Europace Advance Access originally published online on March 11, 2008
Europace 2008 10(4):489-495; doi:10.1093/europace/eun059
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RESYNCHRONISATION THERAPY
Resynchronization of the left ventricular contraction by tailored programming of right and left ventricular pacing
Arrhythmologic Centre, Department of Cardiology, Ospedali del Tigullio, Via don Bobbio, 16033 Lavagna, Italy
Manuscript submitted 17 October 2007. Accepted after revision 18 February 2008.
* Corresponding author. Tel: +39 0185 329 567; fax: +39 0185 306 506. E-mail address: mbrignole{at}asl4.liguria.it
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Abstract |
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Aims: The prerequisite and the rationale for the benefit of cardiac resynchronization therapy (CRT) is that it is able to resynchronize left ventricular (LV) walls that have a delayed activation.
Methods and results: In 69 consecutive patients who underwent biventricular (BIV) pacemaker implantation, we assessed the magnitude of intraventricular resynchronization achieved by means of simultaneous (BIV 0) and sequential BIV pacing (with an individually optimized VV interval value among +80 ms and –80 ms) using pulsed-wave tissue Doppler imaging techniques and in particular the measurement of the intra-LV electromechanical delay. The intra-LV delay was defined as the difference between the longest and the shortest activation time in the six basal segments of the LV. An abnormal intra-LV delay was defined as a value >41 ms. The intra-LV delay was 63 ± 28 ms baseline, decreased to 44 ± 26 ms with BIV 0 and to 26 ± 15 ms with optimized BIV (P = 0.001). BIV 0 determined the shortest delay in 28 (41%) patients (23 ± 12 ms). In 41 (59%) patients, a better resynchronization was achieved with optimized VV intervals (LV first in 32 and RV first in 5) or single-chamber pacing (LV in 3 and RV in 1). With BIV 0, the intra-LV delay remained abnormal in 41% and was longer than baseline in 30% of patients compared with 9 and 12% with optimized BIV, respectively (P = 0.001).
Conclusion: A sub-optimal resynchronization is achieved with simultaneous BIV pacing in most patients. A tailored programming of the relative contribution of RV and LV pacing forms the prerequisite for improving CRT results.
Key Words: Cardiac resynchronisation therapy, Dyssynchrony, Tissue Doppler imaging
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Introduction |
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The prerequisite and the rationale for the benefit of cardiac resynchronization therapy (CRT) is that it is able to resynchronize left ventricular (LV) walls that have a delayed activation.1
,2 Thus, there is the need of a method able to measure dyssynchrony before CRT and finally to document an effective resynchronization after this procedure. The aim of this study was to assess the magnitude of intraventricular resynchronization achieved by means of simultaneous and sequential biventricular (BIV) pacing with an individually optimized intra-LV interval using echocardiographic tissue Doppler imaging (TDI) techniques and in particular the measurement of the intra-LV electromechanical delay.
For the purpose of this study we assumed that the improvement in haemodynamic function and clinical outcome observed during CRT may be explained, at least in part, by a significant resynchronization of the regional LV movement and that TDI is a reliable technique able to show such changes. Conversely, the lack of clinical benefit to CRT, consistently observed in around one-quarter to one-half of patients (the so-called ‘non-responders’), may potentially be attributed to an imperfect sub-optimal resynchronization achieved by current methodologies of pacing. These assumptions come from a large consistent number of studies.3–14 Admittedly, the value of TDI is not yet fully proved and some concern exists on its applicability in the clinical practice once used for future large randomized prospective trials which show a benefit in clinical practice.5,15 However, this debate goes beyond the purpose of this study which is aimed to assess a methodology for improving CRT clinical results and to appropriately design future clinical trials.
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Methods |
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The study population consisted of 69 consecutive patients with drug-refractory advanced heart failure and wide QRS (spontaneous or induced by AV junction ablation) who were prospectively selected for CRT between January 2005 and June 2007. Their clinical characteristics are shown in the Table 1.
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Pacemaker implantation and pacing protocol
All patients received a BIV pacing system able to deliver either simultaneous RV and LV pacing (BIV 0) or sequential pacing with a programmable VV interval that allowed to advance RV or LV pacing, respectively, up to 80 ms. Except for six patients, all devices had an ICD back-up feature. The right atrial and RV leads were positioned in the right atrial and the RV apex, respectively. The target for LV leads was the basal or mid-portion of the postero-lateral free wall. Depending on the suitable anatomy of the coronary sinus, this goal was achieved in 55 patients (80%). In the other cases, the site of LV pacing was the apical portion of the postero-lateral free wall except one case in which the lead was positioned in the anterior position. The patients who were in sinus rhythm were paced in the atrial synchronized (VDD) mode. The best AV synchronization was obtained by programming the AV interval in order to initiate the biventricular contraction at the end of the atrial contraction, i.e. to obtain the longest possible AV filling time without truncating the A wave, as assessed by means of pulsed Doppler analysis of transmitral flow.4
,16,17 In order to ensure complete ventricular capture and rate regularity, the patients in atrial fibrillation performed catheter ablation of the AV junction at the time of pacemaker implantation; the BIV pacemaker was programmed at a rate of 80 bpm.
Echocardiographic study
The intra-LV electromechanical delay of the six basal segments was used to measure LV dyssynchrony baseline, after simultaneous BIV pacing and after sequential BIV pacing with an individually optimized VV delay. The intra-LV electromechanical activation was evaluated by echocardiography using pulsed-wave TDI modality. From three apical views (4-chamber, 2-chamber and long-axis view), the sample volume was placed in the middle of the basal segment of each wall (posterior septum and lateral wall in 4-chamber view, inferior and anterior wall in 2-chamber view, anterior septum and posterior wall in long-axis view) and the interval between the onset of QRS complex and the onset of each respective positive component of the regional systolic velocity on tissue Doppler spectral tracing recorded at 100 mm/s was measured. For each basal LV segment, three consecutive beats were measured, and the average value was taken. The intra-LV electromechanical delay was calculated as the time difference between the longest and the shortest interval among the six ventricular walls.9,10,18–20
In a population of 58 controls, the median intra-LV delay was 17 ms; 95% of controls had a value 
41 ms.19 Abnormal intra-LV delay was therefore considered a delay greater than 41 ms. Pulsed-wave DTI had a time resolution of 5 ms. The inter-observer correlation for intra-LV delay was 0.93 in a sample size of 15 patients.19
An electromechanical activation map was constructed first during simultaneous BIV pacing, as shown in the Figure 1, and the intra-LV delay during simultaneous BIV pacing was calculated first. If its value was equal or less than the median of our reference standard (17 ms), LV contraction was considered sufficiently resynchronized and no other measurement was performed. If longer, the VV interval of the pacemaker was modified by advancing the LV stimulus or the RV stimulus up to 80 ms. In order to avoid repeated unnecessary measures, the choice of the VV interval was guided by the analysis of the BIV 0 activation map. If the postero-lateral segments were delayed, LV pacing was advanced to a value which was approximately half of the delay and the intra-LV delay again measured; conversely, if the antero-septal segments were delayed, RV pacing was advanced at the same manner. Fine adjustments of the VV interval were finally performed, if necessary, in order to achieve the goal. If dyssynchrony persisted, LV or RV pacing alone were assessed. Optimized CRT configuration was defined as the modality of pacing corresponding to that of the shortest intra-LV delay among simultaneous, sequential pacing, or single-chamber pacing. For each patient the study was performed by two operators, one of whom performed TDI measurements and was blind to the programmed modalities. In general the time required for a tailored programming of the relative contribution of RV and LV pacing was 60 min.
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All measurements were made manually on-line by one of four operators (R.M., S.C., R.B., G.L.). Moreover, all images were recorded digitally and analysed off-line by one of us (G.L.). This second analysis served as quality control.
Statistical analysis
Comparisons between groups were performed with Student's t-test or the non-parametric Kruskall–Wallis test for continuous variables and with 
2 or Fisher's exact test or McNemar test for proportions, as appropriate. Tests were two-sided and a P-value of 0.05 was considered significant.
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Results |
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The intra-LV delay was 63 ± 28 ms baseline, decreased to 44 ± 26 ms with simultaneous BIV pacing and to 26 ± 15 ms with optimized CRT (P = 0.001). Simultaneous BIV pacing determined the shortest delay—which was 23 ± 12 ms—in 28 (41%) patients (Figure 2). In 41 (59%) patients a better resynchronization was achieved with optimized VV interval (LV first in 32 and RV first in 5) or single-chamber pacing (LV in 3 and RV in 1) (Figure 3). A great variety of VV intervals was selected in order to achieve the best CRT (Figure 4). The intra-LV delay remained abnormal in 28 (41%) patients during simultaneous BIV pacing compared with six (9%) patients during optimized CRT (P = 0.001). Compared with baseline, the intra-LV delay worsened during simultaneous BIV pacing in 21 patients (30%) vs. eight patients (12%) during optimized CRT (P = 0.001).
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The modality of optimal CRT pacing was different in patients with atrial fibrillation compared with those in sinus rhythm: in two-third of atrial fibrillation patients there was an LV pacing pre-activation, whereas in no atrial fibrillation patient there was an RV pacing pre-activation (Table 2). Right ventricular pacing pre-activation was more frequent in the patients with the widest QRS. Apart from these, the choice of pacing modality was independent by any other baseline clinical parameter.
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A follow-up visit was performed every 6 months (mean follow-up 13 ± 6 months). At the end of the follow-up, the New York Heart Association functional class was improved by one or more classes in 67% of the patients, showed no change in 30% and worsened in 3%. During the follow-up, 12 patients died, five of whom of cardiac cause. Hospitalization for heart failure occurred in eight patients. Clinical failure (defined as death due to cardiovascular cause, or hospitalization for heart failure, or subjective and objective signs of worsening heart failure in respect of pre-implant evaluation) occurred in 11 patients (16%). No clinical parameters, among those listed in Table 1, nor the value of intra-LV delay during optimized CRT was able to identify the patients with clinical failure.
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Discussion |
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A sub-optimal resynchronization is achieved with simultaneous BIV pacing in most patients and in some of these there is even a deterioration with respect to baseline conditions. These results give a pathophysiological explanation for the potential ineffectiveness of CRT therapy in some patients and are consistent with the situation seen in the clinical practice in which some patients are showing marked clinical benefit, balanced by other patients with very little benefit.
A tailored programming of the relative contribution of RV and LV pacing was able to determine a better resynchronization and forms the prerequisite for improving CRT clinical results. In most cases, very short intra-LV delay were obtained with our technique of optimized CRT. In general the values we were able to obtain in heart failure patients were similar to those measured in healthy subjects19 suggesting that a ‘pseudo-normalization’ of the timing of the LV contraction could be achieved. Nevertheless, even with this sophisticated technique an abnormal intra-LV delay still persisted and even worsened, compared with baseline, in a minority of cases (around 10%). The results we obtained probably represent the maximum that can be achieved with conventional BIV pacemaker implantation. Whether more sophisticated techniques of multisite pacing, i.e. using three or more leads or alternative pacing sites in the right ventricle in conjunction with LV pacing,21,22 could ‘normalize’ even the difficult cases is a matter of future investigation.
Finally, this study described the real-world practice of a centre performing a medium volume of CRT procedures and it was probably more representative of the general population undergoing CRT than that of the trials. For example, the proportion of patients in atrial fibrillation was 39%, a rate similar to that observed in patients with severe heart failure;23 on the contrary, atrial fibrillation was an exclusion criteria in the major clinical trials. Therefore, our observations extend those of the clinical trials. The study shows that the method of optimization of CRT is reliable and feasible in every day practice in consecutive patients provided that an experienced team of cardiologists trained in CRT implant, TDI echocardiography, and catheter ablation is available.
Tissue-doppler optimization of cardiac resynchronization therapy
Earlier observations10,19,24,25 showed that the myocardial delay is distributed around the entire ventricle and that the site of the latest mechanical activity is very heterogeneous and unpredictable being located virtually in any segment of the LV; moreover, functional lines of block can also be present, as shown in Figure 1. These findings suggest that the optimal assessment of dyssynchrony requires inclusion of all six basal walls of the LV and that a tailored individualized approach is needed to optimize pacemaker settings. It is not surprising, therefore, that in this study the sequence of ventricular pacing which determined the maximum LV synchronization was very broad, ranging from RV pacing only in one extreme to LV pacing only in the other extreme (Figure 4).
Only a few other small studies18,20 have evaluated the electromechanical activation of the six basal segments to assess the magnitude of intraventricular resynchronization achieved with simultaneous and optimized CRT. While in the present study optimized CRT was defined as the VV interval configuration corresponding to the maximal reduction in LV dyssynchrony, in other studies it was identified as that achieving the maximal increase in LV systolic function (cardiac output, LV outflow tract velocity–time integral, etc.). In the study of Bordachar et al.,18 performed on 40 patients, the intra-LV delay decreased, similar to our results, from 68 ± 25 ms baseline to 46 ± 18 during simultaneous pacing and to 31 ± 19 during optimized sequential pacing. The optimal stimulation configuration was simultaneous BIV pacing in six (15%), pre-activation of the LV in 25 (61%), with VV interval ranging between 12 and 40 ms (LV only in 3), and RV pre-activation in 10 (24%), with VV interval ranging between 12 and 20 ms. In the study of Vanderheyden et al.,20 performed on 20 patients, the intra-LV delay decreased from 70 ± 28 ms baseline to 51 ± 34 during simultaneous pacing and to 34 ± 18 during optimized sequential pacing (P = 0.05 vs. our study); the best VV option was LV pre-activation in 12, RV per-activation in five, and simultaneous pacing in three. In the study of Mele et al.,13 performed on 37 patients, the intra-LV delay, measured on six middle and six basal LV segments, decreased from 60 ± 19 ms baseline to 45 ± 10 during simultaneous pacing.
Thus, the present study and the previous study in the literature consistently showed that a sub-optimal resynchronization is achieved with simultaneous BIV pacing and that it can be improved with a proper sequential pacing. The difference in end-point (maximal reduction in dyssynchrony in the present study vs. maximal increase in systolic function in the others) could account for the small differences observed.
The choice of pacing modality was independent by any baseline clinical parameter (Table 2) except for atrial fibrillation. Indeed, more patients in atrial fibrillation required LV pacing first than those in sinus rhythm. We hypothesize that the patients in sinus rhythm have preserved AV conduction, whereas the patients in atrial fibrillation have complete AV block. Preserved AV conduction (with optimized AV timing) allows a fusion between sinus and paced stimuli; on the contrary, the lack of orthodromic activation of the LV through the His-Purkinje system would cause a delay in the activation of the free walls of the ventricle, which required to be corrected by an advanced stimulation in that site. Thus, the practical implication is that, when there is an AV block, a sequential BIV pacing with pre-activation of the LV should be carefully evaluated. Advanced RV pacing was required in the patients with the widest QRS; advanced LV pacing in those with relatively less large; BIV 0 was intermediate. Even if partly due to the interaction with the different prevalence of patients with atrial fibrillation, the reason is unclear and the observation merits further investigation.
Limitations
The end-point of this study, namely the value of intra-LV electromechanical delay achieved with simultaneous and sequential BIV pacing, is clearly a surrogate end-point of cardiac resynchronization and, for this reason, is somehow imprecise. There are some studies in the literature which showed a correlation between reduction in dyssynchrony measured by tissue-Doppler intra-LV delay after BIV pacing and improvement of cardiac function14,18,20,25 and clinical outcome14,18,20,25 or a correlation between optimization of the VV interval and improvement of cardiac function26–30 and clinical outcome,28 but none of these can be regarded as conclusive. Probably the best argument in favour is the strong pathophysiological background, i.e. intra-LV delay is a direct measure of the mechanism by which CRT is supposed to determine its favorable effect. However, this study was aimed to assess the methodology for an effective CRT and was not powered to assess its clinical results, which need to be evaluated in much larger clinical trials in the future.
The TDI methodology for the study of LV dyssynchrony is not established and differs markedly among studies, making comparison between them difficult to perform. The level of the ventricle at which to assess dyssynchrony is unclear. The LV base contains the largest myocardial mass and is potentially of most haemodynamic significance. Basal rather than mid-level assessment may therefore be more important in predicting response to CRT.5 The number of ventricular walls requiring assessment is equally unclear. A compromise is necessary between optimal detection of mechanical delay and feasibility of examining numerous segments in clinical practice. Measuring time between peak velocities in opposing basal septal and lateral segments, without utilizing QRS onset as a reference point, permits rapid analysis (septal-to-lateral delay). However, the wall exhibiting maximal delay was lateral in just one-third of patients, and mainly anterior, inferior, or posterior in the remaining two-thirds.5 Interrogation of only two segments, as made by others,13,31–34 may overlook a significant proportion of delayed myocardium, thus inadequately assessing dyssynchrony. Different softwares have been developed to measure dyssynchrony automatically.14,25 How these algorithms correlate between them and with the manual measure of the time to onset of systolic velocity is unclear. Many studies have used time to peak systolic velocity to assess LV dyssynchrony; we used the time to onset of systolic velocity mainly because the onset of systolic velocity may be easier to identify than its peak, especially in patients with severe LV dysfunction. Bordachar et al.18 have demonstrated that both indexes are equally sensitive to the patient's haemodynamic status. Finally, while a good inter-observer correlation is usually reported in any single-centre study, the inter-center correlation is likely to be worse, rising concern on the reproducibility of measurements in different hospitals.
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Conclusion |
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TopAbstractIntroductionMethodsResultsDiscussionConclusionReferences |
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A sub-optimal resynchronization is achieved with simultaneous BIV pacing in most patients. A tailored programming of the relative contribution of RV and LV pacing forms the prerequisite for improving CRT results.
Conflict of interest: none declared.
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References |
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[1] Blanc JJ, Etienne Y, Gilard M, Mansourati J, Munier S, Boschat J, et al. Evaluation of different ventricular pacing sites in patients with severe heart failure: results of an acute hemodynamic study. Circulation (1997) 96:3273–7.
[2] Kass DA, Chen CH, Curry C, Talbot M, Berger R, Fetics B, et al. Improved left ventricular mechanics from acute VDD pacing in patients with dilated cardiomyopathy and ventricular conduction delay. Circulation (1999) 99:1567–73.
[3] Bax JJ, Abraham WT, Barold S, Breithardt OA, Fung JW, Garrigue S, et al. Cardiac resynchronization therapy. Part 1. Issues before device implantation. J Am Coll Cardiol (2005) 47:2153–67.
[4] Bax JJ, Abraham WT, Barold S, Breithardt OA, Fung JW, Garrigue S, et al. Implantation and unresolved questions cardiac resynchronization therapy: Part 2. Issues during and after device. J Am Coll Cardiol (2005) 46:2168–82.
[5] Hawkins N, Petrie M, MacDonald M, Hogg K, McMurray J. Selecting patients for cardiac resynchronization therapy: electrical or mechanical dyssynchrony? Eur Heart J (2006) 27:1270–81.
[6] Auricchio A, Abraham W. Cardiac resynchronization therapy: current state of the art. Circulation (2004) 109:300–7.
[7] Bax JJ, Bleeker GB, Marwick TH, Molhoek SG, Boersma E, Steendijk P, et al. Left ventricular dyssynchrony predicts response and prognosis after cardiac resynchronization therapy. J Am Coll Cardiol (2004) 44:1834–40.
[8] Yu CM, Chau E, Sanderson JE, Fan K, Tang MO, Fung WH, et al. Tissue Doppler echocardiographic evidence of reverse remodeling and improved synchronicity by simultaneously delaying regional contraction after biventricular pacing therapy in heart failure. Circulation (2002) 105:438–45.
[9] Notabartolo D, Merlino JD, Smith AL, DeLurgio DB, Vera FV, Easley KA, et al. 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) 94:817–20.[CrossRef][Web of Science][Medline]
[10] Ansalone G, Giannantoni P, Ricci R, Trambaiolo P, Fedele F, Santini M. Doppler myocardial imaging to evaluate the effectiveness of pacing sites in patients receiving biventricular pacing. J Am Coll Cardiol (2002) 39:489–99.
[11] Sogaard P, Egeblad H, Kim WY, Jensen HK, Pedersen AK, Kristensen BO, 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) 40:723–30.
[12] Bader H, Garrigue S, Lafitte S, Reuter S, Jais P, Haissaguerre M, et al. Intra-left ventricular electromechanical asynchrony. A new independent predictor of severe cardiac events in heart failure patients. J Am Coll Cardiol (2004) 43:248–56.
[13] Mele D, Pasanis G, Capasso F, De Simone A, Morales MA, Poggio D, et al. Left ventricualr myocardial deformation dyssynchrony indentifies responders to cardiac resynchronization therapy in patients with heart failure. Eur heart J (2006) 27:1070–8.
[14] Yu CM, Fung WH, Lin H, Zhang Q, Sanderson J, Lau CP. Predictors of left ventricualr reverse remodeling after cardiac resynchronization therapy for heart failure secondary to idiopathic dilated or ischemic cardiomyopathy. Am J Cardiol (2002) 91:684–8.[CrossRef][Web of Science]
[15] Vardas P, Auricchio A, Blanc JJ, Daubert JC, Drexler H, Ector H, et al. Guidelines for cardiac pacing and cardiac resynchronization therapy. Europace (2007) doi:10.1093/europace/eum189.
[16] Nishimura RA, Hayes DL, Holmes DR, Tajik AJ. Mechanism of hemodynamic improvement by dual-chamber pacing for severe left ventricular dysfunction: an acute Doppler and catheterization hemodynamic study. J Am Coll Cardiol (1995) 25:281–8.[Abstract]
[17] Auricchio A, Stellbrink C, Block M, Sack S, Vogt J, Klein H, et al. Effect of pacing chamber and atrioventricular delay on acute systolic function of paced patients with congestive heart failure. Circulation (1999) 99:2993–3001.
[18] Bordachar P, Lafitte S, Reuter S, Sanders P, Jais P, Haissaguerre M, et al. Echocardiographic parameters of ventricular dyssynchrony validation in patients with heart failure using sequential biventricular pacing. J Am Coll Cardiol (2004) 44:2157–65.
[19] Badano L, Gaddi O, Peraldo C, Lupi G, Sitges M, Parthenakis F, et al. Left ventricular electromechanical activation in patients with heart failure and normal QRS duration, and in patients with wide QRS complexes. Europace (2007) 9:41–7.
[20] Vanderheyden M, De Backer T, Rivero-Ayerza M, Geelen P, Bartunek J, Verstreken S, et al. Tailored echocardiographic interventricular delay programming further optimizes left ventricular performance after cardiac resynchronization therapy. Heart Rhythm (2005) 2:1066–72.[CrossRef][Web of Science][Medline]
[21] Bulava A, Ansalone G, Ricci R, Giannantoni P, Pignalberi C, Heinc P, et al. Triple-site pacing in patients with biventricular device. Incidence of the phenomenom and cardiac resynchronization benefit. J Interv Card Electrophysiol (2004) 10:37–45.[CrossRef][Web of Science][Medline]
[22] Occhetta E, Bortnik M, Magnani A, Francalacci G, Piccinino C, Plebani L, et al. Prevention of ventricular desynchronization by permanent para-hisian pacing after atrioventricular node ablation in chronic atrial fibrillation. a crossover, blinded, randomized study versus apical right ventricular pacing. J Am Coll Cardiol (2006) 47:1938–45.
[23] McAlister F, Tu J, Newman A, Lee D, Kimber S, Cujec B, et al. How many patients with heart failure are eligible for cardiac resynchronization? Insights from two prospective cohorts. Eur Heart J (2006) 27:323–9.
[24] Auricchio A, Fantoni C, Regoli F, Carbucicchio C, Goette A, Geller C, Kloss M, et al. Characterization of left ventricular activation in patients with heart failure and left bundle-branch block. Circulation (2004) 109:1133–9.
[25] Sogaard P, Eglebad H, Pedersen AK, Kim WY, Kristensen BO, Hansen PS, et al. Sequential versus simultaneous biventricular resynchronization for severe heart failure: evaluation by tissue Doppler imaging. Circulation (2002) 106:2078–84.
[26] van Gelder B, bracke F, Meijer A, Laverveld L, Pijls N. Effect of optimizing the VV interval on left ventricular contractility in cardiac resynchronization therapy. Am J Cardiol (2004) 93:1500–3.[CrossRef][Web of Science][Medline]
[27] Hay I, Melenovsky V, Fetics B, Judge D, Kramer A, Spinelli J, et al. Short-term effects of right-left heart sequential cardiac resynchronization in patients with heart failure, chronic atrial fibrillation and atrioventricular nodal block. Circulation (2004) 110:3404–10.
[28] Leon A, Abraham W, Brozena S, Daubert J, Fisher W, Gurley J, et al. Cardiac resynchronization with sequential biventricualr pacing for the treatment of moderate-to-severe heart failure. J Am Coll Cardiol (2005) 46:2298–304.
[29] Kurzidim K, Reinke H, Sperzel J, Schneider J, Danilovic D, Siemon G, et al. Invasive optimization of cardiac resy nchronization therapy: role of sequential biventricualr and left ventricular ventricular pacing. Pacing Clin Electrophysiol (2005) 28:754–61.[CrossRef][Medline]
[30] Porciani MC, Dondina C, Macioce R, Demarchi G, Pieragnoli P, Musilli N, et al. Echocardiographic examination of atrioventricular and interventricular delay optimization in cardiac resynchronization therapy. Am J Cardiol (2005) 95:1108–10.[CrossRef][Web of Science][Medline]
[31] Breithard O, Stellbrink C, Herbots L, Claus P, Sinha A, Bijnens B, et al. Cardiac resynchronization therapy can reverse abnormal myocardial strain distribution in patients with heart failure and left bundle branch block. J Am Coll Cardiol (2003) 42:486–94.
[32] Bax J, Molhoek S, Marwick T, van erven L, Voogd P, Somer S, et al. Usefulness of myocardial tissue Doppler echocardiography to evaluate left ventricular dyssynchrony before and after biventricualr pacing in patients with idhiopathic dilated cardiomyopathy. Am J Cardiol (2003) 91:94–7.[CrossRef][Web of Science][Medline]
[33] Schuster P, Faerestrand S, Ohm OJ. Reverse remodeling of systolic left ventricular contraction pattern by long term cardiac resynchronisation therapy: colour Doppler shows resynchronisation. Heart (2004) 90:1411–6.
[34] Soliman OI, Theuns DA, Geleijnse ML, Anwar AM, Nemes A, Caliskan K, et al. Spectral pulsed-wave tissue Doppler imaging lateral-to-septal delay fails to predict clinical or echocardiographic outcome after cardiac resynchronization therapy. Europace (2007) 9:113–8.
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