From Pictures to Practice Paradigms |
Imaging Cardiac Resynchronization Therapy
Theodore Abraham, MD*,
David Kass, MD*,
Giovanni Tonti, MD ,
Gery F. Tomassoni, MD ,
William T. Abraham, MD ,
Jeroen J. Bax, MD||,
Thomas H. Marwick, MBBS, PhD¶,*
* Johns Hopkins Medical Institutions, Baltimore, Maryland
Catholic University of Sacred Heart of Campobasso, Campobasso, Italy
Lexington Cardiology Consultants, Lexington, Kentucky
Ohio State University, Columbus, Ohio
|| Leiden University, Leiden, the Netherlands
¶ University of Queensland, Brisbane, Australia
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Abstract
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Although a prognostic benefit has been shown from cardiac resynchronization therapy, questions are often directed toward the prediction of symptomatic or functional benefit. Recent multicenter trials have shown the pitfalls of current mechanical markers of left ventricular synchrony, but these negative trial results have not marked the conclusion of efforts to predict outcome. Potential new contributors to the assessment of mechanical synchrony include echocardiographic and magnetic resonance techniques for the assessment of myocardial deformation. Nonsynchrony markers that seem promising include assessment of the location and extent of myocardial scar and imaging of the coronary venous and phrenic nerve anatomy.
Key Words: heart failure • synchrony • LV dysfunction • echocardiography • cardiac magnetic resonance • computed tomography
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Abbreviations and Acronyms
| | 2D = 2-dimensional | | 3D = 3-dimensional | | CMR = cardiac magnetic resonance | | CRT = cardiac resynchronization therapy | | CS = coronary sinus | | ICE = intracardiac echocardiography | | LV = left ventricle/ventricular | | RV = right ventricle/ventricular | | TDE = tissue Doppler echocardiography |
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In the last 2 years, 2 important multicenter trials involving 172 (1) and nearly 500 (2) patients showed failure of mechanical markers of left ventricular (LV) synchrony to predict outcome after cardiac resynchronization therapy (CRT). These findings contradicted a number of single center studies, reviewed elsewhere (3), suggesting that mechanical markers of LV synchrony could predict outcome after CRT. The negative trial results have not marked the conclusion of efforts to predict outcome from CRT, and indeed, a less well publicized multicenter study of 161 patients (4) showed that imaging of both synchrony and nonsynchrony markers could predict response. The goal of this review is to evaluate the role of imaging (not just of dyssynchrony) to the evaluation of potential candidates for CRT.
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Defining the Benefits of CRT in Populations and Individuals
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The use of CRT began with a series of acute studies in patients with depressed LV function, showing improvement in invasive hemodynamic parameters (5) and echocardiographic manifestations of LV dyssynchrony and stroke volume (6). After encouraging studies of acute and longer-term clinical effects (7–9), several randomized controlled trials involving >4,000 patients established the role for CRT in heart failure (10–16). These results have given a strong mandate for the routine use of CRT in eligible heart failure patients (Table 1).
In the context of this evidence base, the need to use imaging for the identification of mechanical synchrony might reasonably be questioned. However, the therapeutic expectations of patients in advanced heart failure are not restricted to survival but also functional status, which leads to the rather controversial definition as to whether an individual is a responder to CRT. Clinical end points (New York Heart Association functional class, quality of life score, exercise capacity expressed as 6-min walking distance), hemodynamic response, and echocardiographic end points (improved LV systolic function or reverse LV remodeling) have been used to evaluate response to CRT. Clinical assessment is subjective and unreliable given the placebo effect of CRT; 40% of patients randomized to no CRT experienced a significant reduction in symptoms. Acute hemodynamic response may not be predictive of long-term response. Changes in ejection fraction are modest, with most studies reporting an average improvement of 4% to 5%. Evidence of reverse remodeling provides an objective means of assessment of response to CRT—a 15% decrease in LV end-systolic volume (ESV) index with CRT has emerged as a consistent parameter of reverse remodeling and predictive of long-term clinical outcomes (17)—this is attained in about 60% of patients, in contrast with a clinical response rate in around 70%.
The CRT-responder concept should be applied with caution. First, there is little evidence to justify its application to considerations of survival. Although reverse remodeling is an important mediator of improved survival in heart failure, and seems to be associated with the response to CRT (17,18), a 9.5% reduction of ESV has a sensitivity and specificity of only 70% for prediction of mortality, and survival benefit from myocardial revascularization has been documented in the absence of reverse remodeling (19). Second, there are problems with trying to make this distinction on the basis of mechanical markers of LV synchrony. Third, although changes in synchrony has been proposed as the sine qua non of CRT response (20), the effect of therapy could be mediated in other ways (21).
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Definition of Dyssynchrony
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Electrical dyssynchrony.
The measurement of electrical dyssynchrony has ranged from the simple lumped QRS duration, used in all of the large multicenter trials of biventricular pacing therapy, to more complex electrical activation maps. The latter show early right heart stimulation that rapidly moves to the lateral free wall (this delay is about 70 ms in the canine heart). The mechanical map shows a slower spread of contraction but follows a similar pattern.
Electrical dyssynchrony involves the primary activation delay typically manifested by a widened QRS complex. The transformation of electrical into mechanical dyssynchrony is complex because the latter is not solely determined by when the tissue is excited. Rather, mechanical events require the cellular process of excitation–contraction coupling to generate myocyte force, and are thus influenced by processes that control calcium cycling, myofilament calcium interactions, regional loading, fibrosis, and other factors (22). Indeed, disparities in the timing of regional mechanical function may not be coupled to electrical stimulation delay. This might be caused by regional loading differences, fibrosis, and contractile strength of one part of the wall versus another. Mechanical imaging methods detect motion of the muscle but not its activation process, and so cannot necessarily delineate mechanisms for apparent dyssynchrony. This is important because dyssynchrony caused by electrical delay can be targeted by CRT, whereas that caused by regional properties and/or loading disparities may not be.
Mechanical dyssynchrony.
In left bundle branch block or right ventricular (RV) pacing, septal activation occurs first, and results in pre-stretch of the still-quiescent lateral wall, which consequently reduces the peak rate of pressure increase (dP/dtmax). The delayed lateral wall contraction generates systolic forces that are also partly dissipated by re-stretching the now-early-relaxing septal region, lowering net cardiac output. Discoordinate papillary muscle activation can further compromise overall LV function by exacerbating mitral regurgitation (23) (Fig. 1). Disparities in wall stiffening that generate discoordinate motion are most marked in early systole (isovolumic contraction, lowering dP/dtmax), and late systole as one territory enters relaxation ahead of the other (24).
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Figure 1 Contributors to Electrical and Mechanical Dyssynchrony
The contributors to mechanical delays include left ventricular (LV) remodelling, LV systolic and diastolic dysfunction, mitral regurgitation, coronary flow reserve, and neurohormonal changes. LVH = left ventricular hypertrophy.
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Mechanical dyssynchrony has been measured by a range of imaging modalities, with the largest evidence base being accumulated with echocardiography (3). Respectively, 30% and 40% of patients who fulfill eligibility criteria for CRT do not show a symptomatic response or reverse remodeling (18). Thus, electrical dyssynchrony alone, as detected by electrocardiography, may not be the optimal predictor of CRT response. The concept of disconcordance between electrical and mechanical dyssynchrony was supported by an experimental study that showed improvement in ventricular hemodynamics with CRT despite no change in electrical dyssynchrony (25).
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Imaging Approaches to Mechanical Dyssynchrony
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Echocardiography.
Standard echocardiographic markers of LV mechanical synchrony have been recently reviewed (3). The primary source of variation between these markers relates to how timing is assessed: the simplest are maximal time delays between early and late contracting or electrically stimulated regions, total number of regional areas that show delay, and variance in timing of motion around the heart. However, this can miss critical information regarding the geographic distribution of delays that ultimately generate functional dyssynchrony, and conversely, hearts with scattered heterogeneity of activation or contraction may not necessarily have much functional dyssynchrony. The alternative to these segmental approaches are various approaches to index dyssynchrony, including vector mapping that amplifies the index if the delayed regions are clustered together, as well as the so-called CURE (circumferential uniformity ratio estimate) index (26). These approaches can be applied to virtually any way of assessing electrical or mechanical dyssynchrony, and have the potential to enhance its specificity for therapeutic responsiveness. The second important variation relates to the orientation of the dyssynchrony measurements. Most tissue Doppler echocardiography (TDE) techniques provide data in the longitudinal orientation of the myocardium. However, most fibers are circumferentially oriented, and deformation in this dimension seems to provide a more reliable and stronger signal.
Despite a large evidence base with TDE, this form of analysis poses several problems. Signal noise is common, and variability between observers, often caused by the presence of multiple systolic peaks, seems to be a major problem (2). Second, the measurement of TDE time delays is time consuming, especially if multiple segments are interrogated. The development of parametric imaging techniques that color-code the segments based on time delay (27) may reduce spatial variation as well as save time (Fig. 2). Third, TDE examines the timing of contraction in a longitudinal direction, which may not be the optimal orientation for discerning both dyssynchrony and the impact of CRT (28). Recent data obtained using angle-corrected TDE show that radial velocities can also detect dyssynchrony and predict acute response to CRT (29).
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Figure 2 Parametric Display of Tissue Velocity
In this parametric display (often known by its proprietary name, tissue synchronization imaging), delayed activation of the posterolateral wall is evidenced by red coloration of the lateral and yellow coloration of the posterior walls.
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Tissue velocity measures tissue motion relative to the transducer and is therefore susceptible to cardiac translational motion and tethering artifacts. Strain measurements are based on movement of tissue relative to its neighbor and are therefore site specific (30). Unfortunately, TDE-based strain analysis has not been shown to be superior to tissue velocity (31), likely reflecting the angle dependence of TDE analysis as well as signal-noise related problems. In contrast, speckle-tracking-based measurements of radial, circumferential, and longitudinal strain (32,33) seem to be both feasible and reliable (Fig. 3).
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Figure 3 Assessment of Synchrony Using Tissue Doppler and Speckle Strain
Panel A shows synchronous septal (yellow) and lateral (blue) wall motion with tissue Doppler. Panel B shows delay between the septal (green) and posterolateral walls (red and blue) using longitudinal speckle strain, confirmed also with circumferential strain (C). TDE = tissue Doppler echocardiography.
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Quantitative analysis of dyssynchrony with 3-dimensional (3D) echocardiography requires border detection in a number of 2-dimensional (2D) slices, and creation of a 3D model from which time-volume data are obtained (34). The systolic dyssynchrony index, derived from the dispersion of time to minimum regional volume (Fig. 4), decreases after CRT. Unfortunately, the ability to compare timing of all myocardial segments with a 3D echocardiography approach is probably outweighed by limitations in edge detection and frame rates. This technique, speckle strain, and contrast variability imaging (35) are all the focus of current research.
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Figure 4 Evaluation of Synchrony Using 3-Dimensional Echocardiography
Uniform times to minimum volume indicate synchrony (A). The dyssynchronous left ventricle is characterized by variation in times to minimum volume (B).
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Cardiac magnetic resonance (CMR).
Potential advantages of CMR-based techniques for dyssynchrony assessment include high reproducibility, high spatial resolution, and the ability to obtain 3D information including circumferential mechanics (36), which may be superior to that obtained in the longitudinal direction (28). Myocardial tagging allows assessment of radial, longitudinal, and circumferential strain by measurements between dark lines (markers or tags) left in the myocardium by special encoding pulses (Fig. 5). Recent advances that have drastically reduced analysis time include harmonic phase analysis of tagged CMR and strain-encoded CMR (37).
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Figure 5 Use of Tagged Cardiac Magnetic Resonance for the Assessment of Synchrony
The progressive deformation of the grid (A) allows measurement of the time course of deformation in the principal axes of each segment (B). The parametric display (C) shows the time course of contraction, which can be shown to be synchronous (upper row) or dyssynchronous (lower row). RV = right ventricle; other abbreviation as in Figure 1.
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Three CMR indices have been used for measuring dyssynchrony. Regional variance is determined from the variance of strain magnitude in 28 radially displaced segments for each short-axis section (similar to the indices used in TDE), or the number of segments with delayed shortening as a percent of total regions examined (38) (Fig. 6). The regional variance vector is based on the product of a radial magnitude vector with a scalar representing time to maximal shortening (Fig. 6B). The resulting vector sum will only have significant magnitude if delayed versus early regions are geographically clustered (Fig. 6A, upper panel) (28). Lastly, regional strain uniformity is based on regional strain differences at a given moment in time. Time plots of strain (shortening/stretching) are generated at each of 28 evenly distributed segments around a short-axis slice (28). If segments shorten simultaneously (perfectly synchronous contraction), the plot appears as a straight line, whereas regionally clustered dyssynchrony generates an undulating plot. The relative ratio of first/zero-order magnitudes derived by Fourier analysis (Fig. 6C) generates an index known as the circumferential uniformity ratio estimate (28).
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Figure 6 Cardiac Magnetic Resonance Techniques for Strain Measurement
The regional variance of strain (A) cannot differentiate identical variance of time to peak contraction between segments with delayed contraction clustered in 1 portion of the left ventricular wall (A, top), versus dispersion of delay through the heart (A, bottom); only the former displays dyssynchrony. The regional variance vector of principal strain (B) is based on the product of unit vectors with a scalar representing time at maximal shortening or instantaneous magnitude of shortening. Regional strain uniformity (C) provides a relative ratio of first/zero-order magnitudes derived by Fourier analysis. The heart with clustered regions (A, top) shows delays in 1 territory versus the other so this plot appears sinusoidal. Hearts with more variability (A, bottom) yield a higher frequency waveform.
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Potential disadvantages of CMR include cost, long imaging time, availability, complex and long analysis times, and incompatibility with implanted devices. These technical problems will likely be solved, and CMR may become safe in patients with implanted devices.
Nuclear medicine techniques.
When phase imaging is performed on perfusion scan data, segmental counts are proportionate to thickening. Although acquisitions are obtained at 8 frames/s, Fourier transformation of the data is believed to provide an effective temporal resolution of 75 frames/s. The results of nuclear imaging seem to correspond with those obtained with TDE (39), although the limited published data on CRT effectiveness indicate a sensitivity and specificity <80% (40).
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The Role of Imaging in the EP Laboratory
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Standard imaging approaches offer limited value during CRT implantation. Transthoracic echocardiography may disturb the sterile field, and poor acoustic windows are likely when optimal positioning is not possible. Transesophageal echocardiography requires a second operator.
Intracardiac echocardiography (ICE) is useful during implantation of biventricular devices, allows procedural sterility (the catheter is positioned in the right heart via a subclavian venous sheath), eliminates the need for a second operator, and provides excellent target resolution because of its close proximity (Fig. 7). Intraoperative ICE can facilitate cannulation of the coronary sinus (CS) by identifying the ostium, quantify the degree of mechanical dyssynchrony at the time of the procedure, and assess the acute response to CRT.
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Figure 7 ICE
These typical intracardiac echocardiography (ICE) windows from catheter positions at the right ventricular base and apex show representative B-mode images in 2 different patients for short-axis (A) and long-axis (B) imaging. L = lateral wall, S = septum.
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3D rotational angiography is an alternative that allows 3D chamber reconstruction at the time of intervention (Fig. 8) (41). This technique can serve as a helpful tool during the implant by providing: 1) accurate 3D CS reconstruction; 2) multiangle visualization of the entire CS; 3) an endocardial view to evaluate branch take-off and valvular anatomy; and 4) accurate final LV lead tip position in relation to LV anatomy.
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Figure 8 3-Dimensional Rotational Angiography
This representative image from an electrocardiograph gated 3-dimensional rotational angiography show the coronary sinus and venous vasculature.
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Nonresponse to CRT may be multifactorial, but incorrect positioning of the LV lead appears to be important; a lateral LV lead position may not be optimal for all patients. Intraoperative ICE can quantify the degree of mechanical dyssynchrony present at the time of the procedure, and with the use of additional echocardiographic parameters such as tissue Doppler velocity or strain measurements, can provide real-time physiologic information regarding CRT response (42) (Fig. 9).
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Figure 9 Use of On-Line Vector Velocity Imaging Analysis to Examine Synchrony in Short-Axis Images in Native and Paced States
In each state, velocity vectors are graphically represented in time and magnitude in yellow/red in the upper right, a parametric M-mode plot of systole (red) and diastole (blue) is seen below this, and B-mode image is broken into 6 segments automatically and a strain curve plotted for each (bottom). The left ventricular (LV) dyssynchrony (A) is evidenced by nonalignment of strain and velocity vectors and a lack of clear separation of contracting and relaxing elements on the parametric M-mode plot. The biventricular (BiV) pacing with the LV lead in the anterior interventricular vein results to a significant reduction of dyssynchrony (B). During BiV pacing with the LV lead in a posterolateral vein (C), dyssynchrony does not seem to be improved.
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Anatomical visualization and 3D reconstruction of cardiac chambers during implantation of CRT devices may be useful for facilitating lead localization and assess response. As technology continues to advance, cardiac imaging during EP interventions will contribute to better procedural success, reduce complications, and aid in the understanding of the interaction between electrical activation and anatomical substrates.
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Post-Implantation Assessment in the CRT Patient
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Echocardiography is a useful tool for the evaluation of therapeutic success during follow-up. Patients who do not show LV resynchronization do not show reverse remodeling after CRT (20). However, reverse remodeling needs time to occur, and more immediate effects of successful CRT include an improvement in LV ejection fraction and a reduction in mitral regurgitation, related to both increased closing force and improvement in interpapillary muscle synchrony (43). Late follow-up studies can be expected to show improved LV ejection fraction and reduced LVESV and LV end-diastolic volume, however, follow-up is usually at 6 months post-implantation and improvement may take up to 12 months, particularly in ischemic cardiomyopathy. Reverse remodeling is associated with a reduction in LV annular size and normalization of LV geometry, resulting in a further reduction in mitral regurgitation (44). Other changes include a reduction in RV size and decreases in tricuspid regurgitation and pulmonary artery pressure.
Echocardiographic atrioventricular optimization improves LV dP/dtmax and stroke volume acutely, and was performed in many effectiveness studies (45). The iterative method uses pulsed-wave Doppler imaging of mitral inflow (Fig. 10). Contemporary CRT devices permit programming of the ventricular-ventricular (VV) interval, but the contribution of VV optimization to improved systolic performance is controversial (45) (Fig. 11).
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Figure 10 The Iterative Method for Atrioventricular Optimization
The sequence starts at a long atrioventricular (AV) delay (180 ms, shorter than intrinsic PR interval to ensure capture) and then shortening by 20-ms increments, until A-wave truncation appears (80 ms). Then atrioventricular delay is lengthened by 10-ms increments until A-wave truncation disappears and maximum E- and A-wave separation is provided.
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Figure 11 LV Stroke Volume During VV Optimization
Using 20-ms increments (starting at the left ventricle [LV] activated 80 ms before the right ventricle [RV], and ending at the RV activated 80 ms before the LV), the optimal ventricular-ventricular (VV) delay is the delay associated with the largest LV outflow tract velocity time integral.
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Patient Selection for CRT: Clinical Versus Imaging Criteria
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Current criteria for CRT implantation include drug-refractory heart failure (New York Heart Association functional class III to IV), LV ejection fraction <35%, and a wide QRS complex (46). In the large CRT trials, Mollema et al. (47) showed that QRS duration alone yielded only a sensitivity and specificity of 53%, with an optimized cutoff value of 163 ms. Conversely, echocardiographic studies have shown that approximately 30% of patients with a wide QRS complex do not have evidence of LV dyssynchrony (as assessed by tissue Doppler imaging). As noted above, although single-center studies have shown a high accuracy of a variety of parameters to predict CRT response, reliable measurement of LV dyssynchrony remains a work in progress. None of these different techniques was definitively superior in the PROSPECT (Predictors of Response to CRT) trial (2). Indeed, the message of this trial was that the reproducibility for these parameters was limited, and that both the sensitivity and the specificity of the echocardiographic techniques were modest.
How should these observations be incorporated into decision making? Patients with heart failure and a wide left bundle branch block but no mechanical dyssynchrony should not be denied CRT (3), although it is reasonable to have a dialog with the patient regarding the possibility of symptomatic or functional nonresponse. In the patient with congestive heart failure, systolic dysfunction, mechanical dyssynchrony and a narrow QRS, trial data do not currently justify the use of CRT (1).
Perhaps the focus on mechanical synchrony has been a distraction from more important contributions of imaging: the detection of scar, correspondence of pacing site and maximum VV delay, and RV and LV status. The presence of scar tissue in the target zone of the LV lead may limit response to CRT (48), and the total scar burden is also important (18). Contrast-enhanced CMR may provide delineation of scar tissue with the highest spatial resolution (Fig. 12). The LV lead is frequently not positioned in the site of latest mechanical activation, and patients with this lead position show a worse outcome (49–51). Provision of information on venous anatomy (Fig. 13) (52) or the cardiophrenic bundle (e.g., with multislice computed tomography) is important before CRT implantation.
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Figure 12 Contrast-Enhanced Cardiac Magnetic Resonance to Identify the Location and Thickness of Myocardial Scar
These examples of lateral scar show nontransmural (A) and transmural (B) scar thickness.
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Figure 13 Use of Computed Tomographic Coronary Venography to Plan Lead Localization
This electrocardiograph-gated image shows the relationship of the right coronary artery (RCA) and left circumflex artery (CX) to the coronary sinus (CS), great cardiac vein (GCV) and superior cardiac vein (SCV), posterior interventricular vein (PIV) and left marginal veins (LMV), and posterior vein of the left ventricle (PVLV) and side branches ( ). Reprinted with permission from Van de Veire et al. (52).
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Conclusions
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Problems with the reproducibility of the current generation of imaging techniques has led to a degree of nihilism about imaging in resynchronization therapy. In fact, imaging has important contributions such as the characterization of LV and RV function and the assessment of myocardial viability and atrioventricular delay. Robust techniques of high temporal resolution are needed for the assessment of LV synchrony. At present, multiple imaging modalities contribute components of the decision matrix to proceed with this useful but not uniformly effective treatment modality.
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Footnotes
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Drs. Abraham and Kass are consultants and receive research support from Boston Scientific. Dr. Tonti has received research grants from Siemens. Dr. Tomassoni received honoraria or is a consultant for Siemens and Biosense Webster. Dr. Bax has received research grants from GE Healthcare, BMS Medical Imaging, Edwards Lifescience, St. Jude, Boston Scientific, Medtronic, and Biotronik. Dr. Marwick has received research grant support from GE Medical Systems, Philips, and Siemens. Supported in part by a Program grant (519823) from the National Health and Medical Research Council, Canberra, Australia.
Section Editor: Mani A. Vannan, MBBS
* Reprint requests and correspondence: Dr. Thomas H. Marwick, University of Queensland School of Medicine, Princess Alexandra Hospital, Ipswich Road, Brisbane, Qld 4102, Australia (Email: t.marwick{at}uq.edu.au).
Manuscript received November 18, 2008;
revised manuscript received December 30, 2008,
accepted January 9, 2009.
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REFERENCES
|
|---|
- Beshai JF, Grimm RA, Nagueh SF, et al. Cardiac-resynchronization therapy in heart failure with narrow QRS complexes N Engl J Med 2007;357:2461-2471.[CrossRef][Web of Science][Medline]
- Chung ES, Leon AR, Tavazzi L, et al. Results of the Predictors of Response to CRT (PROSPECT) trial Circulation 2008;117:2608-2616.[Abstract/Free Full Text]
- Gorcsan III J, 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.[CrossRef][Web of Science][Medline]
- Parsai C, Bijnens B, Sutherland GR. Toward understanding response to cardiac resynchronization therapy: left ventricular dyssynchrony is only one of multiple mechanisms Eur Heart J 2008Nov 11 [E-pub ahead of print].
- Saxon LA, Kerwin WF, Cahalan MK, et al. Acute effects of intraoperative multisite ventricular pacing on left ventricular function and activation/contraction sequence in patients with depressed ventricular function J Cardiovasc Electrophysiol 1998;9:13-21.[Web of Science][Medline]
- Auricchio A, Stellbrink C, Block M, et al. Pacing Therapies for Congestive Heart Failure Study Group and the Guidant Congestive Heart Failure Research Group Effect of pacing chamber and atrioventricular delay on acute systolic function of paced patients with congestive heart failure Circulation 1999;99:2993-3001.[Abstract/Free Full Text]
- Leclercq C, Cazeau S, Le Breton H, et al. 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]
- Kass DA, Chen CH, Curry C, et al. Improved left ventricular mechanics from acute VDD pacing in patients with dilated cardiomyopathy and ventricular conduction delay Circulation 1999;99:1567-1573.[Abstract/Free Full Text]
- Gras D, Mabo P, Tang T, et al. Multisite pacing as a supplemental treatment of congestive heart failure: preliminary results of the Medtronic Inc. InSync Study Pacing Clin Electrophysiol 1998;21:2249-2255.[CrossRef][Medline]
- 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;344:873-880.[CrossRef][Web of Science][Medline]
- Leclercq C, Walker S, Linde C, et al. 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]
- Abraham WT, Fisher WG, Smith AL, et al. Cardiac resynchronization in chronic heart failure N Engl J Med 2002;346:1845-1853.[CrossRef][Web of Science][Medline]
- Young JB, Abraham WT, Smith AL, et al. Combined cardiac resynchronization and implantable cardioversion defibrillation in advanced chronic heart failure: the MIRACLE ICD Trial JAMA 2003;289:2685-2694.[Abstract/Free Full Text]
- Higgins SL, Hummel JD, Niazi IK, et al. 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]
- Cleland JG, Daubert JC, Erdmann E, et al. The effect of cardiac resynchronization on morbidity and mortality in heart failure N Engl J Med 2005;352:1539-1549.[CrossRef][Web of Science][Medline]
- Bristow MR, Saxon LA, Boehmer J, et al. Cardiac-resynchronization therapy with or without an implantable defibrillator in advanced chronic heart failure N Engl J Med 2004;350:2140-2150.[CrossRef][Web of Science][Medline]
- Yu CM, Bleeker GB, Fung JW, et al. Left ventricular reverse remodeling but not clinical improvement predicts long-term survival after cardiac resynchronization therapy Circulation 2005;112:1580-1586.[Abstract/Free Full Text]
- St John Sutton M, Keane MG. Reverse remodelling in heart failure with cardiac resynchronisation therapy Heart 2007;93:167-171.[Abstract/Free Full Text]
- Samady H, Elefteriades JA, Abbott BG, Mattera JA, McPherson CA, Wackers FJ. Failure to improve left ventricular function after coronary revascularization for ischemic cardiomyopathy is not associated with worse outcome Circulation 1999;100:1298-1304.[Abstract/Free Full Text]
- Bleeker GB, Mollema SA, Holman ER, et al. Left ventricular resynchronization is mandatory for response to cardiac resynchronization therapy: analysis in patients with echocardiographic evidence of left ventricular dyssynchrony at baseline Circulation 2007;116:1440-1448.[Abstract/Free Full Text]
- Tang WH, Mullens W, Borowski AG, et al. Relation of mechanical dyssynchrony with underlying cardiac structure and performance in chronic systolic heart failure: implications on clinical response to cardiac resynchronization Europace 2008;10:1370-1374.[Abstract/Free Full Text]
- Sengupta PP, Tondato F, Khandheria BK, Belohlavek M, Jahangir A. Electromechanical activation sequence in normal heart Heart Fail Clin 2008;4:303-314.[CrossRef][Medline]
- Auricchio A, Prinzen FW. Update on the pathophysiological basics of cardiac resynchronization therapy Europace 2008;10:797-800.[Abstract/Free Full Text]
- Leclercq C, Kass DA. Retiming the failing heart: principles and current clinical status of cardiac resynchronization J Am Coll Cardiol 2002;39:194-201.[Abstract/Free Full Text]
- Leclercq C, Faris O, Tunin R, et al. Systolic improvement and mechanical resynchronization does not require electrical synchrony in the dilated failing heart with left bundle-branch block Circulation 2002;106:1760-1763.[Abstract/Free Full Text]
- 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;50:1484-1490.[Abstract/Free Full Text]
- Gorcsan III J, 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][Web of Science][Medline]
- Helm RH, Leclercq C, Faris OP, et al. Cardiac dyssynchrony analysis using circumferential versus longitudinal strain: implications for assessing cardiac resynchronization Circulation 2005;111:2760-2767.[Abstract/Free Full Text]
- Dohi K, Suffoletto MS, Schwartzman D, Ganz L, Pinsky MR, Gorcsan III J. 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][Web of Science][Medline]
- Marwick TH. Measurement of strain and strain rate by echocardiography: ready for prime time? J Am Coll Cardiol 2006;47:1313-1327.[Abstract/Free Full Text]
- Yu CM, Zhang Q, Chan YS, et al. Tissue Doppler velocity is superior to displacement and strain mapping in predicting left ventricular reverse remodelling response after cardiac resynchronisation therapy Heart 2006;92:1452-1456.[Abstract/Free Full Text]
- Suffoletto MS, Dohi K, Cannesson M, Saba S, Gorcsan III J. 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]
- Lim P, Buakhamsri A, Popovic ZB, et al. Longitudinal strain delay index by speckle tracking imaging: a new marker of response to cardiac resynchronization therapy Circulation 2008;118:1130-1137.[Abstract/Free Full Text]
- 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]
- Kawaguchi M, Murabayashi T, Fetics BJ, et al. Quantitation of basal dyssynchrony and acute resynchronization from left or biventricular pacing by novel echo-contrast variability imaging J Am Coll Cardiol 2002;39:2052-2058.[Abstract/Free Full Text]
- Lardo AC, Abraham TP, Kass DA. Magnetic resonance imaging assessment of ventricular dyssynchrony: current and emerging concepts J Am Coll Cardiol 2005;46:2223-2228.[Abstract/Free Full Text]
- Osman NF, Sampath S, Atalar E, Prince JL. Imaging longitudinal cardiac strain on short-axis images using strain-encoded MRI Magn Reson Med 2001;46:324-334.[CrossRef][Web of Science][Medline]
- Nelson GS, Curry CW, Wyman BT, et al. Predictors of systolic augmentation from left ventricular preexcitation in patients with dilated cardiomyopathy and intraventricular conduction delay Circulation 2000;101:2703-2709.[Abstract/Free Full Text]
- Henneman MM, Chen J, Ypenburg C, et al. Phase analysis of gated myocardial perfusion single-photon emission computed tomography compared with tissue Doppler imaging for the assessment of left ventricular dyssynchrony J Am Coll Cardiol 2007;49:1708-1714.[Abstract/Free Full Text]
- Henneman MM, Chen J, Dibbets-Schneider P, et al. Can LV dyssynchrony as assessed with phase analysis on gated myocardial perfusion SPECT predict response to CRT? J Nucl Med 2007;48:1104-1111.[Abstract/Free Full Text]
- Knackstedt C, Muhlenbruch G, Mischke K, et al. Imaging of the coronary venous system: validation of three-dimensional rotational venous angiography against dual-source computed tomography Cardiovasc Intervent Radiol 2008;31:1150-1158.[CrossRef][Web of Science][Medline]
- Calo L, Lamberti F, Loricchio ML, et al. Intracardiac echocardiography: from electroanatomic correlation to clinical application in interventional electrophysiology Ital Heart J 2002;3:387-398.[Medline]
- Ypenburg C, Lancellotti P, Tops LF, et al. Acute effects of initiation and withdrawal of cardiac resynchronization therapy on papillary muscle dyssynchrony and mitral regurgitation J Am Coll Cardiol 2007;50:2071-2077.[Abstract/Free Full Text]
- Ypenburg C, Lancellotti P, Tops LF, et al. Mechanism of improvement in mitral regurgitation after cardiac resynchronization therapy Eur Heart J 2008;29:757-765.[Abstract/Free Full Text]
- Stanton T, Hawkins NM, Hogg KJ, Goodfield NE, Petrie MC, McMurray JJ. How should we optimize cardiac resynchronization therapy? Eur Heart J 2008;29:2458-2472.[Abstract/Free Full Text]
- Vardas PE, Auricchio A, Blanc JJ, et al. Guidelines for cardiac pacing and cardiac resynchronization therapy: the task force for cardiac pacing and cardiac resynchronization therapy of the European Society of Cardiology. Developed in collaboration with the European Heart Rhythm Association. Eur Heart J 2007;28:2256-2295.[Free Full Text]
- Mollema SA, Bleeker GB, van der Wall EE, Schalij MJ, Bax JJ. Usefulness of QRS duration to predict response to cardiac resynchronization therapy in patients with end-stage heart failure Am J Cardiol 2007;100:1665-1670.[CrossRef][Web of Science][Medline]
- Ypenburg C, Schalij MJ, Bleeker GB, et al. Impact of viability and scar tissue on response to cardiac resynchronization therapy in ischaemic heart failure patients Eur Heart J 2007;28:33-41.[Abstract/Free Full Text]
- Becker M, Franke A, Breithardt OA, et al. Impact of left ventricular lead position on the efficacy of cardiac resynchronisation therapy: a two-dimensional strain echocardiography study Heart 2007;93:1197-1203.[Abstract/Free Full Text]
- Becker M, Hoffmann R, Schmitz F, et al. Relation of optimal lead positioning as defined by three-dimensional echocardiography to long-term benefit of cardiac resynchronization Am J Cardiol 2007;100:1671-1676.[CrossRef][Web of Science][Medline]
- Murphy RT, Sigurdsson G, Mulamalla S, et al. Tissue synchronization imaging and optimal left ventricular pacing site in cardiac resynchronization therapy Am J Cardiol 2006;97:1615-1621.[CrossRef][Web of Science][Medline]
- Van de Veire NR, Schuijf JD, De Sutter J, et al. Non-invasive visualization of the cardiac venous system in coronary artery disease patients using 64-slice computed tomography J Am Coll Cardiol 2006;48:1832-1838.[Abstract/Free Full Text]
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M. Bertini, V. Delgado, D. W. den Uijl, G. Nucifora, A. C.T. Ng, R. J. van Bommel, C. J. W. Borleffs, G. Boriani, M. J. Schalij, and J. J. Bax
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Circ Cardiovasc Imaging,
January 1, 2010;
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