AM, Nemes A, Caliskan K, Vletter WB, Jordaens LJ, Cate FJ. Spectral pulsed-wave tissue Doppler imaging lateral-to-septal delay fails to predict clinical or echocardiographic outcome after cardiac resynchronization therapy. Europace. 2007; 9: 113–118.[Abstract/Free Full Text]
- Achilli A, Peraldo C, Sassara M, Orazi S, Bianchi S, Laurenzi F, Donati R, Perego GB, Spampinato A, Valsecchi S, Denaro A, Puglisi A. Prediction of response to cardiac resynchronization therapy: the Selection of Candidates for CRT (SCART) study. Pacing Clin Electrophysiol. 2006; 29 Suppl 2: S11–S19.[CrossRef][Medline]
[Order article via Infotrieve]
- Bax JJ, Marwick TH, Molhoek SG, Bleeker GB, van Erven L, Boersma E, Steendijk P, van der Wall EE, Schalij MJ. Left ventricular dyssynchrony predicts benefit of cardiac resynchronization therapy in patients with end-stage heart failure before pacemaker implantation. Am J Cardiol. 2003; 92: 1238–1240.[CrossRef][Medline]
[Order article via Infotrieve]
- Van de Veire NR, Bleeker GB, De Sutter J, Ypenburg C, Holman ER, van der Wal EE, Schalij MJ, Bax JJ. Tissue synchronisation imaging accurately measures left ventricular dyssynchrony and predicts response to cardiac resynchronisation therapy. Heart. 2007; 93: 1034–1039.[Abstract/Free Full Text]
- Bleeker GB, Schalij MJ, Boersma E, Holman ER, Steendijk P, van der Wall EE, Bax JJ. Relative mertis of M-mode echocardiography and tissue Doppler imaging for prediction of response to cardiac resynchronization therapy in patients with heart failure secondary to ischemic or idiopathic dilated cardiomyopathy. Am J Cardiol. 2007; 99: 68–74.[Medline]
[Order article via Infotrieve]
- Gorcsan J 3rd, Kanzaki H, Bazaz R, Dohi K, Schwartzman D. Usefulness of echocardiographic tissue synchronization imaging to predict acute response to cardiac resynchronization therapy. Am J Cardiol. 2004; 93: 1178–1181.[CrossRef][Medline]
[Order article via Infotrieve]
- Yu CM, Fung WH, Lin H, Zhang Q, Sanderson JE, Lau CP. 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: 684–688.[CrossRef][Medline]
[Order article via Infotrieve]
- Yu CM, Fung JW, Zhang Q, Chan CK, Chan YS, Lin H, Kum LC, Kong SL, Zhang Y, Sanderson JE. 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.[Abstract/Free Full Text]
- Yu CM, Zhang Q, Fung JW, Chan HC, Chan YS, Yip GW, Kong SL, Lin H, Zhang Y, Sanderson JE. A novel tool to assess systolic asynchrony and identify responders of cardiac resynchronization therapy by tissue synchronization imaging. J Am Coll Cardiol. 2005; 45: 677–684.[Abstract/Free Full Text]
- Yu CM, Zhang Q, Chan YS, Chan CK, Yip GW, Kum LC, Wu EB, Lee PW, Lam YY, Chan S, Fung JW. Tissue Doppler velocity is superior to displacement and strain mapping in predicting left ventricular reverse remodeling response after cardiac resynchronization therapy. Heart. 2006; 92: 1452–1456.[Abstract/Free Full Text]
- Yu CM, Gorcsan J 3rd, Bleeker GB, Zhang Q, Schalij MJ, Suffoletto MS, Fung JW, Schwartzman D, Chan YS, Tanabe M, Bax JJ. Usefulness of tissue Doppler velocity and strain dyssynchrony for predicting left ventricular reverse remodeling response after cardiac resynchronization therapy. Am J Cardiol. 2007; 100: 1263–1270.[CrossRef][Medline]
[Order article via Infotrieve]
- Knebel F, Schattke S, Bondke H, Walde T, Eddicks S, Reibis R, Baumann G, Borges AC. Evaluation of longitudinal and radial two-dimensional strain imaging versus Doppler tissue echocardiography in predicting long-term response to cardiac resynchronization therapy. J Am Soc Echocardiogr. 2007; 20: 335–341.[CrossRef][Medline]
[Order article via Infotrieve]
- Cannesson M, Tanabe M, Suffoletto MS, Schwartzman D, Gorcsan J 3rd. Velocity vector imaging to quantify ventricular dyssynchrony and predict response to cardiac resynchronization therapy. Am J Cardiol. 2006; 98: 949–953.[CrossRef][Medline]
[Order article via Infotrieve]
- Søgaard P, Egeblad H, Kim WY, Jensen HK, Pedersen AK, Kristensen BØ, Mortensen PT. Tissue Doppler imaging predicts improved systolic performance and reversed left ventricular remodeling during long-term cardiac resynchronization therapy. J Am Coll Cardiol. 2002; 40: 723–730.[Abstract/Free Full Text]
- Dohi K, Suffoletto MS, Schwartzman D, Ganz L, Pinsky MR, Gorcsan J 3rd. Utility of echocardiographic radial strain imaging to quantify left ventricular dyssynchrony and predict acute response to cardiac resynchronization therapy. Am J Cardiol. 2005; 96: 112–116.[CrossRef][Medline]
[Order article via Infotrieve]
- Suffoletto MS, Dohi K, Cannesson M, Saba S, Gorcsan J 3rd. 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: 960–968.[Abstract/Free Full Text]
- Mele D, Pasanisi G, Capasso F, De Simone A, Morales MA, Poggio D, Capucci A, Tabacchi G, Sallusti L, Ferrari R. Left intraventricular myocardial deformation dyssynchrony identifies responders to cardiac resynchronization therapy in patients with heart failure. Eur Heart J. 2006; 27: 1070–1078.[Abstract/Free Full Text]
- Porciani MC, Lilli A, Macioce R, Cappelli F, Demarchi G, Pappone A, Ricciardi G, Padeletti L. Utility of a new left ventricular asynchrony index as a predictor of reverse remodeling after cardiac resynchronization therapy. Eur Heart J. 2006; 27: 1818–1823.[Abstract/Free Full Text]
- Beshai JF, Grimm RA, Nagueh SF, Baker JH 2nd, Beau SL, Greenberg SM, Pires LA, Tchou PJ; RethinQ Study Investigators. Cardiac-resynchronization therapy in heart failure with narrow QRS complexes. N Engl J Med. 2007: 357; 2461–2471.[Abstract/Free Full Text]
- Weidemann F, Kowalski M, D’Hooge J, Bijnens B, Sutherland GR. Doppler myocardial imaging: a new tool to assess regional inhomogeneity in cardiac function. Basic Res Cardiol. 2001; 96: 595–605.[CrossRef][Medline]
[Order article via Infotrieve]
- Wyman BT, Hunter WC, Prinzen FW, McVeigh ER. Mapping propagation of mechanical activation in the paced heart with MRI tagging. Am J Physiol. 1999; 276: H881–H891.[Medline]
[Order article via Infotrieve]
- Breithardt OA, Stellbrink C, Herbots L, Claus P, Sinha AM, Bijnens B, Hanrath P, Sutherland GR. Cardiac resynchronization therapy can reverse abnormal myocardial strain distribution in patients with heart failure and left bundle branch block. J Am Coll Cardiol. 2003; 42: 486–494.[Abstract/Free Full Text]
- Zhang Q, Yu CM, Fung JW, Zhang Y, Chan YS, Chan HC, Yip GW, Sanderson JE. Assessment of the effect of cardiac resynchronization therapy on intraventricular mechanical synchronicity by regional volumetric changes. Am J Cardiol. 2005; 95: 126–129.[CrossRef][Medline]
[Order article via Infotrieve]
- Kapetanakis S, Kearney MT, Siva A, Gall N, Cooklin M, Monaghan MJ. Real-time three-dimensional echocardiography: a novel technique to quantify global left ventricular mechanical dyssynchrony. Circulation. 2005; 112: 992–1000.[Abstract/Free Full Text]
- Rouleau F, Merheb M, Geffroy S, Berthelot J, Chaleil D, Dupuis JM, Victor J, Geslin P. Echocardiographic assessment of the interventricular delay of activation and correlation to the QRS width in dilated cardiomyopathy. Pacing Clin Electrophysiol. 2001; 24: 1500–1506.[CrossRef][Medline]
[Order article via Infotrieve]
- Bordachar P, Lafitte S, Reuter S, Sanders P, Jais P, Haissaguerre M, Roudaut R, Garrigue S, Clementy J. Echocardiographic parameters of ventricular dyssynchrony validation in patients with heart failure using sequential biventricular pacing. J Am Coll Cardiol. 2004; 44: 2157–2165.[Abstract/Free Full Text]
- Richardson M, Freemantle N, Calvert MJ, Cleland JG, Tavazzi L; CARE-HF Study Steering Committee and Investigators. Predictors and treatment response with cardiac resynchronization therapy in patients with heart failure characterized by dyssynchrony: a predefined analysis from the CARE-HF trial. Eur Heart J. 2007; 28: 1827–1834.
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Introduction
CRT: From Origins to...