Europace Advance Access published online on December 3, 2007
Europace, doi:10.1093/europace/eum269
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ORIGINAL ARTICLE
Baseline Doppler parameters are useful predictors of chronic left ventricular reduction in size by cardiac resynchronization therapy
Department of Cardiology, Charité - Universitaetsmedizin Berlin, Campus Virchow-Klinikum, Augustenburger Platz 1, 13353 Berlin, Germany
Manuscript submitted 5 September 2007. Accepted after revision 7 November 2007.
* Corresponding author. Tel.: +49 30 450653635; fax: +49 30 450553961.E-mail address: martin.stockburger{at}charite.de
| Abstract |
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Aims: The identification of responders to cardiac resynchronization therapy (CRT) in patients with left ventricular (LV) dysfunction and left bundle branch block (LBBB) remains difficult. We aimed to define the predictive value of conventional Doppler parameters.
Methods and results: In 73 patients (65 ± 9 years, 51 male, 36 ischaemic, 37 non-ischaemic cardiomyopathy, QRS 167 ± 31 ms, LVEF 23 ± 6%) with LBBB, a CRT device was implanted. LV pre-ejection interval (PEI), interventricular mechanical delay (IVMD), LV filling time (FT), and myocardial performance index (MPI) were assessed at baseline and on optimized CRT. Left ventricular end-diastolic diameter (EDD) was obtained at baseline and after 10.6 ± 6.7 months. end-diastolic diameter diminished from 66.3 ± 8.1 to 59.9 ± 9.6 mm (P < 0.001). Initial LVPEI (r = 0.41, P < 0.001), baseline IVMD (r = 0.34, P = 0.003), acute LVPEI shortening (r = 0.33, P = 0.006), and baseline LVEDD (r = 0.32, P = 0.007) correlated with LVEDD reduction. An LVPEI
140 ms had a 82% accuracy to predict long-term LVEDD reduction (sensitivity 86%, specificity 67%, positive and negative predictive values 91 and 56%, respectively). Multivariate analysis solely revealed baseline LVPEI as predictor of LVEDD reduction. FT and MPI correlated only with their respective improvements.
Conclusion: Left ventricular pre-ejection interval and IVMD predict favourable LV remodelling on CRT. The additional application of tissue Doppler parameters may further increase specificity and negative predictive value.
Key Words: Cardiac resynchronization therapy, Doppler echocardiography, Left ventricular remodelling, Predictors of response
| Introduction |
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Cardiac resynchronization therapy (CRT) has been shown to improve haemodynamics1
| Methods |
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Study participants
The study population consisted of consecutive patients with severe systolic left ventricular dysfunction (LVEF
35%), symptomatic heart failure, and left bundle branch block (LBBB) who were candidates for CRT according to the guidelines of the European Society of Cardiology.23
Cardiac resynchronization therapy device implantation
The indication for a CRT pacemaker(n = 9) vs. CRT device with additional cardioverter/defibrillator capabilities (CRT-D, n = 64) was defined according to the actual pacemaker/ICD guidelines.24
After an initial coronary venogram lateral veins were selected for lead placement. The implantation was performed in the catheterization laboratory under local anaesthesia. Transvenous LV lead placement was invariably attempted in over-the-wire technique. In case transvenous LV lead placement failed, an epicardial lead was implanted by the cardiac surgeon under general anaesthesia in the operating room.
Echocardiographic follow-up
A General Electric Medical SystemsTM Vivid 7 Pro echocardiography machine with a 3 MHz sector transducer was used for standard transthoracic 2D and Doppler echocardiography at baseline and during follow-up. The examinations were performed by two experienced examiners (S.F.M., M.S.) and the analysis focused on changes of the LV end-diastolic diameter (LVEDD), given the prognostic significance25
,26
and good reproducibility27
of this parameter. Left ventricular end-diastolic diameter was assessed from 2D targeted M-mode echocardiography using the parasternal long-axis view and the left ventricular M-mode perpendicular to the left ventricular main axis at the level of mitral leaflet tips according to the recommendations of the European Association of Echocardiography.28
In addition, the 2D-derived anterioposterior linear left atrial (LA) dimension was assessed from the parasternal long-axis view at the level of the aortic valve. During the first three post-operative days, an optimization procedure was carried out guided by Doppler echocardiography, with the patient at rest in the left lateral supine position. The optimization method has previously been described in detail.29
The pulsed wave Doppler spectra from the mitral, aortic and pulmonary valves were analysed at a horizontal speed of 100 mm/s. Under each modality, three values for all of the following parameters were obtained and averaged. The left ventricular ejection time (LVET) and the left ventricular pre-ejection interval (LVPEI) were measured from the transaortic flow signal. The LVPEI is a combined electromechanical parameter which contains prolonged ventricular activation and delayed ejection. It is easily obtained by measuring the time interval between the beginning of the QRS complex and the onset of transaortic ejection. The right ventricular pre-ejection interval (RVPEI) was measured similarly from the QRS onset to the beginning of the transpulmonary ejection signal. The difference of LVPEI and RVPEI is referred to as the IVMD. Cut-off values of
140 ms for LVPEI and
40 for IVMD have been proposed and used for patient selection within a large trial investigating mortality on CRT14
and were re-examined within the present study. The LV filling time (FT) and the interval between an A-wave and the subsequent E-wave (AET) were obtained from the transmitral left ventricular inflow signal. The absence of truncated A-waves with short AV delays was verified. The myocardial performance index (MPI), reflecting systolic and diastolic LV function, was obtained as described by Tei et al.30
from the transmitral inflow spectrum and the transaortic left ventricular ejection time (LVET) following the formula MPI=(AET–LVET)/LVET. In addition, the LVPEI/LVET ratio was calculated as a measure of systolic LV performance, which corresponds to the renowned PEP/LVET.31
All measurements were done without resynchronization and with optimized CRT.
Statistical analysis
Categorical variables are reported as absolute numbers and percentages. Continuous variables are presented as means±standard deviation. Paired and unpaired Student's t-tests were used for horizontal and longitudinal comparisons as appropriate. The relationship between baseline Doppler parameters, acute changes of the Doppler parameters on one side and long-term change of the LVEDD on the other side, was assessed by univariate linear regression analysis. Sensitivity, specificity, positive, and negative predictive values were determined for the previously proposed cut-off levels of LVPEI and IVMD with regard to LV reduction in size. Multivariate analyses were performed with the changes of Doppler parameters and the change of LVEDD as dependent variables. A P-value <0.05 was considered statistically significant.
| Results |
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Study population characteristics
The study enrolled 73 patients. Baseline data of the study population are outlined in Table 1. The patients represent a typical severely compromised heart failure cohort. Coronary artery disease and non-ischaemic cardiomyopathy were equally represented as the aetiology for left ventricular dysfunction. The average EF was severely depressed and marked intraventricular conduction delay was present.
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Cardiac resynchronization therapy device implantation
The implantation was succesful including transvenous lead placement in 72/73 (99%) patients. The first attempt was succesful in 71/73 (97%) patients, a second procedure was required in one patient. Due to an extremely angulated and tortuous course of the proximal coronary sinus and the targeted lateral side branches one patient required open surgery with epicardial lead placement. An atriobiventricular pacemaker was used in 9/73 (12%) patients and the remainder were treated with a CRT-D device (64/73, 88%). The defibrillator option was not preferred by three elderly patients suffering from coronary artery disease. Fluoroscopy time averaged at 21 ± 15 min, the total procedural time added up to 109 ± 32 min.
Left ventricular and left atrial dimensions
As expected, the average baseline LVEDD was importantly dilated and averaged at 66.3 ± 8.1 mm. Long-term CRT after an average follow-up of 10.6 ± 6.7 months produced a significant reduction in size by 6.4 to 59.9 ± 9.6 mm (P < 0.001). In 58/73 (79%) patients, an LVEDD decrease was found, whereas 5/73 (7%) patients had stable left ventricular size and 10/73 (14%) patients experienced progressive LV dilatation. The initial LVEDD showed a significant correlation to LVEDD reduction (r = 0.32, P = 0.007), indicating that more severely compromised patients benefitted more from CRT. The LA size diminished by 2.4 mm from 48.1 ± 7.2 to 45.7 ± 8.0 mm (P = 0.001). Left ventricular and left atrial changes in size were not significantly correlated (r = 0.12, P = 0.31).
Doppler echocardiographic parameters
At baseline the patients exhibited severe interventricular systolic mismatch as reflected by an average IVMD of 54 ± 22 ms. The IVMD was acutely reduced to 13 ± 22 ms (P < 0.001) on optimized CRT already during the early post-operative measurements. The LVPEI decreased acutely from 164 ± 32 to 129 ± 28 ms (P < 0.001) and the MPI improved from 1.05 ± 0.52 to 0.72 ± 0.27 (P < 0.001). The LVET showed a slight acute increase with CRT from 246 ± 36 to 257 ± 32 ms (P < 0.001). The LVPEI/LVET ratio reduced from 0.69 ± 0.18 to 0.51 ± 0.13 (P < 0.001) and the FT extended from 329 ± 121 to 396 ± 100 ms (P<0.001). Baseline LVPEI/LVET ratio was significantly linked to baseline LVEF (r = –0.40, P = 0.002). Doppler echocardiographic parameters are summarized in Table 2.
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Relationship of baseline Doppler parameters and initial left ventricular end-diastolic diameter, left ventricular ejection fraction, and QRS
LVPEI showed a weak, but significant correlation to the initial LVEDD in the sense that patients with larger ventricles had a longer LVPEI (r = 0.28, P = 0.02). LVPEI was not significantly correlated with initial QRS width (r=0.18, P = 0.12) or LVEF (r = –0.19, P = 0.10), although weak tendencies were perceivable. Interventricular mechanical delay, FT, and MPI were not significantly linked to initial LVEDD, LVEF, or QRS width.
Relationship of baseline Doppler parameters and acute haemodynamic improvement
Baseline Doppler paramters were significantly linked to their respective acute improvements by univariate and multivariate analysis (LVPEI vs. acute change of LVPEI: r=0.59, P < 0.001; IVMD vs. acute change of IVMD: r = 0.61, P < 0.001; FT vs. change of FT: r = –0.42, P < 0.001; MPI vs. change of MPI: r = 0.86, P < 0.001; LVPEI/LVET vs. change of LVPEI/LVET: r = 0.69, P < 0.001). All correlations pointed towards more pronounced benefit from CRT in more severely affected patients.
Relationship of Doppler echocardiographic parameters and left ventricular end-diastolic diameter reduction
Patients with long-term LVEDD reduction had significantly longer initial LVPEI (170 ± 30 ms) and IVMD (56 ± 22 ms) when compared with patients, whose LVEDD was stable or progressively enlarging (LVPEI 136±23 ms, IVMD 39 ± 21 ms, P < 0.001 for comparison of LVPEI and P = 0.015 for comparison of IVMD, see also Figure 1). By univariate analysis, the long-term change of LVEDD was significantly linked to baseline LVPEI (r = 0.41, P < 0.001), baseline IVMD (r = 0.34, P = 0.003), and acute shortening of LVPEI (r = 0.33, P = 0.006). By multivariate analysis, baseline LVPEI remained the only significant predictor of chronic LV reduction in size (P = 0.04). Predictive accuracy of an LVPEI
140 ms for an LVEDD reduction was 82%, accuracy of an IVMD
40 ms was 78%. Sensitivity, specificity, positive, and negative predictive values of an LVPEI
140 ms to predict reduced LVEDD were 86, 67, 91, and 56%, respectively. Sensitivity, specificity, positive, and negative predictive values of an IVMD
40 ms to predict reduced LVEDD were 85, 50, 88, and 44%, respectively. Scatter plots of LVEDD reduction vs. baseline LVPEI and baseline IVMD with the respective cut-off levels indicated are given in Figures 2 and 3. Left atrial change in size showed a significant positive association with baseline LVPEI/LVET (r = 0.31, P = 0.017). Baseline values of FT and MPI were not predictive for chronic structural changes.
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| Discussion |
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The adverse effects of dyssynchronous LV contraction and relaxation secondary to LBBB on left ventricular filling and ejection have been described already almost two decades ago.18
Patient cohort
The patients examined in this study represent a typical contemporary CRT cohort with important QRS prolongation and severe systolic LV dysfunction. This must be kept in mind while interpreting the study results, which refer to this patient group and are not necessarily valid for other populations (e.g. less compromised patients or those with narrow QRS).
Relationship of baseline Doppler parameters and acute post-operative improvement by cardiac resynchronization therapy
For all Doppler parameters, significant univariate correlations signify more pronounced acute improvement on CRT in more severely compromised patients. Multivariate analyses identified all baseline Doppler parameters as sole predictors of their respective acute amelioration. The importance of the initial severity of illness as a predictor of CRT treatment effectiveness has already been described during the early evaluation of CRT3
and should give rise to caution with regard to the extension of CRT indications to less severely affected patients.
Relationship of baseline left ventricular pre-ejection interval and initial left ventricular end-diastolic diameter
The weak correlation between LVPEI and LVEDD at baseline is likely due to the influence on delayed LV activation, which is exerted by mere LV geometry. Despite this correlation, LVPEI turned out to be the only significant multivariate single predictor of LV reduction in size during follow-up.
Left ventricular end-diastolic diameter reduction with long-term cardiac resynchronization therapy
The present study results confirm the remarkably favourable impact of long-term CRT on the dimension of the left ventricle, which has previously been reported.21
,33
CRT over 10.4 months on average produced a significant reduction of the LVEDD by 6.4 mm, which compares well to the results obtained from other studies. For the MIRACLE study patient population, for instance, a diminishment by 3.0 mm after 6 months and by 6.0 mm after 12 months CRT has been published.33
Influencing factors on long-term left ventricular end-diastolic diameter reduction
A clear relationship between baseline LVEDD and chronic LVEDD reduction also pointed at the degree of initial compromise as a meaningful determinant of the long-term CRT effect. An interesting finding was the significant positive correlation of acute LVPEI shortening with chronic LV reduction in size, indicating that acute and chronic benefits are not independent. But since acute improvement of Doppler parameters can only be assessed after placement of the required pacing electrodes, this will not help to pre-operatively identify the appropriate patients for CRT, unless an invasive preselection procedure is carried out.
Univariate analysis revealed significant linkage of baseline LVPEI and baseline IVMD to chronic LVEDD reduction, thereby confirming the hyopthesis implicated by the CARE-HF design, which required LVPEI above 140 ms and IVMD>40 ms as a prerequisite for inclusion patients with borderline QRS width. Both parameters were significantly different between patients with and without long-term reduction in size. By multivariate analysis, LVPEI remained the only significant determinant of favourable long-term remodelling, which emphasizes the relevance of this parameter. The LVPEI/LVET ratio is known to be correlated with the LVEF.34
This finding could be reproduced by the present study. With regard to chronic LVEDD evolution according to our data LVPEI/LVET did not offer an advantage over LVPEI alone.
The cut-off levels proposed by the CARE-HF investigators14
were re-examined with regard to their predictive properties. An LVPEI of at least 140 ms and an IVMD of at least 40 ms were found to have high sensitivity and positive predictive values as to LV reduction in size, whereas specificity and negative predictive values were unsatisfactory for both parameters.
Clinical importance
The findings characterize LVPEI and IVMD as simple and useful parameters for patient selection. In symptomatic patients with severe systolic LV dysfunction and wide LBBB, LVPEI or IVMD values above the proposed cut-off levels are very likely to predict favourable long-term LV remodelling on CRT and require no additional decisive measures as to the identification of potential responders defined according to LV reduction in size. But in case values are beneath cut-off, the situation remains inconclusive and additional criteria must be applied to clarify the probability of favourable future CRT effects. In other words, LVPEI and IVMD values above cut-off are well suited to identify responders, but at the same time these parameters below cut-off are less useful with regard to the identification of non-responders. The first step for practical and appropriate patient selection should consist of straightforward LVPEI and IVMD measurements. The identification of responders in thereafter still ambiguous cases may be facilitated by more complex and time consuming TD-derived measures or 2D strain analysis.
Conflict of interest: M.S. is an educational speaker for Biotronik, Boston Scientific/Guidant, Medtronic, and Sorin Group, and receives research grants from these companies.
| References |
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[1] 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.
[2] Nelson GS, Berger RD, Fetics BJ, Talbot M, Spinelli JC, Hare JM, et al. Left ventricular or biventricular pacing improves cardiac function at diminished energy cost in patients with dilated cardiomyopathy and left bundle-branch block. Circulation (2000) 102:3053–9.
[3] Auricchio A, Stellbrink C, Sack S, Block M, Vogt J, Bakker P. for the Pacing Therapies in Congestive Heart Failure (PATH-CHF) Study Group. Long-term clinical effect of hemodynamically optimized cardiac resynchronization therapy in patients with heart failure and ventricular conduction delay. J Am Coll Cardiol (2002) 39:2026–33.
[4] Cazeau S, Leclercq C, Lavergne T, Walker S, Varma C, Linde C. for the Multisite Stimulation in Cardiomyopathies (MUSTIC) Study Investigators. Effects of multisite biventricular pacing in patients with heart failure and intraventricular conduction delay. N Engl J Med (2001) 344:873–80.
[5] Abraham WT, Fisher WG, Smith AL, DeLurgio DB, Leon AR, Loh E. for the MIRACLE Study Group. Cardiac resynchronization in chronic heart failure. N Engl J Med (2002) 346:1845–53.
[6] Calvert MJ, Freemantle N, Yao1 G, Cleland JGF, Billingham L, Daubert JC. on behalf of the CARE-HF Investigators. Cost-effectiveness of cardiac resynchronization therapy: results from the CARE-HF trial. Eur Heart J (2005) 26:2681–8.
[7] Stockburger M. Strategies to avoid complications and to solve technical problems during the implantation of CRT and CRT-D systems. Herzschr Elektrophys (2006) 17:I20–I27.[CrossRef]
[8] Auricchio A, Stellbrink C, Butter C, Sack S, Vogt J, Misier AR. on behalf of the Pacing Therapies in Congestive Heart Failure (PATH-CHF) II Study Group. Clinical efficacy of cardiac resynchronization therapy using left ventricular pacing in heart failure patients stratified by severity of ventricular conduction delay. J Am Coll Cardiol (2003) 42:2109–16.
[9] Yu CM, Fung WH, Lin H, Zhang Q, Sanderson JE, Lau CP. Predictors of left ventricular reverse remodeling after cardiac resynchronization therapy for heart failure secondary to idiopathic dilated or ischemic cardiomyopathy. Am J Cardiol (2003) 91:684–8.[CrossRef][Web of Science][Medline]
[10] 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.
[11] Pitzalis MV, Iacoviello M, Romito R, Guida P, De Tommasi E, Luzzi G, et al. Ventricular asynchrony predicts a better outcome in patients with chronic heart failure receiving cardiac resynchronization therapy. J Am Coll Cardiol (2005) 45:65–9.
[12] 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]
[13] Bristow MR, Saxon LA, Boehmer J, Krueger S, Kass DA, De Marco T, et al. Comparison of Medical Therapy, Pacing, and Defibrillation in Heart Failure (COMPANION) Investigators. Cardiac-resynchronization therapy with or without an implantable defibrillator in advanced chronic heart failure. N Engl J Med (2004) 350:2140–50.
[14] Cleland JGF, Daubert JC, Erdmann E, Freemantle N, Gras D, Kappenberger L, et al, for the Cardiac Resynchronization-Heart Failure (CARE-HF) Study Investigators. The effect of cardiac resynchronization on morbidity and mortality in heart failure. N Engl J Med (2005) 352:1539–49.
[15] Bernie DH, Tang ASL. The problem of non-response to cardiac resynchronization therapy. Curr Opin Cardiol (2006) 21:20–6.[Web of Science][Medline]
[16] Sogaard P, Egeblad H, Kim WY, Jensen HK, Pedersen AK, Kristensen BO, et al. 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.
[17] Yu CM, Abraham WT, Bax J, Chung E, Fedewa M, Ghio S, et al, PROSPECT Investigators. Predictors of response to cardiac resynchronization therapy (PROSPECT)–study design. Am Heart J (2005) 149:600–5.[CrossRef][Web of Science][Medline]
[18] Grines CL, Bashore TM, Boudoulas H, Olson S, Shafer P, Wooley CF. Functional abnormalities in isolated left bundle branch block. The effect of interventricular asynchrony. Circulation (1989) 79:845–53.
[19] Richardson M, Freemantle N, Calvert MJ, Cleland JG, Tavazzi L. CARE-HF Study Steering Committee Investigators. Predictors and treatment response with cardiac resynchronization therapy in patients with heart failure characterized by dyssynchrony: a pre-defined analysis from the CARE-HF trial. Eur Heart J (2007) 28:1827–34.
[20] Breithardt OA, Stellbrink C, Franke A, Balta O, Diem BH, Bakker P, et al. Acute effects of cardiac resynchronization therapy on left ventricular Doppler indices in patients with congestive heart failure. Am Heart J (2002) 143:34–44.[CrossRef][Web of Science][Medline]
[21] St John Sutton MG, Plappert TJ, Hilpisch KE, Chinchoy E. Baseline aortic preejection interval (bAPEI) as a predictor of response to cardiac resynchronization therapy (CRT). Circulation (2002) 106:II–380.
[22] Bordachar P, Lafitte S, Reuter S, Sanders P, Jaïs P, Haïssaguerre 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.
[23] Swedberg K, Cleland J, Dargie H, Drexler H, Follath F, Komajda M, et al. Guidelines for the diagnosis and treatment of chronic heart failure: executive summary (update 2005). Eur Heart J (2005) 26:1115–40.
[24] Jung W, Andresen D, Block M, Bocker D, Hohnloser SH, Kuck KH, et al. Leitlinien zur Implantation von Defibrillatoren. Clin Res Cardiol (2006) 95:696–708.[CrossRef][Web of Science][Medline]
[25] Anand I, Florea VG, Fisher L. Surrogate end points in heart failure. J Am Coll Cardiol (2002) 39:1414–21.
[26] Lee TH, Hamilton MA, Stevenson LW, Moriguchi JD, Fonarow GC, Child JS, et al. Impact of left ventricular cavity size on survival in advanced heart failure. Am J Cardiol (1993) 72:872–6.
[27] Wallerson DC, Devereux RB. Reproducibility of echocardiographic left ventricular measurements. Hypertension (1987) 9:II6–II18.[Medline]
[28] Lang RM, Bierig M, Devereux RB, Flachskampf FA, Foster E, Pellikka PA, et al. Recommendations for chamber quantification. Eur J Echocardiogr (2006) 7:79–108.
[29] Stockburger M, Fateh-Moghadam S, Nitardy A, Langreck H, Haverkamp W, Dietz R. Optimisation of cardiac resynchronisation guided by doppler echocardiography: hemodynamic improvement and intraindividual variability with different pacing configurations and atrioventricular delays. Europace (2006) 10:881–6.
[30] Tei C, Ling LH, Hodge DO Bailey KR, Oh JK, Rodeheffer RJ, et al. New index of combined systolic and diastolic myocardial performance: a simple and reproducible measure of cardiac function – a study in normals and dilated cardiomyopathy. J Cardiol (1995) 26:357–66.[Medline]
[31] Lang-Jensen T. Blood flow velocity and systolic time intervals measured by pulsed Doppler ultrasound: reproducibility of measurements. Cardiovasc Res (1987) 21:582–6.[Web of Science][Medline]
[32] Cazeau S, Bordachar P, Jauvert G, Lazarus A, Alonso C, Vandrell MC, et al. Echocardiographic modeling of cardiacdyssynchrony before and during multisite stimulation: a prospective study. Pacing Clin Electrophysiol (2003) 26:137–43.[CrossRef][Medline]
[33] Sutton St John MG, Plappert T, Hilpisch KE, Abraham WT, Hayes DL, Chinchoy DE, et al. Sustained reverse left ventricular structural remodeling with cardiac resynchronization at one year is a function of etiology quantitative doppler echocardiographic evidence from the Multicenter InSync Randomized Clinical Evaluation (MIRACLE). Circulation (2006) 113:266–72.
[34] Ambrosi C, Chabrillat Y, Duport G, Valeix B, Berthet-Bondet M, Gerard R. Calculation of the ejection fraction from simultaneously recorded systolic intervals and angiography. Comparative study. Arch Mal Coeur Vaiss (1981) 74:321–8.[Web of Science][Medline]
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