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J Thorac Cardiovasc Surg 1994;108:871-879
© 1994 Mosby, Inc.
SURGERY FOR ACQUIRED HEART DISEASE |
Los Angeles, Calif.
This study was supported by The Burton G. Bettingen Corporation, The Robert and Claire Pasarow Foundation, and The Los Angeles Thoracic and Cardiovascular Foundation.
Address for reprints: Gregory Louis Kay, MD, 123 South Alvarado St., Los Angeles, CA 90057.
Abstract
The advantages of mitral valve repair are well established. Unfortunately, not all valves can be repaired. This presents a dilemma for the surgeon in terms of advising the patient as to the timing of operation and in decision making during operation. Patients requiring correction for pure mitral regurgitation are a heterogeneous group. By classifying the patients according to the cause of mitral regurgitation and the pathologic anatomy, we determined patterns of repair in our surgical practice for 100 consecutive patients with pure mitral regurgitation treated from January 1990 through June 1991. Patients with degenerative valve disease that spares the central portion of the anterior leaflet were likely to undergo valve repair (22/24), whereas those patients with involvement of the central portion of the anterior leaflet were likely to require replacement (15/17). This disparity may be related to the techniques of repair that were used and has spurred us to use other techniques when faced with this problem. Patients with ischemic mitral regurgitation caused by anulus dilatation were likely to undergo repair (15/17), whereas patients with ruptured papillary muscle usually underwent valve replacement (8/9). Operative mortality in this series was accurately predicated by the Parsonnet risk score. Combining knowledge of the expected operative risk and the likelihood of valve repair based on anatomic and pathologic considerations should allow the surgeon to better inform patients of their surgical options. (J THORACCARDIOVASCSURG1994;108:871-9)
Mitral valve repair for the treatment of mitral regurgitation has several advantages over valve replacement. Repair is associated with a lower likelihood of thromboembolism, hemolysis, and infectious endocarditis than replacement.
1-7 Because of the low likelihood of thromboembolism, anticoagulation is rarely required after 6 months, and so the hazards of long-term anticoagulation are avoided. Repair is also associated with improved in-hospital and long-term survivorship, especially for patients with ischemic mitral regurgitation and poor ventricular function. 8-14
Concerns over the durability of valve repair seem to have abated with reports that the 10-year durability of repair exceeds 80% for rheumatic mitral valve disease and ischemic mitral valve disease and 90% for degenerative mitral valve disease. 5,7,11,15-17
For 30 years, whenever possible, our practice has been to repair the mitral valve in all patients with mitral regurgitation. 11,18-21 Valve repair takes time and, unfortunately, not all valves can be repaired. Sometimes this can be recognized before the aortic crossclamp is removed, but sometimes not until cardiopulmonary bypass is discontinued. Whereas valve replacement is predictable in its execution, the techniques and results of valve repair vary with the patient's valve abnormality.
The conflict between improved results and predictability can be frustrating for the surgeon deciding between valve repair and valve replacement for a given patient. This decision can be especially difficult when operating on critically ill patients. It is also clear that the indication for operation will differ if repair rather than replacement is the likely outcome. When successful repair is likely, earlier operation may be appropriate. The indications for operation can be liberalized. If replacement is most likely, continued medical management may be the better long-term strategy.
Enthusiasm for mitral valve repair in the United States has grown for several reasons. First, mitral regurgitation is now most commonly due to degenerative or ischemic processes. 7,22-24 These diseased valves are especially amenable to repair and repair has demonstrated excellent long-term durability. 5-7 Second, the echocardiogram has allowed better preoperative identification of pathologic anatomy in the beating heart and has improved the intraoperative assessment of the results of repair. 25-27 This has made repair more predictable. Third, improved techniques of myocardial protection give the surgeon the time needed to attempt valve repair. Finally, a standard, powerful repertoire of techniques for valve repair has been compiled that can be used on the basis of an improved understanding of the pathologic anatomy of regurgitant mitral valves. 11,14,15,22,24,28
With these considerations in mind, we reviewed our own experience in a contemporaneous patient group.
PATIENTS AND METHOD
The time frame for this review was January 1990 through June 1991. Altogether, the records for 100 consecutive patients with pure mitral regurgitation were analyzed. Analysis was based on retrospective chart review.
Patients with mitral regurgitation associated with mitral stenosis were excluded. Patients with previous cardiac operation were included in the cohort so long as the mitral valve had not been replaced. Specifically, patients who had previous attempts at valve repair were included in the study group. A total of 23 patients in this group had undergone previous cardiac surgical procedures. Eight patients had previous mitral valve repair, four associated with myocardial revascularization, one with simple closure of a secundum atrial septal defect, and one with repair of an endocardial cushion defect. Fourteen patients had previous myocardial revascularization alone and one patient had a previous repair of a secundum atrial septal defect.
Repair was considered for all patients. The basic techniques for repair included ring annuloplasty with a flexible or rigid ring or suture annuloplasty, quadrangular resection and reconstruction for posterior leaflet defects, and papillary muscle and chordal shortening procedures. Reimplantation of the chordae and chordal transfer techniques were not used in this series of patients.
Retrograde blood cardioplegia was used in all patients for myocardial protection during the aortic crossclamp period. Continuous retrograde warm blood cardioplegia was used in 52 patients, and intermittent cold blood cardioplegia was used in 48 patients. The patients' ages ranged from 21 to 85 years (mean 65.5 ± 12.5 years). Forty patients were female.
The pathogenesis of mitral regurgitation was classified according to operative findings. When tissue was excised, pathologic examination supported the operative diagnosis. All patients were classified as having mitral regurgitation resulting from degenerative disease, ischemic disease, rheumatic disease, endocarditis, previous valve repair, or miscellaneous causes (Fig. 1). In patients with concomitant coronary artery disease, mitral regurgitation was considered to be due to degenerative disease if the typical findings of leaflet lobulation, thickening and billowing associated with torn chordae, and chordal elongation were present. The regurgitation was considered to be due to ischemic heart disease if there was papillary muscle infarction with rupture or elongation or isolated annular dilation with a normal-appearing mitral apparatus. An occasional patient with long-standing ischemic mitral regurgitation had scarring and shrinkage of a leaflet edge.
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For patients with degenerative and ischemic disease, the ability to repair the valve was analyzed on the basis of anatomic findings. For those with degenerative disease, annular dilation was noted if present. In addition it was noted whether the anterior leaflet, posterior leaflet, or both leaflets were abnormal. We divide the leaflets into six sections to identify the diseased segment (Fig. 2). For ischemic disease we noted whether the anulus was dilated or whether the papillary muscle showed elongation or rupture as a result of infarction. The numbers of patients with rheumatic disease, previously repaired valves, or endocarditis were insufficient to determine anatomic patterns of disease
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Because of the heterogeneous nature of this group, patients were risk stratified according to the system developed by Parsonnet, Dean, and Bernstein. 29 Risk factors and assigned weights are as indicated in Table I. This report's risk stratification may underestimate the actual risk because we ignored morbid obesity, diabetes, and hypertension, which are included in Parsonnet's method. Catastrophic states such as papillary muscle rupture, cardiogenic shock and acute pulmonary edema are included in Parsonnet's method, which allows scores of 10 to 50 for these factors. In this analysis we assigned only a score of 15, regardless of how desperate the situation. In a previous analysis of valve and revascularization patients we found good agreement between the Parsonnet risk score and our surgical outcomes
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RESULTS
Overall
Altogether, 48 patients (48%) in this series underwent valve repair. Hospital mortality for the entire group was 16%. Mortality was closely linked to the Parsonnet risk score (Fig. 3).
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Overall, 24 of 41 (58.5%) patients in this group underwent successful repair. The probability of repair varied according to anatomy, however. Annular dilatation was more severe in some patients but was not an important factor in determining if a valve could or could not be repaired; leaflet involvement was the most important factor.
POSTERIOR LEAFLET INVOLVEMENT.
Nineteen patients had only posterior leaflet prolapse. Seventeen patients (89.5%) underwent successful repair. Nine patients required only quadrangular resection with annular reconstruction; eight patients underwent quadrangular resection and additional annuloplasty (one suture annuloplasty, eight ring annuloplasties). Two patients required valve replacement: one patient with severe annular calcification and one patient whose entire posterior leaflet was flail (Fig. 4).
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Table II summarizes these profiles. No patient admitted to our service in this category was denied operation on the basis of being too ill.
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This group was characterized by low ejection fraction (0.33 ± 0.12), dilated left ventricle, and a high incidence of previous operations for revascularization. The average risk score was 17.9 ± 6.4. There were five deaths (29.4%). The mean ejection fraction for the patients who died is 0.28 ± 0.06. Three patients died of cardiac failure within 48 hours of operation, one patient who required postoperative balloon support died of multiple organ failure 29 days after operation, and one patient who had a perioperative cerebrovascular accident died 10 days after operation. All five patients who died underwent concurrent revascularization and three of the patients had previous revascularization.
PAPILLARY MUSCLE ELONGATION, REMOTE INFARCTION.
Two patients had successful repair by chordal shortening and ring or suture annuloplasty. Six patients either were in such critical condition or had such extensive disease that replacement was preferred. The repair rate for this group was 25%.
The average risk score was 18.1 ± 10.1 and there were two deaths (25%). One patient had a respiratory arrest because of pulmonary embolism and died 39 days after the operation. The other patient died 46 days after the operation of pulmonary failure. Both patients were doing well from a cardiac perspective.
ACUTE PAPILLARY MUSCLE RUPTURE.
Nine patients were operated on for acute mitral regurgitation caused by papillary muscle rupture. Only one patient underwent repair (11.1%); papillary muscle reimplantation was used. The remaining patients had valve replacement because of the extensiveness of the infarction and the patient's condition. Seven patients underwent concomitant revascularization.
All patients were critically ill. The average Parsonnet risk score for these patients was 32.8 ± 9.7, placing them in Parsonnet's extremely high risk group. Six patients were in cardiogenic shock before the operation; five patients required preoperative intraaortic balloon assistance. There were six deaths in this group (66.9%). Two patients died of cardiac failure within 24 hours of operation; one patient died 18 days after operation of a cerebrovascular accident at operation and three patients died of multiple organ failure after 34, 90, and 138 days.
ANNULAR DILATATION AND LEAFLET SCARRING.
Three patients were found to have annular dilatation associated with anterior leaflet scarring and one patient had annular dilatation associated with posterior leaflet scarring. Each patient had previously undergone revascularization. The ejection fractions ranged from 0.35 to 0.48. There were no valve repairs in this group because of inadequate leaflet tissue for successful repair.
The risk score for this group was 16.3 ± 7.5. There were no deaths in this group.
Reoperation after previous repair (eight patients).
Eight patients had recurrent mitral regurgitation after prior mitral valve repair. One patient underwent rerepair in this group (12.5%). In four patients the previous repair was confined to the posterior leaflet and in four patients the previous repair involved the anterior leaflet, alone or in association with posterior leaflet repair.
The interval between operations was from 6 months to 15 years. Early failures (3 years or less) occurred in three patients in whom an anterior leaflet reconstruction had been performed at the initial operation.
The Parsonnet risk score for this group was 19.9 ± 3.2. There were no deaths in this group.
Other pathogenesis (13 patients).
Two of six patients with pure rheumatic mitral regurgitation underwent repair (33.3%). Four patients had mitral regurgitation caused by infectious endocarditis, and none underwent repair. One patient with a cleft anterior leaflet underwent successful repair. Two patients were classified in the miscellaneous category. One patient had a dilated ventricle and anulus without leaflet prolapse. The patient had had pericardial stripping many years earlier. One patient had a dilated ventricle as a result of aortic regurgitation and also had a dilated anulus without leaflet prolapse. Both patients underwent successful valve repair with ring annuloplasty. Altogether, five of 13 patients (38.5%) underwent repair.
Prerepair and postrepair mitral regurgitation evaluated by intraoperative transesophageal echocardiography.
The degree of prerepair and postrepair mitral regurgitation evaluated by intraoperative transesophageal echocardiography is shown in Fig. 7. Before mitral valve repair, 34 patients had severe mitral regurgitation and 14 had moderate mitral regurgitation. After repair, mitral regurgitation was judged as absent (no) in 42 patients (88%) and mild regurgitation was left in five patients (10%). Only one patient had moderate mitral regurgitation after repair. In all other cases we replaced the mitral valve when postrepair mitral regurgitation was judged as moderate or severe. However, this patient had sickle cell anemia and she required intermittent blood exchange. We believe that any artificial valve has the potential to cause worse hemolysis than a repaired valve. There was also the problem of increased risk of endocarditis. She had severe mitral regurgitation before the operation and her mitral regurgitation was reduced significantly afterward. We decided to accept her moderate mitral regurgitation. When she was last examined 49 months after operation, she had a grade 1 apical murmur and was receiving digoxin as her only medication.
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The merits of mitral valve repair are well established. 1-14 Unfortunately, not all valves can be repaired and the uncertainty as to whether a given valve can be repaired is the single disadvantage of repair vis-à-vis replacement. Although the improved understanding of valvular pathoanatomy and expansion of the repertoire of techniques for repair have increased the number of patients who are candidates for valve repair, 11,14,15,22,24,28 some valves simply cannot be repaired because of the pathoanatomy. For other patients repair may be technically feasible but the consequences of a failed repair are unacceptable. Complex mitral valve repair can be time consuming. If success is likely, this is time well spent. If success is not likely, precious time is wasted. The decision to proceed with repair or replacement should be based on the clinical condition of the patient and the likelihood that the attempted repair will be successful. Although it is true that the more extensive the abnormality the less likely repair will be successful, certain specific pathoanatomies are also less likely to be successfully repaired. Knowing which valves are likely to be repaired and which are likely to require replacement is helpful not only for the surgeon's intraoperative decision making but for deciding the timing of operation. If repair is the likely outcome, operation can reasonably be offered earlier; if replacement is likely, operation should be delayed. This analysis of a single group's experience focuses on intraoperative success, not the durability of repair, to provide the information of the probability of repair for given valve anatomy.
Twenty-two of 24 patients with degenerative valve disease in this series who had posterior leaflet rupture or anterior leaflet involvement sparing the central anterior leaflet underwent successful repair regardless of whether annular dilatation was present or not. Because of the high successful repair rate and low surgical mortality rate in degenerative mitral regurgitation, these two pathoanatomies are amenable to repair.
Reconstruction has been less satisfactory when the central portion of the anterior leaflet is involved (2/17 valves repaired). This pattern was not clear to us until we completed this review. We have attempted to repair anterior leaflet problems with chordal shortening techniques. We believe that centrally prolapsing anterior leaflets are difficult to repair because of the role of the anterior leaflet in ensuring mitral competence. Whether after ring annuloplasty, suture annuloplasty, or quadrangular resection of the posterior leaflet, postrepair echocardiograms have shown us an essentially immobile posterior leaflet that acts as a buttress to the mobile anterior leaflet. It would be expected, then, that any repair that substantially interferes with the mobility of the anterior leaflet will fail. On the basis of this review, we would anticipate no problems reconstructing the posterior leaflet after quadrangular resection for chordal transfer to the anterior leaflet. We plan to use this technique in the future when reconstructing valves with prolapse of the central portion of the anterior leaflet.
Preservation of the mitral apparatus can be expected to best preserve ventricular function and, we believe, provide a better chance of survival for these patients than replacement. 11 Nonetheless, reports indicate mortality rates for patients with ischemic mitral regurgitation between 19% and 55%, dependent on variables in the population such as age, ventricular function, co-morbidities, and urgency of operation. 12,13,30-32 Such variables are considered in the Parsonnet score. 29 The operative mortality in our series was accurately predicted by the Parsonnet score. No comment can be made about the advantages of valve repair in this study. Because either repair or replacement dominated each of the pathoanatomic subgroups, these subgroups cannot be compared and the number of patients within a subgroup is insufficient for analysis.
Annuloplasty for ischemic mitral regurgitation caused by annular dilatation is straightforward and reproducible and was performed in 15 of 17 patients. Patients with stretched papillary muscles frequently required replacement because of the extensive involvement of the muscle with compromise of both the anterior and posterior leaflets. Patients with papillary muscle rupture are critically ill and are rarely candidates for continued medical management. All such patients in our series were operated on in extremis. We were reluctant to attempt repair in these patients because the price of spending the time on an unsuccessful repair is too high and our experience over the past 30 years has been that repair for a necrosed and ruptured papillary muscle is not predictably successful.
Patients requiring surgical correction for pure mitral regurgitation are a heterogeneous group. Mitral regurgitation is a disease of volume overload; as such, preoperative left ventricular function will significantly affect outcome. Even so, other factors (e.g., age, nutritional status, and systemic diseases such as hypertension, congestive failure, and diabetes) all affect outcome. The influence of multiple factors is further reflected in the observation that not all deaths after cardiac surgical procedures are cardiogenic. Some patients die of noncardiac complications despite hearts that are functioning well.
Operative mortality cannot be reflected accurately in a single figure. The operative mortality in this study of patients with pure mitral regurgitation was accurately predicted by the standardized risk score derived by Parsonnet and influenced by the cause of mitral regurgitation.
Risk stratification is necessary if we are to learn whether it is surgical technique or case mix that accounts for an observed outcome. Until standardized schemas for objective, prospective risk stratification are required when mortality data are reported, we will be burdened with data that are difficult to interpret and subject to manipulation.
Mortality and successful valve repair are outcomes that are functions of patient characteristics and surgical skill. Identification of the important factors that influence these outcomes will improve patient care. For patients with mitral regurgitation, risk stratification coupled with a pathoanatomic analysis should provide the framework for deciding on the timing of operation and selecting mitral repair or mitral replacement for a given patient. In analyzing medical-surgical outcome data it is useful to keep in mind a comment made by Albert Einstein, "Everything should be made as simple as possible, but not simpler."
Footnotes
Read at the Eighteenth Annual Meeting of The Western Thoracic Surgical Association, Kauai, Hawaii, June 24-27, 1992. 
References
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