Asian Cardiovasc Thorac Ann 2005;13:267-270
© 2005 Asia Publishing EXchange Ltd
Mitral Valve Repair for Ischemic Mitral Regurgitation in Dilated Cardiomyopathy
Vijay Kohli, MCh,
Harpreet Wasir, MCh,
Sanjay Mittal, DM1,
Anil Karlekar, MD2,
Yatin Mehta, FRCA2,
Naresh Trehan, MD
Department of Cardiovascular Surgery
1 Department of Cardiology
2 Department of Cardiovascular Anesthesia, Escorts Heart Institute & Research Centre, New Delhi, India
For reprint information contact: Vijay Kohli, MCh Tel: 91 11 2682 5000 Fax: 91 11 2682 5013 Email: vijay_k22{at}hotmail.com, Department of Cardiovascular Surgery, Escorts Heart Institute and Research Centre, Okhla Road, New Delhi 110025, India.
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ABSTRACT
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Ischemic mitral regurgitation contributes to poor survival in patients with heart failure. The intermediate-term outcome of mitral reconstruction in 15 patients who had ischemic dilated cardiomyopathy with mitral regurgitation requiring surgical intervention was studied. They underwent mitral valve repair along with coronary artery bypass surgery. The mitral valve coaptation depth was considered an important parameter in deciding on repair. Ages ranged from 43 to 72 years. Left ventricular ejection fractions were 15–38% (mean, 26.5% ± 4.3%). The operative technique in all 15 patients was posterior annuloplasty using Dacron felt. At a mean follow-up of 4.6 ± 1.2 months (1–8 months), postoperative transesophageal echocardiography revealed mild mitral regurgitation in 2 patients and none in 13. There was a significant improvement in New York Heart Association functional class from 3.9 ± 1.1 to 1.9 ± 0.3. Mitral valve repair by posterior felt annuloplasty provides favorable results in the intermediate-term in selected patients with ischemic cardiomyopathy and severe left ventricular dysfunction.
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INTRODUCTION
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Ischemic cardiomyopathy is a known precursor of mitral regurgitation (MR) which results from dilatation of the mitral valve (MV) annulus and its ventricular apparatus, secondary to altered ventricular geometry, and it may be associated with subvalvular apparatus dysfunction.1–2 The appearance of functional MR has a distinct negative impact on the overall survival of such patients, as a result of volume overload of the already dilated left ventricle.3–4 These factors lead to progressive annular dilatation with consequent deterioration of MR, which precipitates congestive heart failure. The results of MR repair using posterior felt annuloplasty in patients with ischemic cardiomyopathy and severe left ventricular (LV) dysfunction were reviewed.
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PATIENTS AND METHODS
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Between June 2003 and January 2004, 15 consecutive patients who qualified for this study were evaluated. The inclusion criteria were significant coronary artery disease needing coronary artery bypass grafting, a left ventricular ejection fraction (LVEF) of 35% or lower, diastolic LV size of 110 mL·m–2 or more, and moderate to severe functional MR (> grade 2/4) without any organic element. There were 11 males and 4 females, aged from 43 to 72 years. All were in New York Heart Association functional class III or IV (mean class, 3.9 ± 1.1). The preoperative variables are shown in Table 1
. Two patients had intraoperative intraaortic balloon counterpulsation immediately post-induction for high pulmonary artery pressure (> 40 mm Hg systolic) and low cardiac output. All patients underwent transesophageal echocardiography preoperatively to assess the degree of MR, the anatomy of the MV along with its subvalvular apparatus and the MV coaptation depth (distance between the mitral annular plane and the plane of coaptation of the mitral leaflets). The MV coaptation depth was the main determinant in deciding if the repair procedure was necessary. In any patient, when the MV coaptation depth is less than 10 mm, a repair is indicated. Irrespective of etiology, the MV coaptation depth is directly related to the functional MR, annulus size, LVEF, and the ultimate geometry of the failing heart.5–6
The MV repair was performed through a median sternotomy with conventional cardiopulmonary bypass and hypothermic blood cardioplegia. The distal coronary artery bypass grafting was performed first. Via a left atrial approach, the MV was inspected and tested for MR using the routine saline test. By definition, there was no structural lesion of the leaflets or the chordae, as assessed preoperatively, which was confirmed intraoperatively. In 4 cases, the posterior mitral leaflet was partially tethered to the annulus and required a small incision along the length of the annulus to release it. The mitral annulus, after being released adequately, was plicated with interrupted 2/0 Ti-Cron non-pledgeted sutures (Sherwood Medical, St. Louis, MO, USA) along its entire length, ensuring that the suture bites were not too deep as this may cause puckering of the leaflet along the annulus. The plicated annulus was reinforced with a short Dacron strip, approximately 40 mm long (corresponding to a 24 ring size), going from the posteromedial to the anterolateral trigone. The MV was converted from a bicuspid to a unicuspid valve. The competence of the MV was checked again using the saline test. Once the aorta had been declamped and the heart had started ejecting, infusion of 5 µg·kg–1·min–1 of dobutamine was started, which was supported by epinephrine or norepinephrine if necessary, before or after discontinuation of cardiopulmonary bypass. Transesophageal echocardiography was continuously performed to rule out residual MR, confirm the LVEF, detect any regional wall motion abnormality, monitor the inotropic support, and measure cardiac output. Echocardiography was repeated once prior to discharge and then at 3-monthly intervals in the outpatient department.
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RESULTS
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Tables 2 and 3 show the intraoperative and postoperative data. Two patients required intraoperative intraaortic balloon counterpulsation (post-induction) for high pulmonary artery pressure (> 40 mm Hg systolic) and low cardiac output; one patient was successfully weaned from it by the 3rd postoperative day. In 2 patients, an associated anterior wall aneurysm was repaired after removal of a clot from the left ventricle. In one patient, a small associated post-infarction ventricular septal defect was closed through the left ventriculotomy. There was one death in a man with persistent low cardiac output requiring heavy inotropic and intraaortic balloon pump support. He remained in right ventricular failure, and died on the 6th postoperative day. Transesophageal echocardiography on the 1st postoperative day had revealed MR grade 1+ and LVEF of 15%.
The mean intensive care unit stay was 32.4 ± 4.6 hours, and the mean hospital stay was 9.6 ± 1.6 days. All patients were discharged on angiotensin-converting enzyme inhibitors, beta blockers, and diuretics. There was no mortality or hospital readmission of any patient during follow-up. Table 4 shows the postoperative echocardiography findings at 1–8 months, during a mean follow-up of 4.6 ± 1.2 months (Figures 1 and 2). There was a marked improvement in the New York Heart Association functional class. Although there was a reduction in cardiac volume and an improvement in LVEF, they were not statistically significant. The functional MR which had been severe (3/4 or 4/4) preoperatively, was reduced to a mean of 1.1 ± 0.6 during follow-up, corresponding to trivial to mild MR. No patient had a recurrence of MR. All of these patients had a MV coaptation depth of 10 mm or less preoperatively.
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DISCUSSION
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The development of MR is important in the natural history of ischemic cardiomyopathy.7 Left untreated, it increases the severity of heart failure and shortens life expectancy.3–4 Although some advocate revascularization alone in patients with poor LVEF, others have shown that not tackling the MR has a direct impact on the functional class and intermediate-term survival.7–10 The pathophysiology of MR secondary to cardiomyopathy is multifactorial. In the absence of any organic etiology, regurgitation is due to papillary muscle dysfunction and progressive dilatation of the mitral annulus, which result in loss of coaptation of the MV leaflets.11 As the annulus enlarges, there is a mismatch in the size of mitral leaflet required for adequate coaptation, resulting in a central jet of MR.1 Therefore, the mitral annulus and dysfunction of the papillary muscle and free LV wall beneath it are the determining factors in the grade of MR.
The LV enlargement causes displacement of the papillary muscles posterolaterally and apically, thereby increasing the distance between the annulus and the leaflets and resulting in restricted closure.12 In our opinion, moderate MR in a patient with symptomatic heart failure mandates surgical treatment. Our decision to repair the valve was based on the MV coaptation depth which is a determinant of the recurrence of MR, as studied by other groups.5 However, in selected patients, the valve may have to be replaced. The advantage of this procedure is that it restores the MV anatomy while providing a competent native valve. Although the long-term outcome of such patients is difficult to predict, this palliative approach gives satisfactory results with an improvement in the quality of life, which may have been otherwise compromised in the ongoing progress of the disease.
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ABSTRACT
INTRODUCTION
