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J Thorac Cardiovasc Surg 2007;134:433-441
© 2007 The American Association for Thoracic Surgery
Surgery for Acquired Cardiovascular Disease |
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 |
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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).
| Introduction |
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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.11
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).12
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 |
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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.7,13
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.14
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 associates15
). 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 |
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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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Figure 1 shows long-term survival stratified by preoperative characteristics of the study group.
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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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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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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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2 test P < .02).
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| Discussion |
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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 Bristow4
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.16
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.4
SVR is a surgical strategy that reduces LV volume, improves geometry, and relieves ischemia.5-7,11,13
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 associates10
was developed as a more physiologic repair of LV aneurysm, compared with simple linear repair,9,17
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.15
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.18
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,19
the use of a patch is mandatory, and more recently they introduced the use of a sizer; Caldeira and McCarthy20
use a double purse-string suture technique; Mickleborough and associates8
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.21
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).
The following are contraindications:
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.
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| See related editorial on page 280.
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| Footnotes |
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| References |
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