Europace Advance Access originally published online on June 14, 2007
Europace 2007 9(9):739-743; doi:10.1093/europace/eum117
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CARDIAC RESYNCHRONISATION THERAPY
Importance of contractile reserve for CRT
1 Department of Cardiology, APHP, Henri Mondor Hospital, 51 Av. du Marechal de Lattre de Tassigny, 94000 Creteil, France
Manuscript submitted 1 March 2007. Accepted after revision 3 May 2007.
* Corresponding author. Tel: +33 1 49 81 21 11.E-mail address: pascal.lim{at}hmn.aphp.fr
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Abstract |
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 Top Abstract IntroductionMethodsResultsContractile reserve and response...DiscussionConclusionsReferences |
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Aims To assess whether response to cardiac resynchronization therapy (CRT) is related to myocardial viability in the paced left ventricular (LV) region, evaluated by contractile reserve (CR). Non-response to CRT may partly be due to inefficient pacing by the LV lead located in a fibrotic area.
Methods and results Nineteen patients (64 ± 13 years, 14 men, 9 ischaemic) with severe heart failure (EF = 27 ± 8%, QRS = 154 ± 25 ms) were included in the week after device implantation. Stroke volume (SV) and LV dyssynchrony (by Tissue Doppler Imaging) were successively assessed with CRT on and CRT off. Afterwards, CRT device was maintained off during dobutamine infusion to assess CR in the LV-pacing region. LV end-systolic volume (ESV) was assessed after 6 months to quantify reverse remodelling. CR in the paced LV region (n = 10, 5/9 ischaemic and 5/10 non-ischaemic) was correlated to a reduction in LV dyssynchrony under CRT (120 ± 76 vs. 78 ± 64 ms, P = 0.02). Conversely, LV dyssynchrony was unchanged (161 ± 100 vs. 163 ± 80 ms) without CR. In desynchronized patients (>65 ms, n = 15), increase in SV under CRT and changes in ESV at 6 months were +22 and –18%, respectively, when CR was present and 0% and +9%, respectively, when absent.
Conclusion Acute haemodynamic response and reverse remodelling under CRT require viability in the target region of LV lead.
Key Words: Dyssynchrony, Cardiac resynchronization therapy, Contractile reserve, Viability
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Introduction |
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TopAbstractIntroductionMethodsResultsContractile reserve and response...DiscussionConclusionsReferences |
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Cardiac resynchronization therapy (CRT) is an additional treatment option in the management of end-stage drug-refractory heart failure. Large clinical trials1
–9 have reported the sustained benefit of CRT in patients with severe heart failure (NYHA III/IV), impaired left ventricular ejection fraction (LVEF 
35%), and a wide QRS complex (>120 ms). Beneficial effects of CRT include improvement of symptoms, stroke volume (SV), ejection fraction, mitral regurgitation, left ventricular (LV) remodelling, and survival. In spite of these encouraging results, 
20 to 30% of patients selected according to QRS duration criteria do not respond to CRT. Several observational studies have demonstrated that the main predictor of responsiveness to CRT is mechanical10–19 rather than electrical dyssynchrony.20 Among available techniques, echocardiographic assessment of LV dyssynchrony [mainly by M mode and Tissue Doppler Imaging (TDI)] seems to provide additional selection criteria for potential candidates to CRT. However, despite the presence of LV dyssynchrony, several patients still do not respond to CRT. It has been suggested21 that LV lead positioning in scar tissue may be a determining factor for poor response to CRT on the basis of anecdotal report22 and recently published trials,23–25 assessing myocardial viability before device implantation. Indeed, LV pacing is likely to be less efficient because advanced tissue fibrosis may have severely altered local myocardial contractility and conduction properties.26,27 The presence of myocardial viability can be evidenced by several validated non-invasive techniques such as nuclear imaging, low-dose dobutamine echocardiography, and contrast magnetic resonance imaging (MRI).28 Contractile reserve (CR) using low-dose dobutamine correlated with the extent of fibrosis29,30 and was a largely available method with high sensitivity and excellent specificity,31 useful for ischaemic and non-ischaemic cardiomyopathy. We sought to assess whether CRT efficiency was related to the presence of CR in the target region of the LV lead, in patients with severe ischaemic or idiopathic cardiomyopathy. |
Methods |
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Population
The study was performed in 19 stable patients, in the week (4 ± 1 days) after successful ventricular lead implantation in the lateral or posterolateral coronary vein for biventricular pacing intended for CRT. Patients with haemodynamic instability, recent acute coronary syndrome (<3 months), poor echogenicity, atrial fibrillation, or requiring permanent pacing were excluded. Informed consent was obtained from all patients, and the protocol was approved by our institutional review board.
Biventricular pacemaker implantation
Three transvenous leads were inserted. The right atrial and ventricular (apical site) leads were positioned conventionally. The LV lead was inserted through the coronary sinus into either the lateral or the posterolateral cardiac vein. The biventricular pacing devices used were Biotronik, Berlin, Germany (n = 2), Saint Jude, Sylmar, CA, USA (n = 3), Guidant, Boston, MA, USA (n = 8), and Medtronic, Minneapolis, MN, USA (n = 6). After implantation, the atrioventricular interval was adjusted for optimal diastolic filling using Doppler echocardiography,32 and no adjustment was made to the VV interval.
Echocardiography
For echocardiography study, patients were allowed to take their prescribed medication with an exception for beta-blocker therapy, which was withdrawn 48 h before the investigation. Before the test was started, baseline characteristics were recorded, and a venous line was secured. Patients were positioned in the left lateral decubitus, and images were obtained using a commercially available system (Vingmed system Seven, General Electric, Horten, Norway) with a 3.5 MHz transducer at a 16 cm depth in the parasternal and apical views. Echocardiographic data were successively acquired with CRT device on, 5 min after CRT deactivation (device programmed in VVI HR 30/min) and finally during low-dose dobutamine infusion. Dobutamine was infused in 3 min dose increments from 5 to 10 
/kg/min to patients with CRT device off under continuous ECG and non-invasive blood pressure monitoring. Echocardiographic recordings consisted of 2D apical views coupled to colour Doppler data and LV outflow tract (LVOT) flow velocities using pulse Doppler flow signal. Echocardiographic data acquisition was repeated for each step (CRT device on, CRT device off, and after dobutamine infusion with CRT device off) and stored on optical disk for further analysis. For each measurement, three consecutive cardiac cycles were acquired during apnoea. For SV measurement, LVOT flow velocity was recorded in the apical view as recommended. Special care was taken to maintain the sample volume location throughout the echocardiographic study. SV was calculated using standard formulae.33 TDI parameters were analysed offline from colour images (EchoPac, GE Vingmed, Horten, Norway). Myocardial velocities were computed from the basal portions of the septum and the LV lateral and posterior wall. LV dyssynchrony was defined as the delay in the peak systolic velocity between septum and LV wall receiving CRT, i.e. posterior or lateral wall according to chest X-ray. Significant LV dyssynchrony was considered when this time interval was 
65 ms.17 For all time measurement, ECG signal was amplified and mean value of three consecutive measures was used for analysis.
Contractile reserve
The apical cine loop sequences were interpreted qualitatively in accordance with previous guidelines34 by two experienced observers blinded to clinical and other echocardiographic data. CR was solely considered for analysis in the target site of the LV-pacing device defined as lateral or posterolateral wall if LV-pacing lead was inserted in the lateral or posterolateral cardiac vein, respectively. Moreover, LV lead position was confirmed on chest X-ray (posterior–anterior and lateral views) systematically performed in days after device implantation. In this setting, regional myocardial function of mid-ventricular lateral and posterolateral walls was analysed at rest and under low-dose dobutamine and defined as (i) normal, (ii) hypokinetic, or (iii) akinetic. CR was considered present (CR+) in dysfunctional myocardium if segmental wall motion improved by one grade under dobutamine.
Follow-up
All patients were clinically and echocardiographically evaluated 6 months after device implantation. Patients without clinical improvement (NYHA class decrease 1) or with an episode of acute heart failure or requiring heart transplantation during the follow-up period were considered as non-responders.
Statistical analysis
Normally distributed continuous variables were expressed as mean ± SD. Dichotomous data were expressed as percentages. To compare numerical data between two or several groups, paired and unpaired student test or analysis of variance was used as appropriate. Dichotomized comparison was assessed by 
2 test or the Fisher's exact test. Two-tailed P-values <0.05 were considered statistically significant. Analysis was performed using StatView® software (Version 5.0 for Windows®, SAS institute Inc., Cary, NC, USA).
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Results |
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Baseline characteristics of the population before CRT device implantation are summarized in Table 1. All patients fulfilled the recommended criteria for CRT.35
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Left ventricular dyssynchrony and Stroke volume changes during cardiac resynchronization therapy
With CRT device off, mean LV dyssynchrony was 140 ± 88 ms and was considered as significant in 15 (79%) patients. Heart rate and blood pressure were unchanged with CRT device on or off (Table 2). On the whole, despite the non-significant decrease of LV dyssynchrony, the SV increased +10% with CRT device on, +10 and 7.5% in patients with and without LV dyssynchrony, respectively.
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Contractile reserve and response to cardiac resynchronization therapy |
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Acute haemodynamic response
According to chest X-ray, LV myocardial segment first stimulated was the lateral in 10 and the posterolateral wall in 9 patients. All these segments were graded as dysfunctional at baseline (10 hypokinetic and 9 akinetic). CR under low dose of dobutamine was observed in 10/19 of them, with no difference between ischaemic and idiopathic cardiomyopathy (5/9 and 5/10, respectively). In patients with CR in the LV target site for pacing, LV dyssynchrony (120 ± 76 vs. 78 ± 64 ms, P = 0.02, Figure 1) was significantly reduced with CRT device on, and likewise absence of CR (161 ± 100 vs. 163 ± 80 ms, ns) was associated with non-significant improvement of mechanical dyssynchrony. Mean increase of SV was 22% and 0% in desynchronized patients (n = 15) with and without CR, respectively (Figure 2).
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After 6 months follow-up
One patient was heart transplanted, two admitted for acute heart failure, and three did not feel improved by CRT. End-systolic volume (ESV) reduction at 6 months was greater in responders than in non-responders (–12 ± 11 vs. +13 ± 27%, P = 0.01, Table 1). All non-responder patients (n = 6) had a LV lead placed in a segment without CR. In contrast, LV lead positioned in a segment with CR+ was observed in 10 of the 13 responders and was associated with greater ESV reduction (P = 0.02, Figure 3). ESV reduction was nearly unchanged (–0.04, 0, and –0.03%, respectively) for three patients with clinical improvement and LV lead in segment without CR.
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Discussion |
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The findings in the present study suggest that for efficient mechanical resynchronization in ischaemic and non-ischaemic cardiomyopathy, CRT requires the presence of myocardial viability in the LV lead target site. This underlines the importance of assessing viability before device implantation in order to guide LV lead position to ensure a pacing efficiency.
In patients with severe heart failure (NYHA III–IV), depressed LV function (ejection fraction<35%), and wide QRS complex (QRS> 120 ms), the beneficial effects of CRT has been largely documented with improvement of symptoms and prognosis.21 Reduced mechanical dyssynchrony under CRT decreases wall stress and mitral regurgitation volume and increases SV and LV dP/dt, and finally participates in reverse remodelling process.36 However, most CRT studies demonstrated that up to 30% of patients were non-responders, because mechanical dyssynchrony could be absent despite wide QRS duration. This electro-mechanical dissociation has been confirmed by several studies,20,37 and in this population, LV dyssynchrony was absent in nearly one-third of the patients with large QRS duration. This suggested that mechanical dyssynchrony would be a more accurate predictor of CRT response. Several observational studies10–19 and our data supported that LV dyssynchrony, and specifically the delay of posterolateral wall contraction, is a determining factor in the prediction of response to CRT. Besides the presence of LV dyssynchrony, some authors21 hypothesized that viability of the stimulated LV area should be required in order to obtain efficient pacing substratum, and therefore successful CRT. In this situation, baseline echocardiography associated to dobutamine echocardiography provides the unique opportunity to assess accurately the CR matched to the desynchronized segment. Using this approach, we identified 8 of 15 desynchronized patients without CR. These patients exhibited a limited increase in SV under CRT (<5%) and reverse remodelling (ESV reduction at 6 months <10%). Unchanged mechanical dyssynchrony under CRT in patients with non-viable LV lead region suggests that lack of haemodynamic response could be partly due to an inefficient pacing. This supports the theory that in myocardium with advanced remodelling process, fibrosis and loss of contractile material may have severely altered myocardial conduction and contractile properties, which impeaches efficient biventricular pacing. Finally, lack of haemodynamic response and reverse remodelling under CRT in patients without CR, despite severe LV dyssynchrony, provide the strong evidence that LV dyssynchrony is necessary but not sufficient for CRT response. Finally, lack of haemodynamic response and reverse remodelling under CRT in patients without CR, despite severe LV dyssynchrony, provide the strong evidence that LV dyssynchrony is necessary but not sufficient for CRT response. Indeed, delayed wall motion is mainly a marker of myocardial dysfunction38,39 and could be exhibited in viable and non-viable40 segment according to load conditions.40,41 Furthermore, extracellular matrix changes induced by remodelling were also found responsible for electrical conduction delay.26,29 Thus, LV dyssynchrony is not a specific marker of response to CRT, and characterization of viability in desynchronized segments appears necessary to improve the selection of patients. This was recently supported by Bleeker et al.23 who showed that in patients with severe ischaemic cardiomyopathy, 95% of responders to CRT have LV dyssynchrony (assessed by TDI) and no scar tissue (using late contrast MRI) in the posterolateral wall. In addition, Hummel et al.24 using contrast ultrasound echocardiography for myocardial viability assessment reported similar findings in the ischaemic population. In our study, we extended these observations to patients with idiopathic-dilated cardiomyopathy, which represents nearly 50% of the population study.
In regards to these concordant results using different approaches, we suggest a routine assessment of myocardial viability together with dyssynchrony assessment before CRT to guide LV-pacing lead implantation. Indeed, the present study did not suggest that CRT should be avoided in the presence of scar, since three patients felt clinically improved despite a LV lead placed in the segment without CR. However, the results underline the importance to optimize the LV lead position, i.e. in a viable myocardial segment to ensure the chance of LV reverse remodelling. Finally, correlation between viability and CRT response raises the potential interest to perform CRT in less advanced stages of heart failure when reverse remodelling is still possible.
Limitations
These results should be regarded cautiously and some limitations should be underlined. First, lack of difference between ischaemic and non-ischaemic patients may be resulted from the small number of patients, and then results should be confirmed by a larger study. Second, response to CRT may be underestimated since RV lead was placed in the RV apex in all patients. Finally, one major difficulty of the study is the unclear correlation of the echocardiographically determined regions and the pacing site even after chest X-ray control. Others studies using NOGA system or CT should be performed to confirm these results.
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Conclusions |
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TopAbstractIntroductionMethodsResultsContractile reserve and response...DiscussionConclusionsReferences |
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In patients with severe, dilated cardiomyopathy, response to CRT required both the presence of LV dyssynchrony and preserved CR of the region where the LV-pacing lead was inserted in order to ensure efficient mechanical resynchronization. It is proposed that the detection of myocardial viability as well as the assessment of LV dyssynchrony should be routinely performed before CRT to guide LV-pacing lead implantation.
Conflict of interest: none declared.
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References |
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[1] Lozano I, Bocchiardo M, Achtelik M, Gaita F, Trappe HJ, Daoud E, et al. Impact of biventricular pacing on mortality in a randomized crossover study of patients with heart failure and ventricular arrhythmias. Pacing Clin Electrophysiol (2000) 23(Pt. 2):1711–2.[Medline]
[2] Cazeau S, Leclercq C, Lavergne T, Walker S, Varma C, Linde C, et al. Effects of multisite biventricular pacing in patients with heart failure and intraventricular conduction delay. N Engl J Med (2001) 344:873–80.
[3] Auricchio A, Stellbrink C, Sack S, Block M, Vogt J, Bakker P, et al. 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] Abraham WT, Fisher WG, Smith AL, Delurgio DB, Leon AR, Loh E, et al. Cardiac resynchronization in chronic heart failure. N Engl J Med (2002) 346:1845–53.
[5] Auricchio A, Stellbrink C, Butter C, Sack S, Vogt J, Misier AR, et al. 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.
[6] Young JB, Abraham WT, Smith AL, Leon AR, Lieberman R, Wilkoff B, et al. Combined cardiac resynchronization and implantable cardioversion defibrillation in advanced chronic heart failure: the MIRACLE ICD Trial. JAMA (2003) 289:2685–94.
[7] Bristow MR, Saxon LA, Boehmer J, Krueger S, Kass DA, De Marco T, et al. Cardiac-resynchronization therapy with or without an implantable defibrillator in advanced chronic heart failure. N Engl J Med (2004) 350:2140–50.
[8] Cleland JG, Daubert JC, Erdmann E, Freemantle N, Gras D, Kappenberger L, et al. The effect of cardiac resynchronization on morbidity and mortality in heart failure. N Engl J Med (2005) 352:1539–49.
[9] Cleland JG, Daubert JC, Erdmann E, Freemantle N, Gras D, Kappenberger L, et al. Longer-term effects of cardiac resynchronization therapy on mortality in heart failure [the CArdiac REsynchronization-Heart Failure (CARE-HF) trial extension phase]. Eur Heart J (2006) 27:1928–32.
[10] Pitzalis MV, Iacoviello M, Romito R, Massari F, Rizzon B, Luzzi G, et al. Cardiac resynchronization therapy tailored by echocardiographic evaluation of ventricular asynchrony. J Am Coll Cardiol (2002) 40:1615–22.
[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] Breithardt OA, Stellbrink C, Kramer AP, Sinha AM, Franke A, Salo R, et al. Echocardiographic quantification of left ventricular asynchrony predicts an acute hemodynamic benefit of cardiac resynchronization therapy. J Am Coll Cardiol (2002) 40:536–45.
[13] Penicka M, Bartunek J, De Bruyne B, Vanderheyden M, Goethals M, De Zutter M, et al. Improvement of left ventricular function after cardiac resynchronization therapy is predicted by tissue Doppler imaging echocardiography. Circulation (2004) 109:978–83.
[14] Ansalone G, Giannantoni P, Ricci R, Trambaiolo P, Laurenti A, Fedele F, et al. Doppler myocardial imaging in patients with heart failure receiving biventricular pacing treatment. Am Heart J (2001) 142:881–96.[CrossRef][ISI][Medline]
[15] 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.
[16] Yu CM, Fung JW, Zhang Q, Chan CK, Chan YS, Lin H, et al. Tissue Doppler imaging is superior to strain rate imaging and postsystolic shortening on the prediction of reverse remodeling in both ischemic and nonischemic heart failure after cardiac resynchronization therapy. Circulation (2004) 110:66–73.
[17] 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.
[18] 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][ISI][Medline]
[19] 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.
[20] Kashani A, Barold SS. Significance of QRS complex duration in patients with heart failure. J Am Coll Cardiol (2005) 46:2183–92.
[21] Bax JJ, Abraham T, Barold SS, Breithardt OA, Fung JW, Garrigue S, et al. Cardiac resynchronization therapy: Part 1–issues before device implantation. J Am Coll Cardiol (2005) 46:2153–67.
[22] Kanhai SM, Viergever EP, Bax JJ. Cardiogenic shock shortly after initial success of cardiac resynchronization therapy. Eur J Heart Fail (2004) 6:477–81.[CrossRef][ISI][Medline]
[23] Bleeker GB, Kaandorp TA, Lamb HJ, Boersma E, Steendijk P, de Roos A, et al. Effect of posterolateral scar tissue on clinical and echocardiographic improvement after cardiac resynchronization therapy. Circulation (2006) 113:969–76.
[24] Hummel JP, Lindner JR, Belcik JT, Ferguson JD, Mangrum JM, Bergin JD, et al. Extent of myocardial viability predicts response to biventricular pacing in ischemic cardiomyopathy. Heart Rhythm (2005) 2:1211–7.[CrossRef][ISI][Medline]
[25] Da Costa A, Thevenin J, Roche F, Faure E, Romeyer-Bouchard C, Messier M, et al. Prospective validation of stress echocardiography as an identifier of cardiac resynchronization therapy responders. Heart Rhythm (2006) 3:406–13.[CrossRef][ISI][Medline]
[26] de Bakker JM, van Capelle FJ, Janse MJ, Tasseron S, Vermeulen JT, de Jonge N, et al. Fractionated electrograms in dilated cardiomyopathy: origin and relation to abnormal conduction. J Am Coll Cardiol (1996) 27:1071–8.[Abstract]
[27] Kawara T, Derksen R, de Groot JR, Coronel R, Tasseron S, Linnenbank AC, et al. Activation delay after premature stimulation in chronically diseased human myocardium relates to the architecture of interstitial fibrosis. Circulation (2001) 104:3069–75.
[28] Kim RJ, Wu E, Rafael A, Chen EL, Parker MA, Simonetti O, et al. The use of contrast-enhanced magnetic resonance imaging to identify reversible myocardial dysfunction. N Engl J Med (2000) 343:1445–53.
[29] Otasevic P, Popovic ZB, Vasiljevic JD, Vidakovic R, Pratali L, Vlahovic A, et al. Relation of myocardial histomorphometric features and left ventricular contractile reserve assessed by high-dose dobutamine stress echocardiography in patients with idiopathic dilated cardiomyopathy. Eur J Heart Fail (2005) 7:49–56.[CrossRef][ISI][Medline]
[30] Nagueh SF, Mikati I, Weilbaecher D, Reardon MJ, Al-Zaghrini GJ, Cacela D, et al. Relation of the contractile reserve of hibernating myocardium to myocardial structure in humans. Circulation (1999) 100:490–6.
[31] Bax JJ, Wijns W, Cornel JH, Visser FC, Boersma E, Fioretti PM. Accuracy of currently available techniques for prediction of functional recovery after revascularization in patients with left ventricular dysfunction due to chronic coronary artery disease: comparison of pooled data. J Am Coll Cardiol (1997) 30:1451–60.[Abstract]
[32] Kindermann M, Frohlig G, Doerr T, Schieffer H. Optimizing the AV delay in DDD pacemaker patients with high degree AV block: mitral valve Doppler versus impedance cardiography. Pacing Clin Electrophysiol (1997) 20(Pt. 1):2453–62.[CrossRef][Medline]
[33] Nishimura RA, Miller FA Jr, Callahan MJ, Benassi RC, Seward JB, Tajik AJ. Doppler echocardiography: theory, instrumentation, technique, and application. Mayo Clin Proc (1985) 60:321–43.[ISI][Medline]
[34] Hoffmann R, Lethen H, Marwick T, Rambaldi R, Fioretti P, Pingitore A, et al. Standardized guidelines for the interpretation of dobutamine echocardiography reduce interinstitutional variance in interpretation. Am J Cardiol (1998) 82:1520–4.[CrossRef][ISI][Medline]
[35] 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 The Task Force for the diagnosis and treatment of chronic heart failure of the European Society of cardiology. Eur Heart J (2005) 26:1115–40.
[36] Bax JJ, Abraham T, Barold SS, Breithardt OA, Fung JW, Garrigue S, et al. Cardiac resynchronization therapy: Part 2–issues during and after device implantation and unresolved questions. J Am Coll Cardiol (2005) 46(12):2168–82.
[37] Zhang Y, Chan AK, Yu CM, Lam WW, Yip GW, Fung WH, et al. Left ventricular systolic asynchrony after acute myocardial infarction in patients with narrow QRS complexes. Am Heart J (2005) 149:497–503.[CrossRef][ISI][Medline]
[38] Ehring T, Heusch G. Left ventricular asynchrony: an indicator of regional myocardial dysfunction. Am Heart J (1990) 120:1047–57.[CrossRef][ISI][Medline]
[39] Jamal F, Szilard M, Kukulski T, Liu XS, D'Hooge J, Bijnens B, et al. Changes in systolic and postsystolic wall thickening during acute coronary occlusion and reperfusion in closed-chest pigs: Implications for the assessment of regional myocardial function. J Am Soc Echocardiogr (2001) 14:691–7.[CrossRef][ISI][Medline]
[40] Ryf S, Rutz AK, Boesiger P, Schwitter J. Is post-systolic shortening a reliable indicator of myocardial viability? An MR tagging and late-enhancement study. J Cardiovasc Magn Reson (2006) 8:445–51.[CrossRef][ISI][Medline]
[41] Dalmas S, Wanigasekera VA, Marsch SC, Ryder WA, Wong LS, Foex P. The influence of preload on post-systolic shortening in ischaemic myocardium. Eur J Anaesthesiol (1995) 12:127–33.[ISI][Medline]
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