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J Thorac Cardiovasc Surg 2007;134:433-441
© 2007 The American Association for Thoracic Surgery


Surgery for Acquired Cardiovascular Disease

Surgical therapy for ischemic heart failure: Single-center experience with surgical anterior ventricular restoration

Lorenzo Menicanti, MDa,1, Serenella Castelvecchio, MDa, Marco Ranucci, MDa, Alessandro Frigiola, MDa, Carlo Santambrogio, MDa, Carlo de Vincentiis, MDa, Jelena Brankovic, MDa, Marisa Di Donato, MDb,1,*

a Cardiac Surgery Department, San Donato Hospital, Milano, Italy
b Critical Care Medicine Department, University of Florence, Florence, Italy.

Read at the Eighty-sixth Annual Meeting of The American Association for Thoracic Surgery, Philadelphia, Pa, April 29-May 3, 2006.

Received for publication June 13, 2006; revisions received November 13, 2006; accepted for publication December 1, 2006.

* Address for reprints: Marisa Di Donato, MD, Cardiac Surgery Department, San Donato Hospital, Via Morandi 30, San Donato Milanese, Milan, Italy. (Email: marad{at}tin.it).


    Abstract
 Top
 Abstract
 Introduction
 Patients and Methods
 Results
 Discussion
 Conclusions
 References
 
Objectives: Our objectives were (1) to report operative and long-term mortality in patients submitted to anterior surgical ventricular restoration, (2) to report changes in clinical and cardiac status induced by surgical ventricular restoration, and (3) to report predictors of death in a large cohort of patients operated on at San Donato Hospital, Milan, Italy.

Methods: A total of 1161 consecutive patients (83% men, 62 ± 10 years) had anterior surgical ventricular restoration with or without coronary artery bypass grafting and with or without mitral repair/replacement. A complete echocardiographic study was performed in 488 of 1161 patients operated on between January 1998 and October 2005 (study group). The indication for surgery was heart failure in 60% of patients, angina, and/or a combination of the two.

Results: Thirty-day cardiac mortality was 4.7% (55/1161) in the overall group and 4.9% (24/488) in the study group. Determinants of hospital mortality were mitral valve regurgitation and need for a mitral valve repair/replacement. Mitral regurgitation (>2+) associated with a New York Heart Association class greater than II and with diastolic dysfunction (early-to-late diastolic filling pressure >2) further increases mortality risk. Global systolic function improved postoperatively: ejection fraction improved from 33% ± 9% to 40% ± 10% (P < .001); end-diastolic and end-systolic volumes decreased from 211 ± 73 to 142 ± 50 and 145 ± 64 to 88 ± 40 mL, respectively (P < .001) early after surgery. New York Heart Association functional class improved from 2.7 ± 0.9 to 1.6 ± 0.7 (P < .001) late after surgery. Long-term survival in the overall population was 63% at 120 months.

Conclusions: Surgical ventricular restoration for ischemic heart failure reduces ventricular volumes, improves cardiac function and functional status, carries an acceptable operative mortality, and results in good long-term survival. Predictors of operative mortality are mitral regurgitation of 2+ or more, New York Heart Association class greater than II, and diastolic dysfunction (early-to-late diastolic filling pressure >2).



Abbreviations and Acronyms AUC = area under the curve; CABG = coronary artery bypass grafting; E/A = early-to-late diastolic filling pressure; EF = ejection fraction; HF = heart failure; LV = left ventricular; MR = mitral regurgitation; NYHA = New York Heart Association; ROC = receiver operating characteristic; STICH = Surgical Treatment of IsChemic Heart failure (trial); SVR = surgical ventricular restoration



    Introduction
 Top
 Abstract
 Introduction
 Patients and Methods
 Results
 Discussion
 Conclusions
 References
 
GoChronic ischemic heart failure (HF) is one of the major health care issues in the Western world in terms of increasing number of patients affected, rate of hospitalization, and costs.1,2Go Despite optimal medical treatment, mortality remains high in patients with ischemic HF and high functional class.3Go The increase in ventricular volume after myocardial infarction is a component of the remodeling process; when left ventricular (LV) volume has increased to a certain extent and geometry is markedly abnormal, HF progresses independently of neurohormonal activation, according to the biomechanical model of HF expressed by Mann and Bristow.4Go The concept of a biomechanical model of HF clearly introduces the need for therapies such as surgical ventricular restoration (SVR) that reduce LV volumes and restore geometry. SVR has proven to be effective in improving pump function, clinical status, and survival.5-8Go The technique, first described by Jatene9Go and Dor and associates,10Go applies not only to the classic aneurysm but also to ischemic dilated cardiomyopathy with akinesia or dyskinesia.6Go

SVR for patients with HF is increasingly performed, but the results are somewhat difficult to compare because the type of damage (ie, true aneurysm or dilated cardiomyopathy) is not well defined in the reported series.11Go Moreover, the reported studies are not randomized, and the question whether adding SVR to coronary artery bypass grafting (CABG) will improve survival and clinical status can only be answered by the ongoing STICH trial (Surgical Treatment of IsChemic Heart failure).12Go

In our center (San Donato Hospital, Milan, Italy), we have been performing SVR for ischemic cardiomyopathy since 1989, and a total of 1300 patients have been operated on. The majority (1161 patients aged 63 ± 10 years) had anterior ventricular repair; the remaining either had posterior repair (n = 108) or an associated procedure other than CABG or mitral repair (eg, ventricular septal defect closure, aortic replacement, or Bentall operation; n = 31). They are not included in the analysis because they deserve a separate description, and the aim of the present study is to describe as homogeneous a population as possible (ie, after anterior myocardial infarction).

The end points of this study are as follows: (1) operative cardiac and all causes long-term mortality in the consecutive series of 1161 patients having anterior SVR (1989–2005); (2) changes in LV volumes, ejection fraction (EF), and New York Heart Association (NYHA) functional class in 488 patients with a complete data set (1998-2005); and (3) predictors of operative mortality.


    Patients and Methods
 Top
 Abstract
 Introduction
 Patients and Methods
 Results
 Discussion
 Conclusions
 References
 
Patient Population
From June 1989 to October 2005, a total of 1300 patients were submitted to SVR at San Donato Hospital, Milan, Italy; 1161 patients had anterior SVR with or without CABG and with or without mitral repair/replacement.

Demographic, clinical, echocardiographic, and procedural data were collected on an Excel database, which has been approved by our local ethics committee. The study group consists of 488 patients (1998-2005) with complete clinical and echocardiographic data available for the analysis (LV volumes, EF, NYHA class, and degree of mitral regurgitation [MR]). Eighty-six were women and 402 men (63 ± 10 years). Main indications for surgery were symptoms of HF, angina, and/or a combination of the two.

Diastolic function was graded as follows: 0 = normal, 1 = abnormal relaxation, 2 = pseudonormal, and 3 = restrictive.

Echo assessment was made by transthoracic echocardiography preoperatively and before discharge (7 to 10 days after the operation); a late echo study has been performed 6 months to 2 years after the operation in patients who return to the hospital for clinical evaluation (n = 300).

Operative mortality was defined as 30-day mortality and late mortality as mortality that occurred at follow-up (time from surgery to death is available).

Follow-up was assessed by telephone interview with the patient, family, or family physicians; we contacted the regional death register if telephone interview failed.

Surgical Technique
The technique has been described previously.7,13Go In brief, the procedure is conducted on the arrested heart, with antegrade crystalloid or cold blood cardioplegia introduced in 2001. CABG is first performed, almost always on the left anterior descending coronary artery to preserve the upper part of the septum and to guarantee a complete revascularization. The mitral valve is repaired, when needed, through the ventricular opening with a double-armed stitch at the posterior annulus, from trigone to trigone, and the mitral orifice is undersized with a 24- to 26-mm Hegar sizer.14Go

Since July 2001 we have systematically introduced the use of a mannequin (TRISVR; Chase Medical, Richardson, Tex) filled at 50 to 60 mL/m2 to optimize size and shape of the new ventricle. The technique is a refinement of the Dor technique and allows standardizing the procedure. The mannequin is useful when the ventricle is not very enlarged (to reduce the risk of too small a residual cavity) or when the infarcted region is not clearly demarcated, as occurs in dilated cardiomyopathy (type III silhouette, as described by Strobeck and associates15Go). In this circumstance, the transitional zone between scarred and nonscarred myocardium is not well defined and the mannequin allows rebuilding the ventricle in an elliptical way and avoiding sphericalization, which, besides the reduction in size, is the objective of the procedure.

Statistical Analysis
To determine the association between independent risk factors and hospital mortality, we applied the unpaired or paired Student t test, analysis of variance, or logistic regression analysis when appropriate. Predictability of the detected independent risk factors was tested by a receiver operating characteristics (ROC) analysis, considering an area under the curve (AUC) of at least 0.7 as predictive, and sensitivity-specificity testing for determination of cutoff values. Long-term survival was analyzed by Kaplan–Meier survival curves, and differences between curves have been tested with a log–rank test. Statistics have been performed with a computerized statistical package (SPSS 11.0; SPSS Inc, Chicago, Ill).


    Results
 Top
 Abstract
 Introduction
 Patients and Methods
 Results
 Discussion
 Conclusions
 References
 
Preoperatively, 278 (57%) of the 488 patients were in NYHA functional class III/IV and 107 (22%) in class IV. Overall, diastolic dysfunction was abnormal in the great majority of patients (96%), with a pattern of abnormal relaxation in 60% of patients, pseudonormal in 21%, and restrictive in 15%.

The great majority had coronary disease suitable for CABG; only 2.8% of the patients had nonsignificant coronary lesions resulting from previous percutaneous transluminal coronary angioplasty. Seventy-two percent had multivessel disease, and CABG was performed in 95% (mean number of anastomoses 2.8 ± 1.4); 92% received a thoracic artery graft on the left anterior descending coronary artery; 50% had patch reconstruction and 50% had a direct suture to close the ventricle. A Q-wave anterior myocardial infarction was present in 66% of patients. MR, graded 1 to 4+ at echo study, was present in 78% of patients; it was mild in the majority of patients and moderate to severe in 79 (18%) of 441; in 47 patients the degree of MR was not assessed. Mitral valve surgery (two mitral replacements) was performed in 18% (90/488); the indication to repair the valve was grade 3/4 regurgitation or grade 2+ regurgitation associated with annulus dilatation (≥40 mm).

Early Outcome
Operative cardiac mortality was 4.7% (55/1161) in the overall consecutive series and 4.9% in the study group (24/488). The main determinants of hospital mortality were severity of MR and the need for mitral valve repair/replacement. Severity of MR (graded 0–4) was significantly associated with hospital mortality at a logistic regression analysis (P < .001), and its predictivity was confirmed by a ROC analysis (AUC of 0.81). Patients requiring mitral valve repair/replacement had a significantly higher (13% vs 3.0%; P < .001) operative mortality rate.

Cardiac function improved postoperatively and the degree of MR significantly decreased (Table 1).


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TABLE 1 Functional and cardiac status changes
 
Late Outcome
Clinical follow-up was completed in 95% of the entire population (average follow-up 56 ± 48 months). Figure E1 shows Kaplan–Meier long-term survival curve.


Figure 3
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Figure E1. Kaplan–Meier survival curve in the whole population.

 
NYHA class improved from 2.7 ± 0.9 to 1.6 ± 0.7 (P < .001). Repaired moderate-to-severe MR (>2+) decreased significantly (P < .001) from 3.0 ± 1 to 0.7 ± 0.8 and to 1.5 ± 1.2 at follow-up (time from surgery 6 months to 2 years; Table 1).

Figure 1 shows long-term survival stratified by preoperative characteristics of the study group.


Figure 1
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Figure 1. Kaplan–Meier survival curve in patients stratified by preoperative characteristics. A, Diastolic diameter (≥70 mm. <70 mm). B, Preoperative ejection fraction (>35%; ≤35%). C, Preoperative New York Heart Association (NYHA) classes I/II and III/IV. D, Preoperative end-systolic volume (>80 mL; ≤80 mL).

 
Recent experience (2001–2005)
A subgroup of 254 patients (65 ± 9 years) operated on in recent years was prospectively collected and received a comprehensive echo assessment before and after the operation, including risk factors, medical treatment, diastolic function parameters (early-to-late diastolic filling pressure [E/A] ratio, isovolumic relaxation time, and deceleration time), rate of hospitalization, cardiac events, and procedures after surgery.

Cardiac operative mortality in this subgroup was 7.0% (18/254), not significantly different from that of the early experience. Preoperative factors being associated with hospital mortality at univariate analysis are listed in Table 2.


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TABLE 2 Factors associated with hospital mortality at the univariate analysis (subgroup of 254 patients)
 
Owing to the relatively low number of events, we tested for predictivity the various factors being associated with hospital mortality at the univariate analysis using a ROC analysis and assuming as cutoff value for predictivity an AUC less than 0.7.

The results of this analysis are reported in Table E1. Five variables demonstrated an acceptable level of predictivity: NYHA class, EF, left atrial diameter, E/A ratio, and MR severity. However, we could not determine an adequate cutoff value for EF, which is evidently associated with the hospital mortality risk in a continuous fashion; the left atrial diameter was strongly dependent on the MR severity; finally, the E/A ratio cutoff was settled at a value of 2.0, to avoid the problem of distinguishing between impaired relaxation profiles and pseudonormal patterns. As a result, we maintained in our model three predictive factors for in-hospital mortality: an NYHA class of III/IV, an E/A ratio greater than 2.0, and an MR grade 2 or more. MR alone does not significantly increase operative mortality risk; conversely, if associated with NYHA class III/IV, it determines a significant (P = .03) increase of the mortality risk; if a severe diastolic dysfunction is also present, the risk is further (P < .001) increased (Figure 2).


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TABLE E1 ROC analysis for the factors being associated with hospital mortality at the univariate analysis
 

Figure 2
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Figure 2. Risk stratification for operative mortality based on our predictive model (see text). NYHA, New York Heart Association; E/A, early-to-late diastolic filling pressure.

 
Follow-up (20 ± 10 months) was 100% complete in this subset of patients. Forty-four patients (18%) of 232 survivors had cardiac hospitalization during the entire period of follow-up. The most frequent causes of hospitalization were progressive HF (18/44), cardiac arrhythmias (8/44), unstable angina (3/44), and stroke (1/44). Five (2.3%) of 215 patients (for whom procedures during hospitalization were available) had implantation of an internal cardioverter device, coupled with biventricular pacing in 2; 4 more patients had biventricular pacing alone, for a total of 6 (2.8%) patients with biventricular pacing; 3 patients received percutaneous transluminal coronary angioplasty. Overall, 82% of patients did not need hospitalization after surgery.

Patients with depressed LV function
A group of 301 (62%) of the 488 patients had a preoperative EF of 35% or less; baseline clinical and hemodynamic characteristics are reported in Table E2.


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TABLE E2 Baseline clinical and hemodynamic characteristics in patients with preoperative EF ≤ 35% (n = 301)
 
Cardiac operative mortality was 6.6% (20/301). Causes of operative cardiac death were low cardiac output in 14, intractable ventricular arrhythmias in 4, sudden death during rehabilitation in 1, and acute thrombosis of the graft in 1. Table 3 shows cardiac function and clinical status before, early postoperatively, and late postoperatively. Volume, EF, and NYHA class improved significantly after surgery; the degree of preoperative moderate-to-severe MR decreased significantly. We compared this group of patients with failing ventricles with the 187 patients with LV dilatation (end-diastolic volume index = 100 ± 36 mL/m2; end-systolic volume index = 58 ± 20 mL/m2) and preoperative EF greater than 35% whose main indication for surgery was need for coronary revascularization. We found that patients with better pump function benefit less from SVR: EF was 43% ± 6% preoperatively and changed to 45% ± 10% early postoperatively (P < .02) and to 44% ± 8% late after surgery (P < .10). Operative cardiac mortality rate was 2.1% (4/187) ({chi}2 test P < .02).


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TABLE 3 Preoperative and postoperative (early and late after surgery) hemodynamic and functional data in patients with preoperative EF ≤ 35% (median)
 

    Discussion
 Top
 Abstract
 Introduction
 Patients and Methods
 Results
 Discussion
 Conclusions
 References
 
The present article describes the largest single-center series of patients with anterior SVR, and it is the largest that extends follow-up observation beyond 5 years.

Major findings from our results are as follow: (1) Significant volume reduction and improvement in EF are observed at the predischarge echo evaluation, and this improvement is still significant at late follow-up, despite a slight but significant increase in volumes and in MR, in respect to early after surgery. The late increase in volume could be ascribed to loading conditions that are lower when the patient is hospitalized, at rest. (2) Clinical status, as evaluated by NYHA functional class, is significantly improved. (3) Eighty-two percent of patients are free from cardiac rehospitalization. (4) Very few patients required an internal cardioverter device and biventricular pacing implantation. (5) Long-term survival is promising also in patients with depressed cardiac function and high functional class.

The Biomechanical Model of HF
In a recent article Mann and Bristow4Go described the concept of a biomechanical model for HF to explain the progression of HF independently of the neurohormonal status of the patient. According to these authors, our current neurohormonal models fail to completely explain disease progression in HF. Current medical therapy acting against neurohormonal activation tends to slow progression but fails to arrest the process of remodeling. In addition, many types of neurohormonal inhibition proved to be ineffective or even harmful in patients with HF.16Go To explain failure of neurohormonal antagonism, the authors focus on LV size and geometry abnormalities as responsible for progression of the disease. Geometric changes lead to structural abnormalities of the myocytes and of the myocardium, which worsen cardiac function and increase neurohormonal activation; this may make the cardiovascular system less responsive to normal homeostatic control mechanisms.

Therapeutic strategies designed to interrupt the vicious cycle will favorably affect the HF phenotype and the natural history of HF progression according to Mann and Bristow.4Go SVR is a surgical strategy that reduces LV volume, improves geometry, and relieves ischemia.5-7,11,13Go

Our patients are left on HF medical therapy after surgery (94% are receiving diuretics, 81% angiotensin-converting enzyme inhibitors, 34% beta-blockers, and almost all are receiving acetylsalicylic acid). In our common practice it is frequent to observe that some patients do clinically better than could be expected from cardiac function status, and this mismatch could be explained on the basis of the biomechanical model of HF in that SVR may not only revert the remodeling process but also may make the cardiovascular system more responsive to treatment and to neurohormonal activation, once dimensions and geometry have improved.

Aneurysm Repair or HF Surgical Therapy?
SVR as described by Dor and associates10Go was developed as a more physiologic repair of LV aneurysm, compared with simple linear repair,9,17Go but along with time and experience it was applied also to dilated ischemic cardiomyopathy, without the classic signs of the true aneurysm, that is, a severe distortion of the chamber with a discrete lesion, most often dyskinetic. In ischemic dilated cardiomyopathy, the demarcation of the ischemic/necrotic lesion is no longer present and the curvature of the ventricle is flattened not only at the apical level but also at the basal portions.15Go In our early experience we mainly treated patients with true aneurysm, but more recently, ventricles that exhibit dilated ischemic cardiomyopathy are more frequently encountered. Ischemic dilated cardiomyopathy is the result of more severe damage of the entire chamber, including damage in the remote zones, as the remodeling process progresses and is associated with more severe hemodynamic abnormalities (higher pulmonary pressure, higher volumes, lower EF, more frequent MR). Moreover, in our more recent experience, patients are significantly older and have more comorbidities, and we have increased the number of mitral repairs (it was 5% in the early experience and it is now 18%), which translates into higher risk patients.

It has been known for many years that a true aneurysm can be successfully treated with surgery, and the European guidelines for diagnosis and treatment of HF give indication for LV aneurysmectomy in patients with large, discrete LV aneurysm in whom HF develops.18Go However, the new challenge is to treat patients with dilated ischemic cardiomyopathy, and we think that SVR should be regarded as a viable option in modern interventional treatment of HF and not only as an aneurysm repair technique.

Surgical Technique
SVR is not a standardized technique. According to Dor and colleagues,19Go the use of a patch is mandatory, and more recently they introduced the use of a sizer; Caldeira and McCarthy20Go use a double purse-string suture technique; Mickleborough and associates8Go use a linear closure and septoplasty, sometimes with a patch, and it is difficult to say which other ways of rebuilding the LV are in the hands of surgeons. We think that the technique should be standardized to compare the results and to find the best way to treat patients with HF. We have been using a sizer and shaper since 2001 in all our patients, and we think that the device is helpful to standardize the procedure, reducing the risk of restriction and of sphericalization of LV chamber.

Mitral Repair
Functional MR is frequently associated with postischemic ventricular dilatation, and its presence worsens prognosis.21Go At present, it has not been established whether, when, and how the mitral valve should be repaired during SVR. The presence of moderate-to-severe MR and its surgical repair carries a higher operative risk in our study group. It is difficult to distinguish whether the higher mortality is due to the surgical procedure per sè, because patients with MR have worse clinical and hemodynamic conditions. In the most recent series, MR alone (≥2+) did not increase the in-hospital mortality risk; conversely, if associated with NYHA class III/IV and with severe diastolic dysfunction, the risk is significantly increased. Our interpretation is that MR becomes a true predictor of hospital mortality only when the LV end-diastolic pressure, and therefore the left atrial pressure, are severely increased (as occurs whenever the E/A ratio exceeds 2.0), leading to congestive HF and severe functional impairment (NYHA class III/IV).

• On the basis of this experience, we consider the following to be the indications for SVR:
• Previous anterior myocardial infarction (either Q or non-Q) as evaluated by electrocardiogram or cardiac magnetic resonance.
• LV dysfunction with dilatation of the ventricle and regional asynergy (either akinetic or dyskinetic). When LV asynergy is severe and diffuse, SVR can be performed only if regions remote from the scar have some degree of contraction detectable at rest or under inotropic stimulus (like dobutamine test).
• HF symptoms are the first indication for SVR, but also patients presenting with ventricular arrhythmias and/or angina who need surgical revascularization represent an indication for SVR (if the previous conditions are present) to avoid further dilatation.
• For patients who are asymptomatic despite postinfarction LV dysfunction, we suggest that serial echocardiographic studies be performed to detect the first signs of deterioration (ie, LV progressive enlargement or decline in EF).

The following are contraindications:

• Severe right ventricular dysfunction (biventricular dilated cardiomyopathy) (absolute).
• Severe pulmonary hypertension not associated with MR (relative).
• Severe regional asynergy without LV dilatation (absolute).
• Restrictive diastolic pattern associated with high functional class and MR (absolute).

When patients have relative or absolute contraindications or when cardiac dysfunction is severe and diffuse, we perform a stress echo dobutamine test. If contractility improves, we perform SVR; if it does not improve and other options such as transplantation are available, heart transplant should be done. However, in some elderly patients when full medical therapy and other devices fail to improve clinical status, SVR can be the only treatment option and both patients and surgeons should be aware of an increased mortality risk.


    Conclusions
 Top
 Abstract
 Introduction
 Patients and Methods
 Results
 Discussion
 Conclusions
 References
 
Our study is observational and not randomized. Collection of data is not uniform, being prospective in a minority of our population, which remains the largest reported until now. The severity of HF was based on NYHA functional class, which has limitations; we did not estimate quality of life, which is critical in this kind of patient with severe HF. We expect the STICH trial to answer all these critical questions.


See related editorial on page 280.

 


    Footnotes
 
1 Drs Menicanti and Di Donato serve as consultants at Chase Medical. Back


    References
 Top
 Abstract
 Introduction
 Patients and Methods
 Results
 Discussion
 Conclusions
 References
 

  1. Nohira A, Lewis E, Stevenson LW. Medical management of advanced heart failure. JAMA 2002;287:628-640.[Abstract/Free Full Text]
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  3. Cowborn PJ, Cleland JG, Coats AJ, Komajda M. Risk stratification in chronic heart failure. Eur Heart J 1998;19:696-710.[Free Full Text]
  4. Mann DL, Bristow MR. Mechanisms and models in heart failure. The biochemical model and beyond. Circulation 2005;111:2837-2849.[Free Full Text]
  5. Athanasuleas CL, Buckberg GD, Stanley AWH, Siler W, Dor V, Di Donato M, et al. RESTORE group Surgical ventricular restoration in the treatment of congestive heart failure due to post-infarction ventricular dilation. J Am Coll Cardiol 2004;44:1439-1445.[Abstract/Free Full Text]
  6. Di Donato M, Sabatier M, Dor V, Toso A, Maioli M, Fantini F. Akinetic versus dyskinetic postinfarction scar: relation to surgical outcome in patients undergoing endoventricular circular patch plasty repair. J Am Coll Cardiol 1997;29:1569-1575.[Abstract]
  7. Menicanti L, Di Donato M. The Dor procedure: what has changed after fifteen years of clinical practice?. J Thorac Cardiovasc Surg 2002;124:886-890.[Free Full Text]
  8. Mickleborough LL, Merchant N, Ivanov J, Rao V, Carson S. Left ventricular reconstruction: early and late results. J Thorac Cardiovasc Surg 2004;128:27-37.[Abstract/Free Full Text]
  9. Jatene AD. Left ventricular aneurysmectomy: resection or reconstruction. J Thorac Cardiovasc Surg 1985;89:321-331.[Medline]
  10. Dor V, Saab M, Coste P, Kornaszewska M, Montiglio F. Left ventricular aneurysm: a new surgical approach. Thorac Cardiovasc Surg 1989;37:11-19.[Medline]
  11. Maxey TS, Reece TB, Ellman PI, Butler PD, Kern JA, Tribble CG, et al. Coronary artery bypass with ventricular restoration is superior to coronary artery bypass alone in patients with ischemic cardiomyopathy. J Thorac Cardiovasc Surg 2004;127:428-434.[Abstract/Free Full Text]
  12. Jones RH. Is it time for a randomized trial of surgical treatment of ischemic heart failure?. J Am Coll Cardiol 2001;37:1210-1213.[Free Full Text]
  13. Menicanti L, Di Donato M. Left ventricular aneurysm/reshaping techniques. MMCTS 2005April 25.
  14. Menicanti L, Di Donato M, Frigiola A, Buckberg GD, Santambrogio C, Ranucci A, et al. RESTORE group. Ischemic mitral regurgitation: intraventricular papillary muscle imbrication without mitral ring during left ventricular restoration. J Thorac Cardiovasc Surg 2002;123:1041-1050.[Abstract/Free Full Text]
  15. Strobeck J, Di Donato M, Costanzo MR, Conte J, Boyce S. Importance of shape and surgically reshaping the left ventricle in ischemic cardiomyopathy. Congestive Heart Fail 2004;10:45-53.
  16. Mann DL, Deswal A, Bozkurt B, Torre-Amione G. New therapeutics for chronic heart failure. Annu Rev Med 2002;53:59-74.[Medline]
  17. Cooley DA. Ventricular endoaneurysmorrhaphy: a simplified repair for extensive postinfarction aneurysm. J Card Surg 1989;4:200-205.[Medline]
  18. Swedberg K, Cleland JG, Dargie H, Drexler H, Follath F, Komajda M, et al. Guidelines for the diagnosis and treatment of chronic heart failure: executive summary (update 2005): The Task Force for the Diagnosis and Treatment of Chronic Heart Failure of the European Society of Cardiology. Eur Heart J 2005;26:1115-1140.[Free Full Text]
  19. Dor V, Sabatier M, Montiglio F, Coste P, Di Donato M. Endoventricular patch reconstruction in large ischemic wall-motion abnormalities. J Card Surg 1999;14:46-52.[Medline]
  20. Caldeira C, McCarthy M. A simple method of left ventricular reconstruction without patch for ischemic cardiomyopathy. Ann Thorac Surg 2001;72:2148-2149.[Abstract/Free Full Text]
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Eur J Cardiothorac SurgHome page
S. M. Adhyapak and V. R. Parachuri
Lessons from a mathematical hypothesis -- modification of the endoventricular circular patch plasty
Eur J Cardiothorac Surg, June 1, 2011; 39(6): 945 - 951.
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Am. J. Physiol. Heart Circ. Physiol.Home page
L. Zhong, Y. Su, L. Gobeawan, S. Sola, R.- S. Tan, J. L. Navia, D. N. Ghista, T. Chua, J. Guccione, and G. S. Kassab
Impact of surgical ventricular restoration on ventricular shape, wall stress, and function in heart failure patients
Am J Physiol Heart Circ Physiol, May 1, 2011; 300(5): H1653 - H1660.
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J. Thorac. Cardiovasc. Surg.Home page
V. Dor, F. Civaia, C. Alexandrescu, M. Sabatier, and F. Montiglio
Favorable effects of left ventricular reconstruction in patients excluded from the Surgical Treatments for Ischemic Heart Failure (STICH) trial.
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Eur J Heart FailHome page
T. Isomura, J. Hoshino, Y. Fukada, A. Kitamura, S. Katahira, T. Kondo, T. Iwasaki, G. Buckberg, and from the RESTORE Group
Volume reduction rate by surgical ventricular restoration determines late outcome in ischaemic cardiomyopathy
Eur J Heart Fail, April 1, 2011; 13(4): 423 - 431.
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Ann. Thorac. Surg.Home page
N. W. Skelley, J. G. Allen, G. J. Arnaoutakis, E. S. Weiss, N. D. Patel, and J. V. Conte
The Impact of Volume Reduction on Early and Long-Term Outcomes in Surgical Ventricular Restoration for Severe Heart Failure
Ann. Thorac. Surg., January 1, 2011; 91(1): 104 - 112.
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J. Thorac. Cardiovasc. Surg.Home page
M. Di Donato, F. Fantini, A. Toso, S. Castelvecchio, L. Menicanti, L. Annest, and D. Burkhoff
Impact of surgical ventricular reconstruction on stroke volume in patients with ischemic cardiomyopathy
J. Thorac. Cardiovasc. Surg., December 1, 2010; 140(6): 1325 - 1331.e2.
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J. Thorac. Cardiovasc. Surg.Home page
E. A. ten Brinke, R. J. Klautz, S. A. Tulner, H. F. Verwey, J. J. Bax, M. J. Schalij, E. E. van der Wall, M. I. Versteegh, R. A. Dion, and P. Steendijk
Long-term effects of surgical ventricular restoration with additional restrictive mitral annuloplasty and/or coronary artery bypass grafting on left ventricular function: Six-month follow-up by pressure-volume loops
J. Thorac. Cardiovasc. Surg., December 1, 2010; 140(6): 1338 - 1344.
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Eur J Heart FailHome page
J. L. Rouleau, R. E. Michler, E. J. Velazquez, J. K. Oh, C. M. O'Connor, P. Desvigne-Nickens, G. Sopko, K. L. Lee, and R. H. Jones
The STICH trial: evidence-based conclusions
Eur J Heart Fail, October 1, 2010; 12(10): 1028 - 1030.
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Eur J Heart FailHome page
G. D. Buckberg, C. L. Athanasuleas, A. S. Wechsler, F. Beyersdorf, J. V. Conte, and J. E. Strobeck
The STICH trial unravelled
Eur J Heart Fail, October 1, 2010; 12(10): 1024 - 1027.
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J Am Coll CardiolHome page
M. Zembala, R. E. Michler, A. Rynkiewicz, T. Huynh, L. She, B. Lubiszewska, J. A. Hill, R. Jandova, F. Dagenais, E. D. Peterson, et al.
Clinical Characteristics of Patients Undergoing Surgical Ventricular Reconstruction by Choice and by Randomization
J. Am. Coll. Cardiol., August 3, 2010; 56(6): 499 - 507.
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J. Thorac. Cardiovasc. Surg.Home page
M. Di Donato, L. Menicanti, M. Ranucci, S. Castelvecchio, C. de Vincentiis, J. Salvia, and T. Yussuf
Effects of surgical ventricular reconstruction on diastolic function at midterm follow-up
J. Thorac. Cardiovasc. Surg., August 1, 2010; 140(2): 285 - 291.
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Eur J Heart FailHome page
D. L. Mann, R. Bogaev, and G. D. Buckberg
Cardiac remodelling and myocardial recovery: lost in translation?
Eur J Heart Fail, August 1, 2010; 12(8): 789 - 796.
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Interact CardioVasc Thorac SurgHome page
M. A. Deja, M. Malinowski, J. Biernat, and S. Wos
Left ventricular aneurysm that grew to rupture
Interact CardioVasc Thorac Surg, August 1, 2010; 11(2): 196 - 198.
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J. Thorac. Cardiovasc. Surg.Home page
E. A. ten Brinke, R. J. Klautz, and P. Steendijk
Balloon sizing in surgical ventricular restoration: What volume are we targeting?
J. Thorac. Cardiovasc. Surg., July 1, 2010; 140(1): 240 - 241.
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Ann. Thorac. Surg.Home page
A. Marui, T. Nishina, Y. Saji, K. Yamazaki, T. Shimamoto, T. Ikeda, and R. Sakata
Significance of Left Ventricular Diastolic Function on Outcomes After Surgical Ventricular Restoration
Ann. Thorac. Surg., May 1, 2010; 89(5): 1524 - 1531.
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J. Thorac. Cardiovasc. Surg.Home page
A. M. Calafiore, A. L. Iaco, D. Amata, C. Castello, E. Varone, F. Falconieri, A. Bivona, S. Gallina, and M. Di Mauro
Left ventricular surgical restoration for anteroseptal scars: Volume versus shape
J. Thorac. Cardiovasc. Surg., May 1, 2010; 139(5): 1123 - 1130.
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Eur J Cardiothorac SurgHome page
M. Pocar, A. Di Mauro, D. Passolunghi, A. Moneta, A. M. T. A. Alsheraei, A. Bregasi, R. Mattioli, and F. Donatelli
Predictors of adverse events after surgical ventricular restoration for advanced ischaemic cardiomyopathy
Eur J Cardiothorac Surg, May 1, 2010; 37(5): 1093 - 1100.
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Eur J Heart FailHome page
M. Di Donato, S. Castelvecchio, and L. Menicanti
End-systolic volume following surgical ventricular reconstruction impacts survival in patients with ischaemic dilated cardiomyopathy
Eur J Heart Fail, April 1, 2010; 12(4): 375 - 381.
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Interact CardioVasc Thorac SurgHome page
A. D'Onofrio, D. Cugola, I. Bolgan, L. Menicanti, A. Fabbri, and M. Di Donato
Surgical ventricular reconstruction with different myocardial protection strategies. A propensity matched analysis
Interact CardioVasc Thorac Surg, April 1, 2010; 10(4): 530 - 534.
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Ann. Thorac. Surg.Home page
S. Castelvecchio, M. Ranucci, M. Di Donato, and L. Menicanti
Diabetes Mellitus and Long-Term Outcome in Heart Failure Patients After Surgical Ventricular Restoration
Ann. Thorac. Surg., November 1, 2009; 88(5): 1451 - 1456.
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J. Thorac. Cardiovasc. Surg.Home page
G. D. Buckberg and C. L. Athanasuleas
The STICH trial: Misguided conclusions.
J. Thorac. Cardiovasc. Surg., November 1, 2009; 138(5): 1060 - 1064.e2.
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CirculationHome page
M. V. Badiwala, S. Verma, and V. Rao
Surgical Management of Ischemic Mitral Regurgitation
Circulation, September 29, 2009; 120(13): 1287 - 1293.
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Eur J Cardiothorac SurgHome page
H. Suma, H. Tanabe, T. Uejima, T. Isomura, and T. Horii
Surgical ventricular restoration combined with mitral valve procedure for endstage ischemic cardiomyopathy
Eur J Cardiothorac Surg, August 1, 2009; 36(2): 280 - 285.
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Eur J Cardiothorac SurgHome page
P. Klein, E. R. Holman, M. I. M. Versteegh, E. Boersma, H. F. Verwey, J. J. Bax, R. A. E. Dion, and R. J. M. Klautz
Wall motion score index predicts mortality and functional result after surgical ventricular restoration for advanced ischemic heart failure
Eur J Cardiothorac Surg, May 1, 2009; 35(5): 847 - 853.
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J. Thorac. Cardiovasc. Surg.Home page
H.-Y. Yu, Y.-S. Chen, W.-Y. Tseng, N.-S. Chi, C.-H. Wang, S.-S. Wang, and F.-Y. Lin
Why is the surgical ventricular restoration operation effective for ischemic cardiomyopathy? Geometric analysis with magnetic resonance imaging of changes in regional ventricular function after surgical ventricular restoration
J. Thorac. Cardiovasc. Surg., April 1, 2009; 137(4): 887 - 894.
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Ann. Thorac. Surg.Home page
M. Di Donato, S. Castelvecchio, T. Kukulski, C. Bussadori, F. Giacomazzi, A. Frigiola, and L. Menicanti
Surgical Ventricular Restoration: Left Ventricular Shape Influence on Cardiac Function, Clinical Status, and Survival
Ann. Thorac. Surg., February 1, 2009; 87(2): 455 - 461.
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Ann. Thorac. Surg.Home page
S. Castelvecchio, L. Menicanti, M. Ranucci, and M. Di Donato
Impact of Surgical Ventricular Restoration on Diastolic Function: Implications of Shape and Residual Ventricular Size
Ann. Thorac. Surg., December 1, 2008; 86(6): 1849 - 1854.
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J. Thorac. Cardiovasc. Surg.Home page
V. Dor, F. Civaia, C. Alexandrescu, and F. Montiglio
The post-myocardial infarction scarred ventricle and congestive heart failure: the preeminence of magnetic resonance imaging for preoperative, intraoperative, and postoperative assessment.
J. Thorac. Cardiovasc. Surg., December 1, 2008; 136(6): 1405 - 1412.
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J. Thorac. Cardiovasc. Surg.Home page
K. Takeda, G. Matsumiya, H. Matsue, S. Hamada, M. Sakaki, T. Sakaguchi, T. Fujita, and Y. Sawa
Use of quantitative analysis of remote myocardial fibrosis with delayed-enhancement magnetic resonance imaging to predict outcomes after surgical ventricular restoration for ischemic cardiomyopathy.
J. Thorac. Cardiovasc. Surg., December 1, 2008; 136(6): 1514 - 1521.
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Asian Cardiovasc. Thorac. Ann.Home page
M. Di Donato, L. Menicanti, and H. Suma
Surgical Ventricular Restoration and the STICH Trial
Asian Cardiovasc Thorac Ann, August 1, 2008; 16(4): 269 - 271.
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Interact CardioVasc Thorac SurgHome page
H. Subramanian, B. Kunadian, and J. Dunning
Is it worth performing surgical ventricular restoration in patients with ischemic cardiomyopathy and akinetic but non-aneurysmal segments in the left ventricle?
Interact CardioVasc Thorac Surg, August 1, 2008; 7(4): 702 - 707.
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J. Thorac. Cardiovasc. Surg.Home page
M. B. Ratcliffe and T. S. Guy
The effect of preoperative diastolic dysfunction on outcome after surgical ventricular remodeling
J. Thorac. Cardiovasc. Surg., August 1, 2007; 134(2): 280 - 283.
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