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© The European Society of Cardiology 2006. All rights reserved. For Permissions, please e-mail: journals.permissions@oxfordjournals.org

Which patients with ischaemic heart disease could benefit from cell replacement therapy?

Janusz Lipiecki*, Nicolas Durel and Jean Ponsonnaille

Department of Cardiology, University Hospital, rue Montalembert, 63000 Clermont-Ferrand, France

* Corresponding author. E-mail address: jlipiecki{at}chu-clermontferrand.fr


   Abstract
Top
 Abstract
Introduction
 LV remodelling: mechanism,...
 Detection of patients at...
 Therapeutic possibilities in...
 References
 
Recently, cell replacement therapy has been investigated as a new tool in patients with ischaemic heart disease (IHD), who are prone to or with already established systolic dysfunction. Different subsets of stem cells have been used for preventive as well as curative purposes. Although cardiac cell transplantation and cytokine mobilization originally began in clinical trials with the explicit goal of myocardial regeneration, more recently, the emphasis has been focused on remodelling attenuation capacities of this approach. Left ventricular (LV) remodelling is a complex process involving changes in size, shape, and function of the LV, which plays an important role in the development of chronic heart failure after acute myocardial infarction (AMI).

Recently, several studies have improved our knowledge about prevalence, clinical importance, and methods predicting the occurrence of LV remodelling after AMI.

In patients with established LV remodelling, the place of cell replacement therapy is to be assessed in function of recent progresses concerning the selection of patients for revascularization therapy as well as for other surgical and electrical methods.

This article deals with the possibilities of screening of patients with IHD for cell replacement therapy.

Key Words: Cell replacement therapy • Left ventricular remodelling • Heart failure


   Introduction
Top
 Abstract
 Introduction
LV remodelling: mechanism,...
 Detection of patients at...
 Therapeutic possibilities in...
 References
 
Recently, cardiac cell transplantation has been extensively studied in patients with ischaemic heart disease (IHD). Different subsets of autologous bone marrow-derived stem cells have been used either as a preventive treatment of left ventricular (LV) dilatation after an acute myocardial infarction (AMI) or as a curative method in patients with a severe depression of LV contractile function and clinical signs of heart failure.1–4 In the latter group of patients, the transplantation of cultured autologous myoblasts has also been tested using different ways of cell transfer.5–7 Although cardiac cell transplantation and cytokine mobilization originally began in clinical trials with the explicit goal of myocardial regeneration, more recently, the emphasis has been focused on remodelling attenuation capacity of transplanted cells because of their paracrine effect.

It is, therefore, very important to know how large is the population of patients suffering from AMI at risk of development of LV remodelling, and how exactly we can predict it.

However, patients with advanced heart failure due to post-ischaemic LV remodelling represent a heterogeneous population with different degrees of residual viability and severity of LV dilatation; factors that can influence different therapeutic approaches. The place of cell replacement therapy in this group of patients is to be assessed in function of recent progresses concerning the selection of patients for revascularization therapy as well as for other surgical and electrical methods.


   LV remodelling: mechanism, prevalence, and clinical implications
Top
 Abstract
 Introduction
 LV remodelling: mechanism,...
Detection of patients at...
 Therapeutic possibilities in...
 References
 
IHD results from the interaction of multiple risk factors with genetic predisposition for the development of atherosclerosis in coronary arteries. The most dramatic expression of IHD is the occurrence of AMI because of the thrombotic occlusion of instable intramural plaque. The natural clinical outcome of patients with AMI depends on a number of important factors including initial infarct size, its degree of transmurality, infarct location, pre-existence of collateral circulation to jeopardized area, and number of significantly stenosed coronary arteries. Early reperfusion of the infarct-related artery by percutaneous coronary intervention or with thrombolytic therapy improves early and mid-term mortality in patients with AMI. Suppression of life threatening ventricular arrhythmias during an acute phase and blunting of neurohormonal activation with angiotensin-converting enzyme-inhibitors (ACE-I), angiotensin receptors blockers, and beta-blockers also improve mortality and morbidity following AMI.

However, in spite of these interventions, a relatively important proportion of patients experience progressive LV dilation cause by a dynamic process known as LV remodelling. LV remodelling is characterized by progressive dilatation and distortion of chamber geometry associated with the deterioration of global contractile function. It involves structural changes in the myocytes and in the extra cellular collagen matrix. LV remodelling of post-MI has both mechanical and biochemical origins. The increase in the wall stress is the most important mechanical parameter that precipitates remodelling. The increased wall stress is the driving force that stimulates dilatation of the chamber and hypertrophy of the non-infarcted regions. Change in the extra cellular matrix is another important factor in the development of remodelling. Activation of a family of proteolytic enzymes called matrix metalloproteinases (MMPs) leads to the degradation of collagen and promotes LV dilatation. The treatment with ACE-I or beta-blockers seems to attenuate the processes of LV remodelling rather than to prevent it completely.8,9 Moreover, the inhibition of MMP failed to reduce LV remodelling or to improve clinical outcome, as reported recently by Hudson et al.10

LV remodelling is currently observed in ~30% of survivors of MI.11–15 Most often, the criterion of the individual increase of >20% of LV end-diastolic volume between the acute phase and the 6-month follow-up is retained for the definition of remodelling.11,13,14 This degree of change is linked to the worsening of long-term outcome in the study of Bolognese et al.11 In this study, patients with LV remodelling had a higher 5-year mortality rate (14 vs. 5%, P=0.005) and a cumulative 5-year combined event rate (18 vs. 10%, P=0.025) than those without. In the study of Mengozzi et al.,14 32% of the patients with LV remodelling suffered from congestive heart failure during 6 months of follow-up when compared with 0% in patients without (P=0.0001). Other authors have used an increase of >15% of end-diastolic volume,16 the decrease of >15% in global LV ejection fraction,17 the 6-month end diastolic volume index >63 mL/m2, end-systolic volume index >30 mL/m2, or the sum of both volume indexes >88 mL/m2 as criteria to define LV remodelling.18 Using the latter criterion, patients with LV remodelling had an increased risk of mortality (RR 1.87, 95% CI 1.48–2.36) and heart failure at 6 months (RR 2.59, 95% CI 2.04–3.28).


   Detection of patients at risk for post-MI LV remodelling
Top
 Abstract
 Introduction
 LV remodelling: mechanism,...
 Detection of patients at...
Therapeutic possibilities in...
 References
 
Recently, several approaches have been proposed for the early detection of patients at risk for post-MI LV remodelling. In patients with initially preserved LV function included in the Stent-PAMI study, Mattichak et al.17 were unable to predict LV systolic deterioration (defined as a decrease of >15% of global ejection fraction) using baseline clinical and angiographic and outcome variables. In contrast, De Kam et al.18 have proposed a dilatation model including data from quantitative baseline echocardiography, gender, peak creatine kinase, and relationship between peak creatine kinase and time after MI. With this model, they could correctly predict the 6-month LV dilatation risk for 81% of the 7842 GISSI-3 patients in whom a pre-discharge echo was available.

ST-segment resolution was initially used for the evaluation of infarct-related patency. When sensitivity analyses are performed, it appears that the resolution of ST-elevation by >70% is the optimal threshold for patients with inferior MI, whereas resolution by >50% may be optimal for anterior MI. Subsequently, it has been demonstrated that the resolution of ST-elevation is a reliable predictor of the risk of death and development of congestive heart failure after AMI.19 With thresholds of >70% reduction for complete, 30–70% for incomplete, and <30% for the absence of ST-resolution, the probability of congestive heart failure decreases in a stepwise fashion (7.1, 13.8, and 17.2%, respectively). In a study of Nicolau et al.,20 the presence of ST-segment resolution precluded more favourable LV remodelling at 6-month follow-up.

A promising tool for the early detection of LV remodelling is the myocardial contrast echocardiography (MCE). This technique allows the appreciation of microvascular dysfunction in dyssynergic segments. Intravenous MCE was performed in 63 patients 5 days after an uncomplicated first AMI, in a study published by Mengozzi et al.14 Patients were considered to have microvascular impairment if <50% of the segments within the infarct-related area showed abnormal contrast effect. With this criterion, the LV remodelling was predicted by MCE with a very high sensitivity (94.7%) and specificity (90.9%). In this study, 35% of acutely revascularized patients were not adequately perfused at MCE, despite TIMI grade 3 flow, which is close to 30% of the rate of LV remodelling. In contrast, in a study of Ujino et al.,21 the intravenous MCE was less accurate for the prediction of LV remodelling in 47 patients treated with reperfusion therapy in the acute phase of MI. Although the specificity remains also high (patients with normal contrast opacification have the risk of remodelling <5%), the sensitivity is less satisfactory (in the case of abnormal opacification, the risk of remodelling is of 35%). The difference in results between these two studies is perhaps due to the different timing of follow-up studies (6 months for Mengozzi and 2 months for Ujino). In a study published by Bolognese et al.,22 124 patients treated by angioplasty in the acute phase of MI underwent intracoronary MCE. Microvascular dysfunction was observed in 19% of them. The prevalence of LV remodelling was significantly greater among patients with microvascular dysfunction than among those without (63 vs. 11%, P<0.0001).

LV remodelling can also be predicted by analysis of mitral deceleration time on Doppler echocardiography. With the cut-off value of <136 ms, Cerisano et al.23 were able to predict 6-month LV remodelling with a sensitivity of 75%, a specificity of 97%, and an accuracy of 81%. Of interest, in this study, mitral deceleration time predicted remodelling with higher accuracy than the dosage of brain natriuretic peptide (BNP).

Mannaerts et al.24 analysed 33 patients 6.4 days after an AMI by 3D echo. Clinical, electrocardiographic, and echocardiographic variables were analysed for the early identification of LV remodelling. The baseline 3D sphericity index was, by far, the most predictive variable with a sensitivity, specificity, and positive and negative predictive values of 100, 90, 87, and 100%, respectively, for a cut-off value of >0.25.

High accuracy in the prediction of LV remodelling was also obtained by Hombach et al.25 using the magnetic resonance imaging (MRI) technique 6 days after AMI in 110 patients, 58% of whom presented ST-elevation MI. The combination of three MRI parameters (infarct size, persistent microvascular impairment, and transmural extent of necrosis) predicted LV remodelling with the sensitivity of 80% and specificity of 84.6%.

We have studied a group of 29 patients with acute MI and early angioplasty by rest Tc-99m-Sestamibi ECG-gated SPECT was performed 21±5 days after angioplasty.15 Myocardial perfusion was quantified using a semi-automatic sectorial analysis. The patients were separated into two groups according to the absence (group I, n=21) or presence (group II, n=8) of LV remodelling. The perfusion index in the infarct sectors was –2.29±2.9 SD in group I and –6.40±2.85 SD in group II (P<0.01). With a perfusion cut-off value of –2.46 SD, the sensitivity and specificity of Tc-99-Sestamibi SPECT for the prediction of end-systolic volume enlargement were 100 and 62%, respectively. When the functional data from ECG-gated acquisitions were added, sensitivity and specificity were 87 and 86%, respectively.

The possibility of prediction of LV remodelling early after the AMI with low dose dobutamine by rest Tc-99m-Sestamibi ECG-gated SPECT is currently investigated in our centre.

Given these data, it appears that at the present time, it is possible to predict the adverse LV remodelling after AMI with relatively high accuracy. Patients who are at low risk for remodelling have a good long-term prognosis and probably will not benefit from cell replacement therapy. The question is open if those at high risk could be efficaciously treated by this approach, keeping in mind that the process of LV remodelling is linked at least, in part, with the microvascular obstruction. The efficacy of intracoronary delivery of stem cells could be impaired in these cases. Other ways of cells delivery might be more useful.


   Therapeutic possibilities in patients with established LV remodelling
Top
 Abstract
 Introduction
 LV remodelling: mechanism,...
 Detection of patients at...
 Therapeutic possibilities in...
References
 
The prognosis of patients with advanced ischaemic cadiomyopathy remains poor, despite progresses in pharmacological therapy. The annual mortality rate can exceed 10% in patients treated with beta-blockers, ACE-I, and aldosterone receptors blockers.26 The surgical revascularization remains still a valuable tool in this subset of patients, improving the long-term mortality and morbidity.27 Efficacy of surgical treatment on the recovery of contractile function depends on the presence of residual myocardial viability. The presence of viable myocardium is a double-edge sword. When revascularized, improved outcome and global function may occur. However, the presence of viable/hibernating tissue, which is not revascularized, is associated with unfavourable outcomes in long-term follow-up of patients with ischaemic cardiomyopathy.28 If more than ~30% of the LV myocardium is dyssynergic but viable, the improvement of global ejection fraction by >5% can be expected with the sensitivity of 86% and specificity of 92%. This recovery of contractility predicts the improvement of heart failure symptoms with positive and negative predictive values of 76 and 71%, respectively.29 In patients with advanced IHD and global ejection fraction <35%, the substantial viability (>30% of LV) can be expected in ~50% of the patients.30 Nevertheless, not all patients with a high amount of hibernating myocardium recover after a successful coronary revascularization. Extensive remodelling has been shown to be a predictive factor of no recovery.31 The cut-off value of pre-operative end-systolic volume >140 mL had a sensitivity of 68% and a specificity of 65% for the prediction of the lack of global LV recovery.32

Interestingly, in patients with ischaemic cardiomyopathy presenting extensive remodelling and residual viability, the endocardial injections of stem cells resulted in the improvement of global ejection fraction and the diminution of LV volumes in the study of Perin et al.4 These interesting data should be confirmed by other studies, including patients who are also good candidates for bypass surgery.

In contrast, patients with advanced ischaemic cardiomyopathy revascularized without substantial viability, even if their symptoms of angina are improved, are at higher risk of event rate at long-term follow-up, as shown by Bax et al.33 The Dor intervention or endoventricular circular patch plasty allows reduction of LV volumes and improvement of global ejection. The mean increase in ejection fraction obtained after this procedure is between 10 and 15% in different series.34 Dor intervention associated with bypass surgery is more efficacious in preventing the recurrence of heart symptoms in heart failure than bypass surgery alone.35 The confirmation of these encouraging results is awaited from ongoing STICH trial.36

The implanted cardioverter-defibrillator improves survival in patients with advanced cardiomyopathy, with a 30–54% reduction in the risk of mortality in several randomized trials. Unfortunately, the reduction in risk of all-cause mortality is associated with an increase in risk of hospitalization for heart failure (HF). In the retrospective analysis of MADIT II trial the 42% reduction of mortality was associated with 39% increase of hospitalization for HF.37

Cardiac resynchronization therapy (CRT) is another important therapeutic option in patients with advanced heart failure because of the systolic dysfunction. In the systematic overview of published randomized trials, Freemantle et al.38 showed the 28% reduction of mortality rate and 45% reduction of hospitalization for worsening heart failure. Chronic CRT has been shown to reduce end-diastolic volume by 6.3–18.00% and end-systolic volume by 8.2–24.7%, accompanied by an increase in global LV ejection fraction by ~10%.39 However, the reduction in LV dimensions seems to be more pronounced in patients with dilated cardiomyopathy than in those with ischaemic cardiomyopathy. In a substudy of MUSTIC trial,40 the reduction in end-diastolic diameter was 12.7±7.9 vs. 3.8±5.5 mm and that of end-systolic diameter was 13.5±7.5 vs. 3.7±5.3 mm in these two groups of patients. Moreover, few heart failure patients are good candidates for CRT. In a study published recently by McAlister et al.,41 only 21% of the patients with ischaemic or dilated cardiomyopathy hospitalized in a specialized clinic met criteria for this treatment.

In conclusion, in patients with advanced ischaemic cardiomyopathy, a very careful analysis of several parameters, including LV volumes, the extent of residual viability, and contractility asynchrony should be performed for the best therapeutic strategy. Probably, multiple approaches can be associated. The place of cell replacement therapy in this association is to be determined.

Conflict of interest: none declared.


   References
Top
 Abstract
 Introduction
 LV remodelling: mechanism,...
 Detection of patients at...
 Therapeutic possibilities in...
 References
 

  1. Strauer BE, Brehm M, Zeus T, Köstering M, Hernandez A, Sorg RV, Kögler G, Wernet P. (2002) Repair of infracted myocardium by autologous intracoronary mononuclear bone marrow cell transplantation in humans. Circulation 106:1913–1918.
  2. Assmus B, Schächinger V, Teupe C, Britten M, Lehman R, Döbert N, Grünwald F, Aicher A, Urbich C, Martin H, Hoelzer D, Dimmeler S, Zeiher A. (2002) Transplantation of Progenotor cells and Regeneration Enhancement in Acute Myocardial Infarction (TOPCARE-AMI). Circulation 106:3009–3017.
  3. Ripa RS, Jorgensen E, Wang Y, Thune JJ, Nilsson JC, Sondergaard L, Johnsen HE, Kober L, Grande P, Kastrup J. (2006) Stem cells mobilization induced by subcutaneous granulocyte-colony stimulating factor to improve cardiac regeneration after acute ST-elevation myocardial infarction. Results of the double-blind, randomized, placebo-controlled stem cells in myocardial infarction (STEMMI) trial. Circulation 113:1983–1992.
  4. Perin E, Dohman HFR, Borojevic R, Silva S, Sousa ALS, Mesquita CT, Rossi MID, Carvalho A, Dutra HS, Dohman HJF, Silva GV, Belém L, Vivacqua R, Rangel FOD, Esporcatte R, Geng YJ, Vaughn WK, Assad J, Mesquita ET, Willerson JT. (2003) Transendocardial, autologous bone marrow cell transplantation for severe, chronic ischaemic heart failure. Circulation 107:2294–2302.
  5. Menasché P, Hagège AA, Vilquin J-T, Desnos M, Abergel E, Pouzet B, Bel A, Sarateanu S, Scorsin M, Schwartz K, Bruneval P, Benbunan M, Marolleau J-P, Duboc D. (2003) Autologous skeletal myoblast transplantation for severe postinfarction left ventricular dysfunction. J Am Coll Cardiol 41:1078–1083.[Abstract/Free Full Text]
  6. Siminiak Fiszer D, Jerzykowska O, Grygielska B, Rozwadowska N, Kalmucki P, Kurpisz M. (2005) Percutaneous trans-coronary-venous transplantation of autologous skeletal myoblastes in the treatment of post-infarction myocardial contractility impairment. Poznan Trial Eur Heart J 26:1189–1195.
  7. Smits PC, van Geuns R-JM, Poldermans D, Bontioukos M, Ondewater EEM, Lee CH, Maat APWM, Serruys PW. (2003) Catheter-based intramyocardial injection of autologous skeletal myoblastes as a primary treatment of ischaemic heart failure. J Am Coll Cardiol 42:2063–2069.[Abstract/Free Full Text]
  8. St John Sutton M, Pfeffer MA, Moye L, Plappert T, Rouleau JL, Lamas G, Rouleau J, Parker JO, Arnold MO, Sussex B, Braunwald E. (1997) Cardiovascular death and left ventricular remodeling two years after myocardial infarction. Baseline predictors and impact of long-term use of captopril: information from the Survival and Ventricular Enlargement (SAVE) trial. Circulation 96:3294–3299.
  9. Doughty RN, Whalley GA, Walsh HA, Gamble GD, Lopez-Sendon J, Sharpe N. (2004) Effects of carvedilol on left ventricular remodeling after acute myocardial infarction. The CAPRICORN echo substudy. Circulation 109:201–206.
  10. Hudson MP, Amstrong PW, Ruzyllo W, Brum J, Cusmano L, Krzeski P, Lyon R, Quinones M, Theroux P, Sydlowski D, Kim HE, Garcia MJ, Jaber WA, Weaver WD. (2006) Effects of selective matrix metalloproteinase inhibitor (PG-116800) to prevent ventricular remodeling after myocardial infarction. J Am Coll Cardiol 48:15–20.[Abstract/Free Full Text]
  11. Bolognese L, Neskovic AN, Parodi G, Cerisano G, Buonamici P, Santoro GM, Antoniucci D. (2002) Left ventricular remodeling after primary coronary angioplasty. Patterns of left ventricular dilation and long-term prognosis implications. Circulation 106:2351–2357.
  12. Cerisano G, Domenico P, Valenti R, Boddi V, Migliorini A, Tommasi MS, Raspanti S, Parodi G, Antoniucci D. (2005) Comparison of the usefulness of Doppler-derived deceleration time versus plasm brain natriuretic peptide to predict left ventricular remodeling after mechanical revascularization in patients with ST-elevation acute myocardial infarction and left ventricular systolic dysfunction. Am J Cardiol 95:930–934.[CrossRef][ISI][Medline]
  13. Husic M, Norager B, Egstrup K, Moller JE. (2005) Usefulness of left ventricular diastolic wall motion abnormality as an early predictor of left ventricular dilation after a first acute myocardial infarction. Am J Cardiol 96:1186–1189.[CrossRef][ISI][Medline]
  14. Mengozzi G, Rossini R, Palagi C, Musumeci G, Petronio AS, Limbruno U, Caravelli P, Di Bello V, Mariani M. (2002) Usefulness of intravenous myocardial contrast echocardiography in the early left ventricular remodeling in acute myocardial infarction. Am J Cardiol 90:713–719.[CrossRef][ISI][Medline]
  15. Lipiecki J, Cachin F, Durel N, de Tauriac O, Ponsonnaille J, Maublant J. (2004) Influence of infarct-zone viability detected by rest Tc-99 m sestamibi gated SPECT on left ventricular remodeling after acute myocardial infarction treated by percutaneous transluminal coronary angioplasty in the acute phase. J Nucl Cardiol 11:673–681.[CrossRef][ISI][Medline]
  16. Bigi R, Mafrici A, Colombo P, Gregori D, Corrada E, Alberti A, De Biase A, Orrego PS, Fiorentini C, Klugman S. (2005) Relation of terminal QRS distortion to left ventricular functional recovery and remodeling in acute myocardial infarction treated with primary angioplasty. Am J Cardiol 96:1233–1236.[CrossRef][ISI][Medline]
  17. Mattichak SJ, HArjai KJ, Dutcher JR, Boura JA, Stone G, Cox D, Brodie BR, O'Neill WO, Grines CL. (2005) Left ventricular remodeling and systolic deterioration in acute myocardial infarction: findings from the Stent-PAMI study. J Interv Cardiol 18:255–260.[CrossRef][Medline]
  18. De Kam PJ, Nicolosi GL, Voors AA, van den Berg MP, Brouver J, van Veldhuisen DJ, Barlera S, Maggioni AP, Gianuzzi P, Temorelli PL, Latini R, van Gilst WH. (2002) Prediction of 6 months left ventricular dilatation after myocardial infarction in relation to cardiac morbidity and mortality. Eur Heart J 23:536–542.[Abstract/Free Full Text]
  19. De Lemos JA and Braunwald E. (2001) ST segment resolution as a tool for assessing the efficacy of reperfusion therapy. J Am Coll Cardiol 38:1283–1294.[Abstract/Free Full Text]
  20. Nicolau JC, Maia LN, Vitola J, Vaz VD, Machado MN, Godoy MF, Giraldez RR, Ramirez JA. (2003) St-segment resolution and late (6-month) left ventricular remodeling after acute myocardial infarction. Am J Cardiol 91:451–453.[CrossRef][ISI][Medline]
  21. Ujino K, Hillis GS, Mulvagh SL, Hagen ME, Oh JK. (2005) Usefulness of real-time intravenous myocardial contrast echocardiography in predicting left ventricular dilatation after successfully reperfused acute myocardial infarction. Am J Cardiol 96:17–21.[ISI][Medline]
  22. Bolognese L, Carraba N, Parodi G, Santoro GM, Buonamici P, Cerisano G, Antoniucci D. (2004) Impact of microvascular dysfunction on left ventricular remodeling and long-term clinical outcome after primary coronary angioplasty for acute myocardial infarction. Circulation 109:1121–1126.
  23. Cerisano G, Domenico P, Valenti R, Boddi V, Migliorini A, Tommasi MS, Raspanti S, Parodi G, Antoniucci D. (2005) Comparison of the usefulness of Doppler-derived deceleration time versus plasm brain natriuretic peptide to predict left ventricular remodeling after mechanical revascularization in patients with ST-elevation acute myocardial infarction and left ventricular systolic dysfunction. Am J Cardiol 95:930–934.[CrossRef][ISI][Medline]
  24. Mannaerts HFJ, van der Heide JA, Kamp O, Stoel MG, Twisk J, Visser CA. (2004) Early identification of left ventricular remodelling after myocardial infarction, assessed by transthoracic 3D echocardiography. Eur Heart J 25:680–687.[Abstract/Free Full Text]
  25. Hombach V, Grebe O, Merkle N, Waldenmaier S, Höher M, Kochs M, Wöhrle J, Kestler HA. (2005) Sequelae of acute myocardial infarction regarding cardiac structure and function and their prognostic significance as assessed by magnetic resonance imaging. Eur Heart J 26:549–557.[Abstract/Free Full Text]
  26. Pitt B, Remme W, Zannad F, Neaton J, Martinez F, Roniker B, Bittman R, Hurley S, Kleiman J, Gatlin M. (2003) Eplerenone, a selective aldosterone blocker, in patients with left ventricular dysfunction after myocardial infarction. N Engl J Med 348:1309–1321.[Abstract/Free Full Text]
  27. Samady H, Elefteriades JA, Abott BG, Mattera JA, McPherson CA, Wackers FJTh. (1999) Failure to improve left ventricular function after coronary revascularization for ischaemic cardiomyopathy is not associated with worse outcome. Circulation 100:1298–1304.
  28. Lee KS, Marwick TH, Cook SA, Go RT, Fix JS, James KB, Sapp SK, MacInery WJ, Thomas JD. (1994) Prognosis of patients with left ventricular dysfunction, with and without viable myocardium after myocardial infarction. Relative efficacy of medical therapy and revascularization. Circulation 90:2687–2694.
  29. Bax JJ, Visser FC, Poldermans D, Elhendy A, Cornel JH, Boersma E, Valkema R, van Lingen A, Fioretti PM, Visser CA. (2001) Relationship between preoperative viability and postoperaitive improvement in LVEF and heart failure symptoms. J Nucl Med 42:79–86.[Abstract/Free Full Text]
  30. Schinkel AFL, Bax JJ, Boersma E, Elhendy A, Roelandt JRTC, Poldermans D. (2001) How many patients with ischaemic cardiomyopathy exhibit viable myocardium? Am J Cardiol 88:561–564.[CrossRef][ISI][Medline]
  31. Bax JJ, Schinkel AFL, Boersma E, Elhendy A, Rizello V, Maat A, Roelandt JRTC, van der Wall EE, Poldermans D. (2004) Extensive left ventricular remodeling does not allow viable myocardium to improve in left ventricular ejection fraction after revascularization and is associated with worse long-term prognosis. Circulation 110:II18–II22.
  32. Schinkel AFL, Poldermans D, Rizello V, Vanoverschelde J-L J, Elhendy A, Boersma E, Roelandt JRTC, Bax JJ. (2004) Why do patients with ischaemic cardiomyopathy and a substantial amount of viable myocardium not always recover in function after revascularization? J Thorac Cardiovasc Surg 127:385–390.[Abstract/Free Full Text]
  33. Bax JJ, Poldermans D, Elhendy A, Cornel JH, Boersma E, Rambaldi R, Roelandt JRTC, Fioretti P. (1999) Improvement of left ventricular ejection fraction, heart failure symptoms and prognosis after revascularization in patients with chronic coronary artery disease and viable myocardium detected by dobutamine stress echocardiography. J Am Coll Cardiol 34:163–169.[Abstract/Free Full Text]
  34. Dor V, Di Donato M, Sabatier M, Civaia F. (2006) Other surgical or device-based approaches to treating cardiac remodeling. In Greenberg B (Ed.). Cardiac Remodeling Mechanism and Treatment(Taylor & Francis, New York, London).
  35. Ribeiro GCA, Antonialli F, Lopes MM, Costa CE, Albuquerque AN, Franchini KG. (2006) Left ventricular reconstruction brings benefit for patients with ischaemic cardiomyopathy. J Cardiac Fail 12:189–194.[CrossRef][ISI][Medline]
  36. Ratcliffe MB. (2006) The treatment of ischaemic heart failure with surgical ventricular restoration (SVR): new evidence of benefit. J Cardiac Fail 12:195–198.[CrossRef][ISI][Medline]
  37. Goldenberg I, Moss AJ, Hall WJ, McNitt S, Zareba W, Andrews ML, Cannom DS. (2006) Causes and consequences of heart failure after prophylactic implantation of a defibrillator in the Multicenter Automatic defibrillator Implantation Trial II. Circulation 113:2810–2817.
  38. Freemantle N, Tharmanathan P, Calvert MJ, Abraham WT, Ghosh J, Cleland JGF. (2006) Cardiac resynchronization for patients with heart failure due to left ventricular systolic dysfunction—a systematic review and meta-analysis. Eur J Heart Fail 8:433–440.[CrossRef][ISI][Medline]
  39. Kass DA. (2003) Ventricular remodeling: chamber dyssynchrony and effects of cardiac resynchronization. Eur Heart J 5:Suppl. I, I54–I63.[CrossRef]
  40. Duncan A, Wait D, Gibson D, Daubert J-C. (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 (Multisite Stimulation in Cardiomyopathies) trial. Eur Heart J 24:430–441.[Abstract/Free Full Text]
  41. McAlister FA, Tu JV, Newman A, Lee A, Lee DS, Kimber S, Cujec B, Amstrong PW. (2006) How many patients with heart failure are eligible for cardiac resynchronization? Insights from two prospective cohorts. Eur Heart J 27:323–329.[Abstract/Free Full Text]

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