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Eur J Cardiothorac Surg 2000;17:213-221
© 2000 Elsevier Science NL
a Department of Thoracic and Cardiovascular Surgery, The Cleveland Clinic Foundation, 9500 Euclid Avenue, Cleveland, OH 44195, USA
b The Kaufman Center for Heart Failure, The Cleveland Clinic Foundation, Cleveland, OH, USA
c Department of Cardiology, The Cleveland Clinic Foundation, Cleveland, OH, USA
d Department of Biostatistics and Epidemiology, The Cleveland Clinic Foundation, Cleveland, OH, USA
Corresponding author. Tel.: +1-216-444-0648; fax: +1-216-445-3272
e-mail: mccartp{at}ccf.org
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Abstract |
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 Top Abstract 1. Introduction2. Patients and methods3. Results4. Discussion5. ConclusionsAppendix A. Conference...References |
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Key Words: Mitral valve surgery • Left ventricular dysfunction
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1. Introduction |
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TopAbstract1. Introduction2. Patients and methods3. Results4. Discussion5. ConclusionsAppendix A. Conference...References |
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These observations were largely made with traditional mitral valve replacement with disruption of the subvalvular apparatus. Since being first described by Lillehei et al. [4], the importance of conservation of the subvalvular apparatus in the preservation of systolic function postoperatively has been reaffirmed in numerous clinical trials involving both mitral valve repair and chordal preserving techniques of mitral valve replacement [5–9]. More recently, this knowledge has been applied with good results in the management of mitral regurgitation in patients with ischemic and idiopathic dilated cardiomyopathies [10–13].
Furthermore, emerging left ventricular remodeling techniques, such as the Batista and the Dor procedures, often employ mitral valve repair as an integral part of the treatment of mitral regurgitation associated with a dilated cardiomyopathy. This raises the question as to how much of the favorable postoperative remodeling and symptomatic improvement is a result of the correction of the mitral regurgitation and whether mitral valve surgery alone can suffice in these patients. Thus, we set out to examine our experience in the surgical correction of mitral regurgitation in patients with severe left ventricular dysfunction.
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2. Patients and methods |
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TopAbstract1. Introduction2. Patients and methods3. Results4. Discussion5. ConclusionsAppendix A. Conference...References |
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Since one objective of this study was to examine the impact of correction of mitral regurgitation on left ventricular dimensions and function, the study group was further refined by medical chart review, excluding patients having concomitant coronary artery, aortic valve, or left ventricular remodeling (Batista and Dor) operations. Patients having concomitant tricuspid valve repairs were retained.
2.2. Patient characteristics
The mean age of the patients at the time of operation was 66±11 years (range 41–84 years); 28 (64%) patients were over the age of 65 years. Twenty-three (52%) were women. The etiology of mitral regurgitation was based on operative findings, pathological examination and preoperative echocardiographic findings and was the result of ischemia in 13 (30%), valvular causes in 18 (40%) and secondary to a dilated idiopathic cardiomyopathy in 13 (30%) patients.
All patients with ischemic mitral regurgitation had a prior remote history of myocardial infarction with nine patients having had previous coronary bypass grafts (CABG) and four having had more than one prior CABG. Coronary angiography demonstrated significant coronary artery disease but patent grafts in the nine patients with previous CABG surgery. The remaining four patients with ischemic mitral regurgitation had lesions not amenable to grafting. Mitral regurgitation in all patients was the result of regional left ventricular wall motion abnormalities with a structurally normal mitral valve and restricted leaflet motion.
All patients were receiving maximized medical therapy for congestive heart failure, including digoxin, angiotensin converting enzyme inhibitors, diuretics and more recently beta-blockers. Seven (16%) patients were initially referred for consideration of transplantation. Three patients were operated on an urgent basis, two after decompensated episodes of heart failure and one for refractory ventricular tachycardia. Every patient had been hospitalized at least once before referral for symptoms of congestive heart failure, with a mean number of admissions of 2.3±1.5 (range 1–6) in the year before surgery. However, at the initial office visit, 17 (39%) patients were relatively asymptomatic (New York Heart Association (NYHA) functional class II), whereas 27 (61%) patients had severe ongoing symptoms of dyspnoea, edema and fatigue on minimal exertion or at rest (NYHA III, n=15 (34%); NYHA IV, n=12 (27%)). The preoperative functional status was documented according to the metabolic exercise testing result if this was performed. The mean preoperative NYHA functional class for the 44 patients was 2.9±0.8.
The preoperative heart rhythm was atrial fibrillation in 27 (61%) patients, five (11%) patients were permanently paced and three (7%) patients had a preoperative history of ventricular tachycardia (one with a prior sudden death episode), with two requiring the placement of an internal defibrillator. The remaining patients were in sinus rhythm. Preoperative echocardiographic and hemodynamic data are listed in Table 1.
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Measurements of left ventricular dimensions were made from two-dimensional echocardiographic images in the parasternal long axis view and M mode echocardiography. Left ventricular volumes and ejection fraction were calculated by using a modification of Simpson's method with two apical views [14]. Stroke volume was calculated as the difference between the diastolic and systolic volumes, and ejection fraction was calculated as the ratio of stroke volume to end-diastolic volume. Left ventricular chamber sphericity was described by the ratio of maximal ventricular diameter to length. Mitral and tricuspid regurgitation were assessed with color flow Doppler; severity was graded as mild (1), moderate (2), moderate-severe (3), and severe (4). Twelve (27%) patients had 3+, and 32 (73%) 4+ mitral regurgitation.
2.4. Surgical techniques
Mitral valve reconstruction was performed through a median sternotomy in 36 (82%) patients and through a minimally invasive approach in four (9%) patients with antegrade and retrograde cold blood cardioplegia. A right thoracotomy and fibrillatory arrest was used in four (9%) patients who had undergone previous coronary artery bypass operations.
Mitral valve repair was performed in 35 (80%) patients and replacement was performed in nine (20%) patients. All patients undergoing mitral valve repair had an annuloplasty as part of the repair. Annuloplasty techniques varied during the period of the study. Techniques used included Cosgrove–Edwards annuloplasty bands (Baxter Healthcare Corp, Irvine, CA), Carpentier–Edwards classic annuloplasty ring (Baxter Healthcare), and posterior pericardial plication with autologous pericardium or Periguard graft (Baxter Healthcare). The average ring size used was 29 mm. Concomitant valve repair techniques varied according to the etiology of the mitral regurgitation and included posterior leaflet quadrangular resection in seven patients, chordal transfer in two patients, papillary shortening in one patient and edge to edge leaflet approximation (Alfieri repair) in seven patients. Concomitant tricuspid valve repair was performed in 13 (30%) patients. The mean duration of cardiopulmonary bypass was 76±29 min (range 41–193 min), with an aortic cross-clamp time of 45±28 min (range 0–143 min).
2.5. Reasons for replacement
Reasons for replacement included rheumatic mitral etiology in two patients, failed chordal transfer for a flail middle scallop of the anterior leaflet in one patient, failed leaflet cleft closure in one patient, failed repair for bileaflet leaflet prolapse secondary to ruptured chordae in one patient, and surgeon's preference in four patients. Of the nine patients undergoing replacement, eight had Carpentier–Edwards tissue prosthesis and one had a St. Jude mechanical valve prosthesis. Valve replacement in all nine patients was performed using subvalvular preserving techniques with preservation of at least one leaflet.
2.6. Follow-up
Systematic CVIR follow-up every 2 years was supplemented by telephone interview with the patient or referring cardiologist, or both. A standardized questionnaire was used for symptomatic evaluation and compared with preoperative functional status. Complete follow-up information was available in all 43 hospital survivors. Patients were followed up for a total 141 patient years, with a mean follow-up among survivors of 40±21 months, ranging from 9 months to 7 years. Postoperative admissions for congestive heart failure were documented as well as the date and cause of death. Sudden cardiac death was defined as the unexpected death of a patient who was symptomatically stable, with no obvious clinical deterioration requiring hospitalization or a change in medication within 24 h of death.
2.7. Data analysis
The endpoints for this study were (1) all cause mortality from the time of mitral valve surgery, (2) readmission for heart failure, and (3) reoperation.
All data are expressed as mean±standard deviation. Data were available preoperatively and postoperatively for certain variables and matched for comparison. The normality of the distribution of these variables and of their paired differences was considered. Where not normally distributed, the logarithmic transformation (geometric mean) was found to be normally distributed and used in the paired t-tests. Ordinal data, such as the change in the echocardiographic grade of mitral regurgitation and the postoperative change in NYHA functional class, were assessed by means of the sign rank test.
Initial survival analysis was conducted and freedom from hospital readmission for heart failure was analyzed using the non-parametric methods of Kaplan and Meier. Potential risk factors for death and readmission for heart failure were then examined with parametric, multivariable analysis in the hazard function domain [15]. The analysis used a directed technique of entry of variables into the multivariable model [16]. Because of the small sample size, variables were retained when P<0.1.
Because patients could be readmitted for heart failure more than once after surgery, the cumulative incidence of all readmission was analyzed non-parametrically by the repeated events method of Nelson [17], and parametrically by the hazard function methodology. In addition, the times to second readmission after a first were investigated by the Kaplan–Meier method and parametrically.
Variables examined included demographic data (age, gender), history and symptoms (number of admissions preoperatively for heart failure, NYHA functional class, preoperative inotropes, prior history of myocardial infarction and cardiac surgery, cardiac rhythm), non-cardiac comorbidity (diabetes, serum creatinine), etiology of mitral valve disease (ischemic, idiopathic, intrinsic valve disease), right heart catheterization data (pulmonary systolic, diastolic, mean and capillary wedge pressures), echocardiographic data (left ventricular end-systolic and -diastolic diameters and volumes, stroke volume, grade of mitral regurgitation and ejection fraction), and surgical variables (approach, valve replacement versus repair, repair technique including annuloplasty ring type, aortic cross-clamp time and cardiopulmonary bypass duration).
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3. Results |
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TopAbstract1. Introduction2. Patients and methods3. Results4. Discussion5. ConclusionsAppendix A. Conference...References |
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One in-hospital death occurred 9 days after mitral valve repair, which had consisted of closure of an anterior mitral valve leaflet cleft and annuloplasty. This patient deteriorated on the second postoperative day developing acute non-oligouric renal failure and respiratory failure with adult respiratory distress syndrome requiring veno-arterial extracorporeal membrane oxygenation. The cause of death, confirmed by autopsy examination, was severe right ventricular failure secondary to acute bronchopneumonia.
Important morbidity occurred in 12 patients (Table 2). The mean length of intensive care stay was 41±34 h, the mean duration of intubation was 20±11 h, and the mean total length of hospital stay was 9±5 days.
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0.0001) was greater than after valve replacement (1.2±0.75, P=0.06), P=0.11.
3.4. Follow-up echocardiography
Follow-up echocardiography was available for 18 patients at a mean of 2.6±2 years postoperatively (15 after repair and three after valve replacement). These were compared with the matched preoperative echocardiographs and the results are summarized in Table 4. All measurements of left ventricular size decreased and stroke volume increased, with the decrease in the end-diastolic diameter being highly significant and consequently resulting in a decrease in LV chamber sphericity. The combination of a reduction in end-diastolic volume and a significant decrease in end-systolic volume resulted in a somewhat increased stroke volume and contributed to the significant increase in the ejection fraction. This together with the decrease in mitral regurgitation has probably resulted in an increase in the forward cardiac output (not measured).
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4. Discussion |
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TopAbstract1. Introduction2. Patients and methods3. Results4. Discussion5. ConclusionsAppendix A. Conference...References |
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4.2. Management
The issues regarding the appropriate management of patients with mitral regurgitation and advanced left ventricular dysfunction are controversial. Part of this controversy arises due to difficulty in the characterization of ventricular function in the setting of mitral regurgitation because of the favorable unloading effect of the regurgitation into the low-pressure left atrium. Hence, virtually all measures of left ventricular systolic function, including the ejection fraction, tend to overestimate the true level of ventricular performance. Despite this, ejection fraction is one of the most important determinants of long-term survival after mitral valve surgery for mitral regurgitation. Patients with normal preoperative ejection fraction have an excellent postoperative survival, whereas those with moderate to severely reduced ejection fraction are at considerable risk [1–3].
In this study group the causes of the mitral regurgitation were valvular, ischemic, and secondary to idiopathic dilated cardiomyopathy. The operative mortality associated with operation for ischemic mitral regurgitation is higher than that for other forms of mitral valve regurgitation, particularly when the regurgitation is due to restricted leaflet motion secondary to severe left ventricular impairment, as was seen in all of our ischemic group [18,19]. In this series all patients survived the procedure, including the 13 (30%) patients with ischemic mitral regurgitation, with only one hospital death following closure of a cleft mitral leaflet. Furthermore, literature is scant with regard to mitral valve surgery for the correction of mitral regurgitation in patients with idiopathic dilated cardiomyopathy. It has, however, been shown that the presence of mitral regurgitation in these patients is a marker of a poor prognosis [20]. Therefore, the patients in this study represented a high-predicted mortality and yet our results show both acceptable survival and freedom from hospital admissions for heart failure.
The knowledge that preservation of the mitral subvalvular preserves left ventricular function postoperatively has made both valve repair and replacement, with preservation of the subvalvular apparatus, particularly applicable to patients with severe left ventricular dysfunction preoperatively. Bolling et al. [10–13] have shown that patients with severe ventricular dysfunction and severe mitral regurgitation secondary to dilated ischemic and idiopathic cardiomyopathies can be managed with mitral valve repair alone with very acceptable morbidity and mortality. Furthermore, they demonstrated that the left ventricle remodels to a smaller more ellipsoid ventricle with an increase in both the stroke volume and the ejection fraction postoperatively. Our results support in part those of Bolling et al. [10–13] and in addition, we have demonstrated that this management strategy can be extended to mitral regurgitation of a valvular etiology and also to include subvalvular apparatus preserving mitral valve replacement.
4.3. Postoperative remodeling
Interest has recently focused on left ventricular remodeling procedures, namely partial LV ventriculectomy (Batista), in the management of dilated cardiomyopathies. Since mitral regurgitation is commonly associated with dilated cardiomyopathy, mitral valve repair is usually an integral part of this procedure. In our Batista experience, all of the 57 patients reported had a mitral valve repair attempted (two of these required replacement) [21,22]. The question as to whether the beneficial effect seen was due to the ventriculectomy or simply the mitral repair has been a contentious one and gave us the impetus to carry out this study. From the limited follow-up echocardiography we present in this series, we saw a trend for a smaller less spherical ventricle with increased stroke volume and ejection fraction. Importantly there was no progression of the preoperative ventricular dysfunction. This we feel is achieved partly by preservation of the subvalvular apparatus during replacement and repair, and partly by correction of the volume overload on the left ventricle allowing a more physiological gradual remodeling than that achieved by left ventriculectomy. A greater number of follow-up echocardiographs, perhaps in a serial fashion, are needed to support our preliminary findings.
To compare the outcome between the left ventriculectomy and mitral valve repair and the patients presented in this series would be comparing two different patient groups. Patients in our Batista series were more acutely ill with 44% of the patients being in hospital receiving inotropes preoperatively and 95% awaiting cardiac transplantation of which 40% were status I [21,22]. Whilst three patients in this series were operated on an urgent basis (one for refractory ventricular tachycardia), the majority of the patients enjoyed a prolonged period of medical stabilization before coming to surgery with 17 (39%) in NYHA functional class II. Also the patients in the Batista series had a lower mean ejection fraction and larger left ventricles than the patients presented in this series.
4.4. Study limitations
This series excluded, by design, patients undergoing concomitant cardiac procedures (with the exception of tricuspid valve repair). Therefore, the numbers involved are small and the results of this study may not be extrapolated to patients with severe left ventricular dysfunction undergoing mitral valve surgery in association with the treatment of coronary artery disease, aortic valve disease, or other coexisting conditions. Furthermore, due to the small numbers involved with a small number of events (deaths and readmission for heart failure), it was difficult to identify significant risk factors for these events that one would have expected. The rationale for excluding patients having concomitant coronary bypass grafting was that one of the primary objectives of this study was to investigate the change in left ventricular dimensions and function following correction of the mitral regurgitation. If re-vascularization is simultaneously performed it is hard to resolve whether the improvement in dimension and function is due to the re-perfusion of ischemic myocardium or due to the correction of the left ventricular volume overload.
The non-invasive methods used to measure left ventricular volumes and function have limitations, in particular when performed in a retrospective fashion. Measurements used, particularly end-diastolic volume and diameter, are very load dependent and changes in both blood pressure or filling pressures can confound the data. Also echocardiographic follow-up was available only in 18 patients. A greater number of serial echocardiographs would be more informative with regard to postoperative remodeling.
Finally the assessment of functional status both preoperatively and postoperatively is subjective. Where possible we documented the preoperative functional status according to the metabolic exercise testing result if this was performed.
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5. Conclusions |
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TopAbstract1. Introduction2. Patients and methods3. Results4. Discussion5. ConclusionsAppendix A. Conference...References |
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Acknowledgments |
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Footnotes |
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Appendix A. Conference discussion |
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TopAbstract1. Introduction2. Patients and methods3. Results4. Discussion5. ConclusionsAppendix A. Conference...References |
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Dr Bishay: That’s a very interesting point. The actual mean duration of symptoms for the entire group was 3 years. What we did see, is some patients, particularly in the idiopathic group, who have documented left ventricular dysfunction, and perhaps 1- or 2-plus MR, who are managed medically for 2 or 3 years, that with the increase in the mitral regurgitation, they decompensated quickly and actually required hospital admissions. Some of the other patients just presented with severe left ventricular dysfunction and mitral regurgitation at the first presentation. The duration of symptoms we looked at, but it didn't seem to make any difference in terms of the outcome.
Dr M. Sussman (Johannesburg, South Africa): I have two questions if I may. The first is, do you have information differentiating your different subgroups, the idiopathic dilated cardiomyopathies versus the primary valvular disease with subsequent LV dysfunction, because I would imagine the outcomes should be different?
And the second is, how many of the patients, if any, needed mechanical assistance after surgery?
Dr Bishay: In answer to your first question, we did. I must point out however, obviously that with 44 patients it was hard to get statistical significance. We did look at the etiology as a risk factor for both readmissions for heart failure and death, and we didn’t see any significant difference between the etiologies.
Only one patient required an intra-aortic balloon pump postop. No patients required LVAD support.
Dr R. Dion (Brussels, Belgium): I would like to know if you can give an idea of the LV end-diastolic diameter of these patients? And is there a correlation with the postoperative outcome, for instancein patients above or under 70 mm? Indeed, if the results are less good in these patients with severe LV dilatation, shouldn't we add a resection, a Batista?
Dr Bishay: The mean end-diastolic diameter for the group was 6.6 cm and the end-systolic was 5.1 cm. Now, I think this group is very different, for example, from the Batista group where the inclusion criteria was an end-diastolic diameter greater than 7 cm. So these patients had definitely smaller hearts than that from our Batista experience.
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References |
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TopAbstract1. Introduction2. Patients and methods3. Results4. Discussion5. ConclusionsAppendix A. Conference...References |
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T. A. Timek, P. Dagum, D. T. Lai, D. Liang, G. T. Daughters, F. Tibayan, N. B. Ingels Jr, and D. C. Miller Tachycardia-induced cardiomyopathy in the ovine heart: Mitral annular dynamic three-dimensional geometry J. Thorac. Cardiovasc. Surg., February 1, 2003; 125(2): 315 - 324. [Abstract] [Full Text] [PDF]
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A. M. Gillinov and D. M. Cosgrove III Mitral Valve Repair Card. Surg. Adult, January 1, 2003; 2(2003): 933 - 950. [Full Text]
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V. Badhwar and S. F. Bolling Nontransplant Surgical Options for Heart Failure Card. Surg. Adult, January 1, 2003; 2(2003): 1515 - 1526. [Full Text]
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L. Menicanti, M. Di Donato, A. Frigiola, G. Buckberg, C. Santambrogio, M. Ranucci, and D. Santo Ischemic mitral regurgitation: Intraventricular papillary muscle imbrication without mitral ring during left ventricular restoration J. Thorac. Cardiovasc. Surg., June 1, 2002; 123(6): 1041 - 1050. [Abstract] [Full Text] [PDF]
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K. Kuwaki, M. Tsukamoto, K. Komatsu, and T. Abe Endoventricular circular patch plasty for end-stage valvular cardiomyopathy Eur. J. Cardiothorac. Surg., October 1, 2001; 20(4): 886 - 888. [Abstract] [Full Text] [PDF]
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A. M. Calafiore, S. Gallina, M. Di Mauro, F. Gaeta, A. L. Iaco, S. D'Alessandro, V. Mazzei, and G. Di Giammarco Mitral valve procedure in dilated cardiomyopathy: repair or replacement? Ann. Thorac. Surg., April 1, 2001; 71(4): 1146 - 1152. [Abstract] [Full Text] [PDF]
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