European Heart Journal Advance Access originally published online on August 1, 2006
European Heart Journal 2006 27(20):2426-2432; doi:10.1093/eurheartj/ehl179
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Comparison of segmental and global markers of dyssynchrony in predicting clinical response to cardiac resynchronization
Department of Echocardiography, Royal Brompton Hospital and, Imperial College, Sydney Street, London SW3 6NP, UK
Received 8 March 2006; revised 2 June 2006; accepted 14 July 2006; online publish-ahead-of-print 1 August 2006.
* Corresponding author. Tel: +44 207 351 8209; fax: +44 207 351 8604. E-mail address: a.duncan{at}imperial.ac.uk
See page 2380 for the editorial comment on this article (doi:10.1093/eurheartj/ehl247)
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Abstract |
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Aims Cardiac resynchronization therapy (CRT) reduces inter- and intraventricular dyssynchrony and shortens total isovolumic time (t-IVT). We compared the extent to which the values of ventricular dyssynchrony and t-IVT predict clinical benefits of CRT.
Methods and results Ventricular dyssynchrony was assessed in 39 patients with heart failure before and 6 months after CRT. Segmental dyssynchrony was identified from time to onset and peak systolic velocity of wall motion. T-IVT (s/min) was derived as [60–(total ejection time+total filling time)]. The difference between ventricular pre-ejection periods (D-PEP) was calculated. Outcome measures were fall in New York Heart Association (NYHA) class and increase in cardiac output (CO). Following CRT, NYHA class fell in 29/39 patients, CO increased (by 1.0 L/min, P<0.001), and intraventricular delay (Intra-VD), interventricular delay (Inter-VD), t-IVT, and D-PEP shortened (by 25 ms, 72 ms, 6 s/min, and 38 ms, P<0.01). NYHA class and CO were unchanged with CRT in 10/39, and Intra-VD, Inter-VD, t-IVT, and D-PEP lengthened (by 43 ms, 52 ms, 7 s/min, and 35 ms, P<0.05). Though univariate predictors of CO increment with CRT were Intra-VD, Inter-VD, t-IVT, and D-PEP, only pre-CRT values of CO (P<0.001), t-IVT (P<0.001), and D-PEP (P=0.025) were independent.
Conclusion Global, rather than segmental, measures of ventricular dyssynchrony are powerful, independent predictors of clinical response to CRT.
Key Words: Cardiac resynchronization therapy • Interventricular delay • Intraventricular delay • Total isovolumic time
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Introduction |
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Cardiac resynchronization therapy (CRT) is a treatment of intractable heart failure with intraventricular conduction disturbances. Clinical trials have demonstrated the benefits of CRT on symptoms, exercise capacity, quality of life, heart failure hospitalization, and long-term prognosis.1–4 However, individual responses may vary; indeed, up to 30% of patients receiving CRT fail to respond clinically.5 Widened QRS complex on the surface electrocardiogram, baseline New York Heart Association (NYHA) function class, age, sex, and ejection fraction (EF) correlate poorly with outcome.6,7 In contrast, the predictive value of direct measures of segmental dyssynchrony using a variety of outcome measures based on different imaging types such as M-mode,8 Doppler,5 tissue Doppler,9–11 tissue synchronization12 and strain-rate analysis13 have demonstrated predictive accuracies of 85–100%. However, segmental measures of mechanical dyssynchrony do not necessarily reflect the overall effect of CRT on global cardiac function.
Segmental dyssynchrony decreases peak rates of left ventricular (LV) pressure rise and fall,14 but also prolongs total isovolumic time (t-IVT: time in the cardiac cycle when the LV is neither ejecting nor filling).15 In patients with coronary artery disease, t-IVT prolongs as mechanical dyssynchrony increases during dobutamine stress15 and shortens with surgical revascularization.16 CRT also shortens t-IVT.17 Our working hypothesis was that when correction of dyssynchrony increases cardiac output (CO), it does so by shortening t-IVT. We therefore compared the predictive value of t-IVT in identifying responders to CRT with that of several global and segmental measures of LV dyssynchrony. We aimed not only to identify patients most likely to benefit clinically from CRT but also to predict its extent.
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Methods |
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Study population
We retrospectively studied 39 patients with end-stage heart failure who received clinically indicated CRT during the period 2003–04. All patients included in the study fulfilled the AHA/ACC/NASPE criteria for resynchronization, that is, symptomatic NYHA classes III–IV, drug-refractory heart failure, stable sinus rhythm, LVEF
35%, dilated cardiomyopathy (LV end-diastolic diameter 
55 mm), and prolonged QRS complex (130 ms). Ischaemic or non-ischaemic heart disease was defined by the WHO criteria.18 Exclusion criteria were acute heart failure, unstable angina, coronary artery bypass graft surgery or myocardial infarction within the previous 3 months, prior pacemaker or defibrillator insertion, valvular stenosis, previous valve replacement, uncomplicated RBBB, and a history of chronic atrial fibrillation. Clinical response to CRT was defined as a fall in NYHA class 1 functional class. The project was approved by The Royal Brompton and Harefield Research Ethics Committee, and the study complied with the Declaration of Helsinki.
Protocol
All patients underwent a clinical examination, 12-lead electrocardiography, and echocardiographic assessment at baseline and at after 6 months of pacing in biventricular mode with optimal atrioventricular delay. Patients were closely monitored in a specialist heart failure clinic where functional status was assessed and NYHA class independently documented at each visit. The therapeutic regime was unaltered between the two echocardiographic assessments. All echocardiographic studies and analyses were performed by operators not involved in the clinical follow-up and were blinded at all times to the clinical data.
Echocardiographic assessment
Transthoracic echocardiography was performed using a Phillips Sonos 5500 echocardiograph and a multifrequency transducer (Andover, MA, USA). Standard two-dimensional parasternal long- and short-axis views and apical four-, five-, and two-chamber views were performed. Cross-sectional two-dimensional guided M-mode recordings of the LV minor axis were obtained. EF and end-systolic volume (ESV) were calculated by Simpson's method. Mitral regurgitation (MR) was recorded using colour-flow Doppler and continuous-wave Doppler in the apical four- and two-chamber views, and its duration, expressed as percentage of the RR interval, was calculated.
Subaortic flow velocity was obtained by pulsed-wave Doppler from the apical five-chamber view, with the sample volume placed in the LV outflow tract, 1 cm below the aortic cusps. LV ejection time (ET) was measured using leading edge methodology as the interval between the onsets of forward aortic flow and aortic valve closure artefact. Stroke distance was calculated as the time integral of aortic velocity, stroke volume as the product of stroke distance and subaortic area, and CO as stroke volume multiplied by heart rate. A pre-determined increment in CO of 15% was used to signify an increase in CO after CRT.
Transmitral flow velocities were recorded from the apical four-chamber view using pulsed-wave Doppler. Isovolumic relaxation time (IVRT: the interval between A2 and the onset of mitral flow) and peak E (early diastolic) and A (atrial) velocities were obtained in all patients. Filling time (FT) was measured using leading edge methodology from the onset of the E-wave to the end of the A-wave. Isovolumic contraction time (IVCT) was calculated by subtracting the sum of IVRT (ms), ET (ms), and FT (ms) from RR interval.
Total LV ejection and filling periods were derived as the product of the corresponding time interval and heart rate, expressed in s/min, e.g. total ET (s/min)=ET (ms)*heart rate/1000. T-IVT, also in s/min, was derived as [60–(total ET+total FT)]15–17 (Figure 1). LV pre-ejection period (LV-PEP) and RV pre-ejection period (RV-PEP) were measured from the onset of the QRS complex to the onsets of aortic and pulmonary flow, respectively. With CRT, the pacing artefact was taken as the onset of ventricular activation. The difference (D-PEP) was calculated as LV-PEP minus RV-PEP.
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LV long axis M-mode and pulsed-wave tissue Doppler recordings were obtained with the cursor positioned at the lateral, septal, and posterior angles of the mitral ring and at the lateral ring of the tricuspid valve for the RV. A Doppler velocity range of ±30 cm/s displayed systolic and early diastolic velocities. Intraventricular delay (Intra-VD) and interventricular delay (Inter-VD) were calculated using the following two methods.
M-mode imaging
Segmental electromechanical delay was measured from the onset of the QRS to the onset of long-axis shortening (TOS) (Figure 2, top). Intra-VD (TOS-Intra-VD) was calculated as the difference between the longest and shortest regional electromechanical coupling time (irrespective of site). Inter-VD (TOS-Inter-VD) was calculated as the difference between regional electromechanical coupling time at the RV free wall and the most delayed LV site (i.e. longest regional electromechanical coupling time).
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Tissue Doppler imaging
Tissue Doppler imaging was used to measure the time to peak systolic velocity (TS), taken from the onset of the QRS complex to the peak velocity during ejection (Figure 2, bottom). Intraventricular (TS-Intra-VD) delay was calculated as the difference between the longest and shortest time to peak systolic velocity (irrespective of site), and Inter-VD (TS-Inter-VD) as the difference between time to peak systolic velocity at the RV free wall and the most delayed LV segment.
Pacemaker implantation
Seventeen of 39 patients were implanted with a biventricular pacemaker (Guidant Contak TR CHFD, Guidant Inc., St. Paul, MN, USA or Medtronic InSync III 8040, Medtronic Inc., Minneapolis, MN, USA), and 22/39 received a biventricular cardioverter-defibrillator (Guidant Contak CD CHFD or Contak Renewal, Guidant Inc., or Medtronic InSync ICD 7272, Medtronic Inc.). Implantation was performed as previously described17 and was uncomplicated in all cases. The final LV lead position was lateral (in 23 cases), posterolateral (in 10 cases), and posterior (in six cases). The biventricular pacing mode was programmed in DDD, and the lower rate set at 40 bpm. The atrioventricular interval was optimized for maximal diastolic filling by Doppler echocardiography19 while ensuring atrial sensing and ventricular pacing (78% A-sensed and 98% Bi-V paced). The Inter-VD was set at zero.
Data analysis
Statistical analyses were performed using Statview 4.5 (Abacus Concepts, Berkley, CA, USA) and S Plus 6.2 (Insightful, Seattle, WA, USA). Normally distributed continuous variables were expressed as mean±standard error. Continuous variables within and between groups were compared using two-tailed paired and unpaired Student's t-tests. Categorical variables were expressed as number (percentage) and compared using a 
2 or Fisher's exact test as appropriate. Agreement between reduction in NYHA class, improvement in CO, and reduction in ESV was assessed using the kappa statistic. The influence of t-IVT vs. a number of pre-determined global and segmental measures of LV dyssynchrony in predicting the increment in CO with CRT was assessed with multiple-regression analysis (ANCOVA). Correlation was performed by linear-regression analysis. A significance level of P<0.05 was employed throughout the study.
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Results |
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Thirty-nine patients (aged 65±10 years, QRS duration 154±18 ms, 30 male) were studied before [median 2.0 months, interquartile range (IQR) 0.5–2.5 months] and after (median 6.3 months, IQR 4.2–8.9 months) pacemaker implantation. Before pacing, 37/39 patients were in NYHA class III and two were in NYHA class IV. NYHA class fell by
1 functional class with CRT in 29/39 patients (‘responders’) and did not change in 10 (‘non-responders’).14 The demographic, clinical, and therapeutic characteristics of the patient population are presented in Table 1. Half of all responders and 90% of non-responders had an ischaemic aetiology (2=5.3, P<0.03). There was no difference in LV lead placement between responders vs. non-responders (lateral LV lead: 66 vs. 50%, posterolateral lead in 10 vs. 20%; posterior lead: 24 vs. 30%, all P=NS). Similarly, there was no difference in medical therapy or in the programmed resting atrioventricular interval between responders (89±19 ms) and non-responders (93±19 ms, P=0.77).
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Relation between changes in NYHA class, CO, and ESV
Resting CO increased with CRT in 31/39 patients (in whom NYHA class fell
1 class in 29/31). ESV fell by >15% in 32/39 patients (in whom NYHA class fell 1 class also in 29/31). The agreement between fall in NYHA class and increase in CO (>15%) was associated with a kappa statistic of 0.85 (P<0.001); similarly, fall in NYHA class and reduction in ESV (>15%) were associated with a kappa statistic of 0.78 (P<0.001). In the event, we used post-implantation CO as a quantitative measure to determine the predictors of clinical response to CRT.
Comparison between responders and non-responders at baseline
When compared with non-responders, responders had lower baseline values for mitral E-wave velocity (by 35 cm/s, P<0.001) and longer values for t-IVT, LV-PEP, and D-PEP (by 7 s/min, P<0.001; 33 ms, P=0.008; 50 ms, P<0.001, respectively; Table 2). Segmental dyssynchrony was more pronounced at baseline in responders (Table 3), with Intra-VD and Inter-VD up to 51 and 71 ms longer, respectively, than that in non-responders (both P<0.001).
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Effect of CRT on global LV function
Responders
With CRT, there were significant mean (±SE) increases in CO (by 1.0±0.1 L/min), EF (by 10±2%), and total LV FT (by 5±1 s/min), and significant mean (±SE) reductions in ESV (by 58±31 mL), MR duration (by 10±7%), and IVCT (by 50±39 ms, all P<0.001, Table 2). The combination of shorter IVCT and longer FT resulted in a significant fall in t-IVT (by 6±4 s/min, P<0.001). D-PEP shortened in responders (by 38±23 ms, P<0.001).
Non-responders
There were no significant mean changes in resting CO, EF, or duration of MR with CRT (Table 2), and ESV decreased by 30±21 mL (P<0.05 compared to responders). In contrast to responders, IVCT lengthened (by 73±95 ms, P=0.037) and FT shortened (by 5±4s/min, P=0.024), so that t-IVT increased (by 7±4s/min, P=0.001). D-PEP increased with CRT in non-responders (by 35±12 ms, P<0.001).
Effect of CRT on segmental LV function
Responders
The LV lead was placed at the site of longest electromechanical delay in 76% of patients. Intra-VD and Inter-VD fell with CRT in responders (Table 3): TOS-Intra-VD and TOS-Inter-VD both shortened (by 25±42 ms, P=0.003 and 72±37 ms, P<0.001 respectively), as did TS-Intra-VD and TS-Inter-VD (by 25±67 ms, P=0.043 and 51 ms, P<0.001 respectively).
Non-responders
The LV lead was placed at the site of longest electromechanical delay in 70% of patients (P=NS compared with responders). Intra-VD and Inter-VD increased with CRT in non-responders (Table 3): TOS-Intra-VD and TOS-Inter-VD both increased (by 43±13 ms P=0.015 and 52±10 ms P<0.001 respectively), as did TS-Inter-VD (by 28±18 ms P<0.001). Mean TS-Intra-VD was unchanged.
Predictors of the extent of increase in CO with CRT
Other than baseline values of CO, there were several univariable predictors of the CO increment with CRT; TOS-Intra-VD, TOS-Inter-VD, D-PEP, t-IVT, total FT, IVCT, LV-PEP, and TS-Inter-VD (Table 4). After adjusting for baseline values of CO, the only independent variables that predicted CO-increment with CRT were t-IVT (P<0.001) and D-PEP (P=0.025, Table 4). The combination of pre-CRT values for CO, t-IVT, and D-PEP explained 87% (R2=0.87) of the total variance in observed CO with CRT (Figure 3), considerably more than any of these variables singly. Overall, responders tended to have longer t-IVT and D-PEP before CRT (Figure 4A) and shorter t-IVT and D-PEP with CRT (Figure 4B). The reverse was true for non-responders.
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Reproducibility
We have previously published the reproducibility of measurements used in our analysis; reproducibility, expressed as root mean square, was 3.5 s/min for t-IVT, 1.26 L/min for CO, and 11 ms for TOS.16 In the present study, the root mean square was 21 ms for D-PEP, 31 ms for TS, and 42 mL for ESV.
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Discussion |
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The principal aim of CRT is to improve clinical outcome or to prolong prognosis. We thus chose an independently determined, previously validated,14,20 clinical marker of response to CRT (fall in NYHA class >1 grade) as an endpoint to identify clinical responders to CRT. There was a close agreement between fall in NYHA class (clinical response to CRT) and increase in resting CO and reduction in ESV (echocardiographic response). Fall in NYHA class agreed with an increase in CO with a higher kappa statistic than that for reduction in ESV, which lent credence to using CO increment with CRT as an endpoint. Measurement of CO is a clinically valid and reliable outcome measure in patients with end-stage heart failure, with the advantage of eliminating any placebo effect on NYHA class.
Findings
Our results demonstrate that patients who responded to CRT with a fall in NYHA class and rise in resting CO had more pronounced segmental dyssynchrony and greater values for t-IVT and D-PEP before implantation when compared with non-responders. A positive clinical response to CRT was also accompanied by shortening of t-IVT, as previously demonstrated in the MUSTIC trial,17 and of D-PEP, as previously demonstrated in the CARE-HF21 trial, compatible with lessening of the degree of segmental dyssynchrony. Indeed, resynchronization by CRT augmented stroke volume to the extent that resting CO increased, despite a significant reduction in heart rate after pacing. In contrast, segmental dyssynchrony became more apparent after pacing in non-responders, in whom t-IVT and D-PEP both increased.
In line with previous studies,8–13 we found that patients who responded to CRT had more pronounced segmental dyssynchrony, whether measured by M-mode or tissue Doppler. Furthermore, their baseline values proved to be significant univariate predictors of response to CRT. However, these segmental measures of dyssynchrony were subsumed in multivariate analysis, and the only independent predictors of CO increment with CRT were baseline values of CO, t-IVT, and D-PEP. Indeed, the combination of baseline values of CO, t-IVT, and D-PEP accounted for 87% of the variance in CO increment with CRT. Moreover, combining t-IVT and D-PEP in a simple two-dimensional display demonstrated clustering of patients with almost complete separation between responders and non-responders (Figure 4).
Mechanisms
It is clear from Figure 4 that responders were patients in whom pre-implantation values of both t-IVT and D-PEP were greatly and abnormally prolonged. We have previously shown that t-IVT is prolonged by segmental dyssynchrony16 and shortens as a result of reduction of dyssynchrony with CRT.10 We have also previously shown that it is a powerful predictor of peak VO2 in patients with dilated cardiomyopathy,22 which might explain its significance in predicting the clinical response to CRT. The reason why D-PEP is as sensitive to t-IVT, as well as being synergistic with it, is not entirely clear. We previously demonstrated that dyssynchronous LV contraction is a determinant of PEP in patients with LV disease.23 Owing to uncertainty in determining the onset of the QRS on the surface ECG in some patients with LBBB, this correlation is apparent only as prolonged D-PEP, rather than in absolute values of LV-PEP in isolation. We assume, therefore, that D-PEP, like t-IVT, can be regarded as an index of the overall effects of dyssynchrony on LV function.
In keeping with previous investigations, 
25% of our patients were non-responders. From Figure 4, it is clear that in all non-responders, values of t-IVT and D-PEP were within the normal range prior to implantation.22 This strongly suggests that in these patients, failure to respond to CRT was associated with pre-existing coordinate contraction rather than dyssynchrony uncorrected by biventricular pacing, caused, for instance, by inappropriate positioning of the LV lead due to unfavourable coronary sinus anatomy. Furthermore, it was disquieting to observe that in nearly every non-responder, implementation of CRT was associated with prolongation of both t-IVT and D-PEP to values well outside the normal range. The possibility that CRT had actually induced dyssynchrony was reinforced in these patients by the observation that measures of segmental dyssynchrony had also deteriorated (Table 3).
Limitations
Although the study sample size was relatively small, the results are compatible with previous conclusions that the absence of baseline dyssynchrony is the main basis for non-response. Similar to other studies,14,20 only basal LV sites were interrogated; this may have led to the loss of precision in localizing intraventricular dyssynchrony, thereby favouring t-IVT and D-PEP on multivariate analysis. However, any potential intraventricular dyssynchrony at mid-cavity or apical level would have been reflected in reciprocal dyssynchrony at the base of the heart which we studied. Furthermore, basal segmental function is closely related to global cardiac function (EF), so basal intraventricular dyssynchrony, if present, would be more likely to have an effect on global cardiac function than dyssynchrony elsewhere in the myocardium. We chose a clinical rather than an echocardiographic marker of response to CRT (reduction in LV ESV>15%), as the aim of our study was to predict clinical, not echocardiographic, improvement with CRT. Although the assessment of NYHA class may be subjective, there was a good agreement between clinical and echocardiographic response to CRT on an individual patient basis. As in all CRT studies, the possibility exists of spontaneous improvement, independent of pacing, which may confound the results. Finally, the statistical analysis implicitly assumes that the effects of CRT are constant with time (i.e. patients do not have an initial improvement and subsequently decline).
Clinical implications
To be of value in a clinical setting, any measurement should be easy to quantify and interpret. Individuals with pronounced evidence of global LV dyssynchrony (long t-IVT and D-PEP) are more likely to respond clinically to CRT, regardless of baseline demographics, QRS duration, NYHA class, or EF. T-IVT and D-PEP can be measured rapidly and compared with those on a display as in Figure 4, allowing a clinical decision to be made. Using these simple intervals avoids multiple determinations of segmental function, which may be time consuming to perform. Furthermore, we have previously demonstrated the close association between resting t-IVT and peak VO2;17 the shorter the t-IVT, the greater peak VO2. This might explain the favourable clinical outcome in patients who responded to CRT. The contrasting observation that CRT may apparently induce dyssynchrony in patients with coordinate contraction requires further investigation.
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Conclusion |
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The consequence of segmental dyssynchrony in patients with end-stage heart failure appears to be reflected in simple measurements of timing within the cardiac cycle, namely t-IVT and the difference between the ventricular pre-ejection periods. These measures of global LV function, which can readily be made in routine clinical conditions using simple and well-validated techniques, independently predict the extent of clinical response to biventricular pacing and together afford the possibility of predicting the outcome of CRT in individual patients with some precision.
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Acknowledgement |
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A.D. is supported by Imperial College, London.
Conflict of interest: None declared.
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References |
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- Cazeau S, Leclercq C, Lavergne T, Walker S, Varma C, Linde C, Garrigue S, Kappenberger L, Haywood GA, Santini M, Bailleul C, Daubert JC. (2001) Effects of multisite biventricular pacing in patients with heart failure and intraventricular conduction delay. N Engl J Med 344:873–880.
[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. (2002) Multicenter insync randomized clinical evaluation. Cardiac resynchronization in chronic heart failure. N Engl J Med 346:1845–1853.
[Abstract/Free Full Text] - Gras D, Leclercq C, Tang AS, Bucknall C, Luttikhuis HO, Kirstein-Pedersen A. (2002) Cardiac resynchronization therapy in advanced heart failure the multicenter insync clinical study. Eur J Heart Fail 4:311–320.[CrossRef][Web of Science][Medline]
- 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, Defibrillation in Heart Failure (COMPANION) Investigators. (2004) Cardiac-resynchronization therapy with or without an implantable defibrillator in advanced chronic heart failure. N Engl J Med 350:2140–2150.
[Abstract/Free Full Text] - Reuter S, Garrigue S, Barold SS, Jais P, Hocini M, Haissaguerre M, Clementy J. (2002) Comparison of characteristics in responders vs nonresponders with biventricular pacing for drug-resistant congestive heart failure. Am J Cardiol 89:346–350.[CrossRef][Web of Science][Medline]
- Leclercq C, Faris O, Tunin R, Johnson J, Kato R, Evans F, Spinelli J, Halperin H, McVeigh E, Kass DA. (2002) Systolic improvement and mechanical resynchronization does not require electrical synchrony in the dilated failing heart with left bundle-branch block. Circulation 106:1760–1763.
[Abstract/Free Full Text] - Krahn AD, Snell L, Yee R, Finan J, Skanes AC, Klein GJ. (2002) Biventricular pacing improves quality of life and exercise tolerance in patients with heart failure and intraventricular conduction delay. Can J Cardiol 18:380–387.[Web of Science][Medline]
- Pitzalis MV, Iacoviello M, Romito R, Guida P, De Tommasi E, Luzzi G, Anaclerio M, Forleo C, Rizzon P. (2005) Ventricular asynchrony predicts a better outcome in patients with chronic heart failure receiving cardiac resynchronization therapy. J Am Coll Cardiol 45:65–69.
[Abstract/Free Full Text] - Yu CM, Fung WH, Lin H, Zhang Q, Sanderson JE, Lau CP. (2003) Predictors of left ventricular reverse remodeling after cardiac resynchronization therapy for heart failure secondary to idiopathic dilated or ischaemic cardiomyopathy. Am J Cardiol 91:684–688.[CrossRef][Web of Science][Medline]
- Penicka M, Bartunek J, De Bruyne B, Vanderheyden M, Goethals M, De Zutter M, Brugada P, Geelen P. (2004) Improvement of left ventricular function after cardiac resynchronization therapy is predicted by tissue Doppler imaging echocardiography. Circulation 109:978–983.
[Abstract/Free Full Text] - Bax JJ, Bleeker GB, Marwick TH, Molhoek SG, Boersma E, Steendijk P, van der Wall EE, Schalij MJ. (2004) Left ventricular dyssynchrony predicts response and prognosis after cardiac resynchronization therapy. J Am Coll Cardiol 44:1834–1840.
[Abstract/Free Full Text] - Yu CM, Zhang Q, Fung JW, Chan HC, Chan YS, Yip GW, Kong SL, Lin H, Zhang Y, Sanderson JE. (2005) A novel tool to assess systolic asynchrony and identify responders of cardiac resynchronization therapy by tissue synchronization imaging. J Am Coll Cardiol 45:677–684.
[Abstract/Free Full Text] - Sogaard P, Egeblad H, Kim WY, Jensen HK, Pedersen AK, Kristensen BO, Mortensen PT. (2002) Tissue Doppler imaging predicts improved systolic performance and reversed left ventricular remodeling during long-term cardiac resynchronization therapy. J Am Coll Cardiol 40:723–730.
[Abstract/Free Full Text] - Gibson DG and Brown DJ. (1976) Assessment of left ventricular systolic function in man from simultaneous echocardiographic and pressure measurements. Br Heart J 38:8–17.
[Abstract/Free Full Text] - Duncan AM, Francis DP, Henein MY, Gibson DG. (2003) Limitation of cardiac output by total isovolumic time during pharmacologic stress in patients with dilated cardiomyopathy: activation-mediated effects of left bundle branch block and coronary artery disease. J Am Coll Cardiol 41:121–128.
[Abstract/Free Full Text] - Duncan A, Francis D, Gibson D, Pepper J, Henein MY. (2004) Electromechanical left ventricular resynchronisation by coronary artery bypass surgery. Eur J Cardiothorac Surg 26:711–719.
[Abstract/Free Full Text] - Duncan A, Wait D, Gibson D, Daubert JC. (2003) Left ventricular remodelling and haemodynamic effects of multisite biventricular pacing in patients with left ventricular systolic dysfunction and activation disturbances in sinus rhythm: sub-study of the MUSTIC trial. Eur Heart J 24:430–441.
[Abstract/Free Full Text] - Richardson P, McKenna W, Bristow M, Maisch B, Mautner B, O'Connell J, Olsen E, Thiene G, Goodwin J, Gyarfas I, Martin I, Nordet P. (1996) Report of the 1995 Cardiology Task Force on the definition and classification of cardiomyopathies. Circulation 93:841–842.
[Free Full Text] - Brecker SJ and Gibson DG. (1996) What is the role of pacing in dilated cardiomyopathy? Eur Heart J 17:819–824.
[Free Full Text] - Bleeker GB, Bax JJ, Fung JW, van der Wall EE, Zhang Q, Schalij MJ, Chan JY, Yu CM. (2006) Clinical vs echocardiographic parameters to assess response to cardiac resynchronization therapy. Am J Cardiol 97:260–263.[CrossRef][Web of Science][Medline]
- Cleland JG, Daubert JC, Erdmann E, Freemantle N, Gras D, Kappenberger L, Tavazzi L. Cardiac Resynchronization-Heart Failure (CARE-HF) Study Investigators. (2005) The effect of cardiac resynchronization on morbidity and mortality in heart failure. N Engl J Med 352:1539–1549.
[Abstract/Free Full Text] - Duncan AM, Francis DP, Gibson DG, Henein MY. (2004) Limitation of exercise tolerance in chronic heart failure: distinct effects of left bundle-branch block and coronary artery disease. J Am Coll Cardiol 43:1524–1531.
[Abstract/Free Full Text] - Chen W and Gibson D. (1979) Mechanisms of prolongation of pre-ejection period in patients with left ventricular disease. Br Heart J 42:304–310.
[Abstract/Free Full Text]
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 C. Parsai, B. Bijnens, G. R. Sutherland, A. Baltabaeva, P. Claus, M. Marciniak, V. Paul, M. Scheffer, E. Donal, G. Derumeaux, et al. Toward understanding response to cardiac resynchronization therapy: left ventricular dyssynchrony is only one of multiple mechanisms Eur. Heart J., April 2, 2009; 30(8): 940 - 949. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 N. Antonio, R. Teixeira, L. Coelho, C. Lourenco, P. Monteiro, M. Ventura, J. Cristovao, L. Elvas, L. Goncalves, and L. A. Providencia Identification of 'super-responders' to cardiac resynchronization therapy: the importance of symptom duration and left ventricular geometry Europace, March 1, 2009; 11(3): 343 - 349. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 G. Bajraktari, A. Duncan, J. Pepper, and M. Henein Prolonged total isovolumic time predicts cardiac events following coronary artery bypass surgery Eur J Echocardiogr, November 1, 2008; 9(6): 779 - 783. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 R Chung, R Sutton, and M Y Henein Beyond dyssynchrony in cardiac resynchronisation therapy Heart, August 1, 2008; 94(8): 991 - 994. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 T. H. Marwick Hype and Hope in the Use of Echocardiography for Selection for Cardiac Resynchronization Therapy: The Tower of Babel Revisited Circulation, May 20, 2008; 117(20): 2573 - 2576. [Full Text] [PDF]
|
|
|
|
|
|
C. Miyazaki, B. D. Powell, C. J. Bruce, R. E. Espinosa, M. M. Redfield, F. A. Miller, D. L. Hayes, Y.-M. Cha, and J. K. Oh Comparison of Echocardiographic Dyssynchrony Assessment by Tissue Velocity and Strain Imaging in Subjects With or Without Systolic Dysfunction and With or Without Left Bundle-Branch Block Circulation, May 20, 2008; 117(20): 2617 - 2625. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
L. J. Anderson, C. Miyazaki, G. R. Sutherland, and J. K. Oh Patient Selection and Echocardiographic Assessment of Dyssynchrony in Cardiac Resynchronization Therapy Circulation, April 15, 2008; 117(15): 2009 - 2023. [Full Text] [PDF]
|
|
|
|
 |
|
 B. W.L. De Boeck, M. Meine, G. E. Leenders, A. J. Teske, H. van Wessel, J. H. Kirkels, F. W. Prinzen, P. A. Doevendans, and M. J. Cramer Practical and conceptual limitations of tissue Doppler imaging to predict reverse remodelling in cardiac resynchronisation therapy Eur J Heart Fail, March 1, 2008; 10(3): 281 - 290. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
G. B Bleeker, C.-M. Yu, P. Nihoyannopoulos, J. de Sutter, N. Van de Veire, E. R Holman, M. J Schalij, E. E van der Wall, and J. J Bax Optimal use of echocardiography in cardiac resynchronisation therapy Heart, November 1, 2007; 93(11): 1339 - 1350. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. Uebing, D. G. Gibson, S. V. Babu-Narayan, G. P. Diller, K. Dimopoulos, O. Goktekin, M. S. Spence, K. Andersen, M. Y. Henein, M. A. Gatzoulis, et al. Right Ventricular Mechanics and QRS Duration in Patients With Repaired Tetralogy of Fallot: Implications of Infundibular Disease Circulation, October 2, 2007; 116(14): 1532 - 1539. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 F. A. McAlister, J. Ezekowitz, N. Hooton, B. Vandermeer, C. Spooner, D. M. Dryden, R. L. Page, M. A. Hlatky, and B. H. Rowe Cardiac Resynchronization Therapy for Patients With Left Ventricular Systolic Dysfunction: A Systematic Review JAMA, June 13, 2007; 297(22): 2502 - 2514. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. E. Sanderson Assessment of ventricular dyssynchrony: global or regional function? Eur. Heart J., October 2, 2006; 27(20): 2380 - 2381. [Full Text] [PDF]
|
|
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