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Ann Thorac Surg 2001;71:1146-1152
© 2001 The Society of Thoracic Surgeons
a Department of Cardiology and Cardiac Surgery, University "G. D’Annunzio" of Chieti, Chieti, Italy
Accepted for publication October 20, 2000.
Address reprint requests to Dr Calafiore, "G. D’Annunzio" University, Division of Cardiac Surgery, "San Camillo de’ Lellis" Hospital, Via C. Forlanini 50, 66100 Chieti, Italy
e-mail: calafiore{at}unich.it
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Abstract |
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 TopFootnotes Abstract IntroductionMaterial and methodsResultsCommentReferences |
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Methods. From January 1990 to May 2000, 49 patients with dilated cardiomyopathy (12 idiopathic and 37 ischemic) underwent MV operation, 29 repair and 20 replacement. Preoperative evaluation included measurement of MV coaptation depth (CD) as a mirror of the abnormalities of MV apparatus leading to functional mitral regurgitation.
Results. Thirty-day mortality was 4.2% (2 patients). One-, 3-, 5-, and 10-year actuarial survival was, respectively, 90%, 87%, 78%, and 73%. The possibility of survival with at least one New York Heart Association functional class improvement was 88%, 76%, 71%, and 65%. Return of functional mitral regurgitation after MV repair was nearly inevitable; however, using a scale from 0 to 4, mean postoperative functional mitral regurgitation was 1.2 ± 0.8 when preoperative MVCD was 10 mm or less and 2.5 ± 0.7 when preoperative MVCD was 11 mm or higher (p < 0.05). Globally, functional results were not influenced by the strategy of treatment (MV repair or replacement).
Conclusions. Mitral valve operation can give satisfying survival and good palliation of dilated cardiomyopathy. The MVCD can be helpful in the choice of the surgical strategy on the MV.
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Introduction |
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TopFootnotesAbstractIntroductionMaterial and methodsResultsCommentReferences |
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The appearance of FMR has a negative impact on survival of patients with DCM [1–3], with a mortality rate from 40% to 70% after 12 months from the diagnosis of FMR. It is noteworthy that patients with mild FMR also showed a lower survival, about 40% after 12 months [2].
Recently [4, 5] mitral valve (MV) annuloplasty was proposed in selected patients to reduce left ventricle overload and, consequently, end-diastolic pressure. The competence of the MV has a direct effect on the stroke volume, which, independently from the ejection fraction, becomes antegrade, with a favorable effect on the cardiac output. As these concepts are becoming more popular, more patients undergo conventional operation for DCM [6–8].
We reviewed our experience with MV operation in DCM, both idiopathic and ischemic, to evaluate from the analysis of our early and late results if the MV can be always preserved or if there are indications for MV replacement and, in case, what they are.
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Material and methods |
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TopFootnotesAbstractIntroductionMaterial and methodsResultsCommentReferences |
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Clinical experience
From January 1990 to May 2000, 49 patients with DCM (12 idiopathic and 37 ischemic) underwent isolated MV operation. None of them had organic MV disease. Age ranged from 42 to 79 years (mean, 64 ± 10 years) and 17 patients (34.7%) were 70 years or older. Seventeen patients (34.7%) were younger than 60 years and 5 (10.2%) were previously scheduled for cardiac transplant. Five patients (10.2%) were women. Twenty-five patients (51.0%) were in New York Heart Association functional class IV and 24 (49.0%) were in class III (mean, 3.5 ± 0.6). Mean duration of symptomatic heart failure was 2.5 ± 1.7 years. Preoperative ejection fraction ranged from 15% to 35% (mean, 27% ± 7%) and was 25% or less in 14 patients (28.6%). Patients with postischemic DCM had concomitant coronary disease, but none of them had angina or ischemic symptoms. Moreover, the dobutamine stress test did not show any evidence of segmental ischemia in 34 patients. Hemodynamic findings showed a mean pulmonary artery pressure of 34 ± 14 mm Hg and a mean cardiac index of 2.04 ± 0.84 L · min-1 · m-2.
Echocardiographic evaluation of functional mitral regurgitation
The degree of FMR was not the only key point to indicate MV operation, being changeable from time to time. The anatomy of the MV and of its subvalvular apparatus was carefully studied using transesophageal echocardiography. The distance between the mitral annular plane and the coaptation point of the mitral leaflets (MV coaptation depth, MVCD) was mainly taken into consideration.
The MVCD is an early consequence of all the mechanisms that can influence the function of the MV apparatus. It is directly related to the left ventricular sphericity (transversal length/longitudinal length), one of the main determinants of FMR both in the clinical [9] and the experimental settings [10], to the annular size and to the ejection fraction (Fig 1). A single value is the mirror of the perturbations of the geometry of the heart and, consequently, of the MV. In 20 healthy controls, its mean value was 4.1 ± 1.6 mm and did not exceed 6 mm (Fig 2). Table 1 shows the preoperative echocardiographic data.
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If FMR is moderate to severe (3/4) or severe (4/4), operation is clearly indicated. In our opinion, in presence of moderate FMR (2/4), MV operation is always indicated. This FMR degree, with a normally contracting heart and normal volumes, represents a small portion of the cardiac output. In a dilated heart with a low ejection fraction (50% of the stroke volume), there is a need for correction.
Surgical technique
Intermittent antegrade warm blood cardioplegia was always used for myocardial protection [11]. If necessary, coronary artery bypass grafting was performed first. The MV was exposed through the interatrial septum; if the visual field was not satisfactory, the superior approach [12] was used. For this purpose, the superior vena cava was always cannulated directly.
Mitral valve annuloplasty (n = 29) was obtained by two different techniques. A gluteraldehyde-treated homologous pericardium, 52 mm long, was inserted between the two trigons in 10 patients; as the length was equivalent to a 26-ring size, the annulus was overreduced. In the remaining 19 patients, a De Vega-like annuloplasty with a single 2/0 TICRON (TI-CRON, Sherwood Medical, St. Louis, MO) was performed, going twice from the posteromedial to the anterolateral trigon and tying the suture at this level on a pledget. A 26 sizer was applied inside the valve to evaluate if the mitral annulus was reduced to the proper size.
Mitral valve replacement was done on 20 patients limiting the excision of the valve only to a triangle of the anterior leaflet, which leaves in place all the chordae and, consequently, the papillary muscles. The interrupted pledgeted U sutures are brought to the limit of the leaflets, attaching the papillary muscles to the annulus. In this way the subvalvular apparatus and its function are preserved.
When a tricuspid annuloplasty was needed (17 patients), it was performed after the MV operation. A De Vega-like procedure with a 2/0 Ticron was used.
Coronary bypass grafting was performed in 33 patients, even if no ischemia was detected. Seventy-four coronary vessels were grafted (mean, 2.2 ± 1.0 distal anastomoses per patient): 27, left anterior descending artery; 4, diagonal; 17, obtuse marginal; and 19, right coronary artery or one of its branches.
Before unclamping the aorta, all the patients received electively 5 µg · kg-1 · min-1 of dobutamine. If necessary, stronger inotropic support with adrenaline and intraaortic balloon pump was used. If preoperative creatinine was higher than 1.4 mg/L when the pump was off, a continuous infusion of dopamine (3 µg · kg-1 · min-1, renal range) and furosemide (20 mg/h) was always started.
Choice between mitral valve repair and replacement
At the beginning of our experience (1990 to 1993, 9 patients) the MV was always replaced. Later on, we tried to repair the MV at each occasion. However, as we considered MV replacement in these patients, our strategy changed.
The anatomy of the MV is the key point of the choice of technique. If the MVCD is between 7 and 10 mm, MV annuloplasty must be performed. However, if the MVCD exceeds 10 mm, the alterations of the MV subvalvular apparatus are such that FMR is expected to return in a short period of time (Fig 3). In this situation MV replacement must be performed.
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Follow-up data were obtained 3, 6, 9, and 12 months after operation and then every 6 months. Echocardiographic examination was performed every time patients were seen at our outpatients clinic; if the patient could not come to the clinic, the referring cardiologist sent us clinical information. Follow-up was 100% complete.
Statistical analysis
Results are expressed as mean value ± standard deviation unless otherwise indicated. Statistical analysis comparing two groups was performed with unpaired two-tailed t tests for the means or 
2 test for categoric variables. Survival and event-free survival curves were obtained with the Kaplan-Meier method (SPSS Software, Chicago, IL). The statistical significance was calculated with the log-rank. p value less than 0.05 was considered significant.
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Results |
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TopFootnotesAbstractIntroductionMaterial and methodsResultsCommentReferences |
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Late survival
After a mean of 28 ± 27 months, 11 patients (23.4%) died; 5 of them had MV repair and 6 MV replacement. Causes of death were cardiac in 10 (2 sudden death and 8 heart failure) and noncardiac in 1 (malignancy). One-, 3-, 5-, and 10-year actuarial survival was, respectively, 90%, 87%, 78%, and 73% (Fig 4). Five-year survival in ischemic and idiopathic patients was similar (78% ± 10% versus 75% ± 14%, p = not significant). Patients who had MV repair had better 5-year survival than patients who had MV replacement, although not statistically significant (83% ± 7% versus 70% ± 10%).
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Comment |
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TopFootnotesAbstractIntroductionMaterial and methodsResultsCommentReferences |
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Mechanisms of FMR are several. Left ventricular enlargement causes displacement of both papillary muscles posterolaterally and apically. Geometric distortion of the mitral apparatus is its natural consequence. These changes increase the distance over which the mitral leaflets are tethered from the papillary muscles to the anterior annular ring and restrict their possibility to close at the annular level [13]. The leaflets take a tented geometry, the length of leaflet coaptation is reduced, the excursion angle of the posterior leaflet decreases, and the coaptation depth of the leaflets increases.
When FMR starts, the mitral annular area increases together with the dilatation of the mitral annulus and a consequent increase of the base of the heart. With the same level of papillary muscle displacement, dilation of the annulus causes a higher degree of FMR. The combination of posterolateral and apical displacement and dilated annulus gives the highest degree of FMR.
Mitral regurgitation that follows postischemic DCM can have, if a papillary muscle is involved in the ischemic event, a different start, as restricted motion of a leaflet (generally the posterior one) can be the basis of the process. However, when left ventricular dilation starts, the further mechanisms of FMR are similar to those described previously.
Surgical possibilities, when heart failure is not controlled pharmacologically, are directed to the restoration of the competence of the MV, with a concomitant reduction of the base of the heart [4, 5]. This effect causes a reduction of the left ventricular volume, as the base of the cardiac cone becomes smaller. With time, a favorable remodeling of the left ventricle can follow, with further reduction of the volume; however, as demonstrated by our experience, this is not always the case. The purpose of operation is to maintain the same stroke volume as preoperatively, which is antegrade, with a concomitant increase in cardiac output. According to this viewpoint, as operation being only palliatory, the possibility of returning to the situation where symptoms could be more easily controlled by medical treatment, can be considered a success of the procedure.
To decide when FMR has to be treated, moderate to severe or severe FMR is the obligatory surgical indication. However, in our opinion, moderate FMR, in any patient symptomatic of heart failure, is huge enough to justify its correction. An accurate study of the anatomy of the MV will provide the real potential for FMR that, at the moment of the evaluation, can change according different factors (relative hypovolemia, vasodilation, vasoconstriction due to anxiety, etc). The higher the ventricular volume, the lower the ejection fraction, the more aggressive the MV operation must be.
To correct FMR, MV can be repaired or replaced. Mitral annuloplasty was considered the standard to correct mitral regurgitation [4, 5]. However, FMR can reappear in the follow-up of patients treated with ring annuloplasty [14]. The reduction of posterior annulus limits annular area, improving coaptation. However, ring insertion shifts the posterior annulus toward the fixed anterior annulus, increasing the distance between the papillary muscles and the posterior annulus and further reducing its ability to move anteriorly and to coapt. This can still cause FMR [13], even with an annular overreduction [15]. In our opinion, in certain patients FMR is difficult to correct due to the deep geometric alterations among the components of the MV apparatus, and MV replacement has to be considered.
We found that MVCD is a simple measurement that can give us an indication of the altered leaflet tethering geometry. If it is 11 mm or more, MV, preserving intact its subvalvular apparatus, must be replaced. Two goals are fulfilled: the mitral annulus is fixed to a certain size, reducing the base of the heart (a 25- or 27-mm prosthetic valve is generally inserted) and FMR will not be a problem in the future. In these patients, if MV repair is performed, return of FMR is very likely to happen, with a degree that can impair the functional result of the procedure.
We observed that when MV repair was performed in patients with a MVCD 11 mm or more, return of FMR was the rule and all the patients had some degree of FMR (mean, 2.5). On the contrary, when MVCD was 10 mm or less, FMR was generally mild to moderate (mean, 1.2). This was not attributable to mitral annulus redilation, as its size remained constant with time.
We believe that there are indications both for MV repair and for MV replacement and, in selected patients, this latter solution has to be preferred. The MVCD gives the indication of the geometry of the left ventricle and can identify the patients in whom recurrence of mitral regurgitation is more likely to occur.
Midterm results in our patients and in the series of other investigators [4, 5, 7, 8, 16] show satisfactory survival rates and functional palliation. A small increase in ejection fraction and stroke volume was observed, but this was not significant. However, stroke volume becomes mainly antegrade, with a concomitant increase in cardiac output. The great benefit of the procedure is the restoration of MV competence or the reduction of FMR, as observed in patients who had MV replacement or MV repair with MVCD 10 mm or less. Modifications of left ventricle volume were not important and were not related to the clinical improvement.
How long this situation will remain constant is difficult to say. As patients always have DCM and remain with a DCM after operation, our purpose is to obtain a palliation that will reduce symptoms and increase life expectancy, often related to the competence of the MV. Aggressive medical treatment, which has recently made gigantic improvements, will allow an improvement in the quality of life, reducing as much as possible the progression of the disease.
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