- Email: [email protected]
Results of valve reconstruction for mitral regurgitation secondary to mitral valve prolapse
Results of Valve Reconstruction for Mitral Regurgitation Secondary to Mitral Valve Prolapse PATRICIA A. PENKOSKE, MD, F. HENRY ELLIS, Jr., MD, PhD, SIDNEY ALEXANDER, and ELTON WATKINS,
MD,
Jr., MD
Mitral valve prolapse (MVP), often the result of myxomatous degeneration of the mitral valve, is the most commonly known pathologic entity leading to pure mitral regurgitation (MR). Reconstruction of the mitral valve rather than replacement is particularly applicable to this pathologic defect, but is not often used in the U.S. Experience with reconstruction of the mitral valve for MR secondary to MVP during the period January 1970 to January 1984 was reviewed. A total of 479 patients with mitral valve disease underwent operation during this period, 82 (17 % ) of whom had MR secondary to MVP. Thirty-one patients (6%) had valve reconstruction by a technique of leaflet plication and posteromedial anuloplasty. Eleven of these patients had associated cardiac disease requiring correction: 2 requiring
aortic valve replacement and 9 requiring coronary artery bypass grafting procedures. One hospital death (3%) and 6 late deaths (19%) occurred, of which only 3 were related to cardiac factors. Major complications included recurrent MR in 5 patients and cerebral embolus in 1 patient. The adjusted 5-year survival rate was 89 ZIZ6 (mean ZJZ standard error of the mean), and the overall survival rate of patients free of cardiac-related complications was 73 f 9%. Thus, reconstruction of the mitral valve is a highly effective surgical approach to the management of symptomatic patients with MR secondary to MVP, and its use is favored over replacement in the management of these patients.
Mitral valve prolapse (MVP), often the result of myxomatous degeneration of the mitral valve and sometimes described as the floppy valve, is the most usual pathologic entity that leads to pure mitral regurgitation (MR).l Although replacement of the valve is the technique most frequently used in the U.S. for surgical correction of this defect, its pathology is such that reconstruction of the valve is often technically feasible. Many surgeons, particularly those from England and Europe, prefer reconstruction to replacement to minimize the threat of thromboembolicand warfarin-related complications that accompany the use of prosthetic valves. We present our experience with valve reconstruction for pure MR in patients with MVP with and without ruptured chordae tendineae.
Methods
(Am J Cardiol 1985;55:735-738)
Case material: From January 1970 to January 1984,479 patients with disease of the mitral valve were operated on at the New England Deaconess Hospital, Boston. Of these patients, 82 (17%) had MR secondary to MVP, and in 31 patients (6%) valve reconstruction was performed (Fig. 1). Clidical characteristics: The median age of patients was 63 years, and 17 were men and 14 were women. Twenty-seven
patients were in New York Heart Association (NYHA) class III, 2 were in class II and 2 were in class IV. At presentation, 18 patients had atria1 fibrillation, and the others had normal sinus rhythm. Eleven had associated cardiac disease requiring correction at the time of valve reconstruction: 2 requiring aortic valve replacement and 9 having coronary artery bypass grafting procedures. Pathology: Appearance of the mitral valve was similar in all patients. The surface area of the valve leaflets was increased. The chordae tendineae were lengthened and thinned and the interchordal spaces widened, resulting in ballooning of the tissue of the leaflets and giving them a hooded appearance. The posterior leaflet was involved more frequently (22 patients) than the anterior leaflet (8 patients); in only 1 patient were both leaflets involved. Chordal rupture was present in 19 of the 31 patients and usually involved 1 to 3 chordae. Anular dilatation was present in most patients. No patient had mitral stenosis.
From the Section of Thoracic and Cardiovascular Surgery, Section of Cardiology, and Sias Surgical Research Unit, Lahey Clinic Medical Center, Burlington, Massachusetts, and the Division of Thoracic and Cardiovascular Surgery, New England Deaconess Hospital, and Harvard Medical School, Boston, Massachusetts. Manuscript received May 23, 1984; revised manuscript received November 19, 1994, accepted November 20, 1984. Address for reprints: F. Henry Ellis, Jr., MD, PhD, Section of Thoracic and Cardiovascular Surgery, Lahey Clinic Medical Center, 41 Mall Road, Box 541, Burlington, Massachusetts 01805. 735
736
VALVE
RECONSTRUCTION
FOR MITRAL
REGURGITATION
Surgical techniques: The reconstructive procedures were performed by one of us (FHE). When reconstructive attempts failed because of valve distortion, the valve was replaced. Competence was restored by the technique originally described by McGoon,2 which essentially excludes the flail portion of the leaflet by plication with sutures of fine nonabsorbable material that approximate the points on the leading edge of the involved leaflet to which normal chordae remain attached (Fig. 2). The procedure serves the dual purpose of stabilizing the flail segment and decreasing the surface area of the leaflet. To assure coaptation of the 2 leaflets, anuloplasty was performed by the figure-eight suture technique when anular dilatation was recognized (Fig. 3). One figureeight anuloplasty suture was used posteromedially in 14 patients. Additional sutures were needed posteromedially in 4 patients, and 9 patients also required an anuloplasty suture placed anterolaterally. Clefts identified in the leading edge of the posterior leaflet were approximated with interrupted sutures of fine nonabsorbable material in 3 patients. Narrowing of the mitral anulus is an essential part of the reconstructive procedure. The goal is to achieve a degree of overcorrection in anticipation of possible subsequent loosening of the anuloplasty stitch. An opening of 2 fingerbreadths is considered ideal, and competence is tested intraoperatively by intraventricular injection of saline solution under pressure using a handheld syringe. Follow-up data: All surviving patients were available for follow-up evaluation either by personal interview or~by letter within the past 6 months. The mean follow-up interval was 44 months. Factors considered in analysis of results included NYHA classification, cardiac rhythm, presence or absence of apical systolic murmur, thromboembolic and warfarin-related complications, valvular dysfunction, need for repeat operation and death. Statistical methods: Survival patterns and actuarial analysis of complication-free periods were determined by life-table analysis with calculation of standard error values.3 The significance of differences between life-table or complication-incidence plots was determined by logrank analysis.4 Results Complications:
Mortality:
One (3%) of the patients
died in the hospital. This patient with combined aortic and mitral disease was in NYHA class IV. Death occurred 12 days after replacement of the aortic valve and reconstruction of the mitral valve from complications of a cerebrovascular accident. during the perioperative period.
q
Reumstmctim
Six late deaths (19%) occurred, of which only 3 were related to cardiac factors. One patient. died after valve replacement that was undertaken because of persistent MR 2 months after reconstruction. One patient died suddenly at home 4 months after operation, presumably of an arrhythmia before which he was well, and 1 patient. who refused repeat surgery despite residual MR died from heart failure 2 months after reconstruction. The other 3 late deaths were caused by noncardiac factors: 1 patient died after closure of a colostomy 28 months postoperatively, 1 died from a ruptured abdominal aneurysm 9 months after valve reconstruction, and 1 died from unspecified causes 2 years after operation. The actuarial overall 5-year survival rate was 78 f 8% (mean f standard error of the mean), and the adjusted figure excluding non-cardiac-related deaths was 89 f 6% (Fig. 4). Persistent or recurrent mitral regurgitation: Five patients (16%) had either persistent or recurrent MR postoperatively. One of these was the patient who refused to undergo repeat operation and later died from cardiac failure. Another patient had successful repeat operation and repeat valvuloplasty 4 months after the original operation and is well 3 years later. Three patients with recurrent MR required replacement of the mitral valve at 6,11 and 20 months, respectively, after reconstruction. One of these patients died postoperatively and the other 2 are well. Of the 21 surviving patients who did not require repeat operation, 1 has a residual systolic murmur of significance (greater than grade 2 on the basis of 1 to 6), and she is well 12 years after valve reconstruction. Thromboembolic or warfarin-related complications: One patient who had atria1 fibrillation but was not taking anticoagulant medication had a cerebrovascular accident 6 days after operation.
All patients
now receive anticoagulant drugs for at least 6 weeks postoperatively. No bleeding problem was identified in any patient. Cardiac status: All 24 surviving patients are in NYHA class I or II. Twenty patients remained free of cardiac-related complication for an average of 33/4follow-up years. Actuarial curves of survival free of cardiac-related complication are displayed in Figure 4.
(31)
FIGURE 1. Distribution of operations on the mitral valve at the New England Deaconess Hospital by years 1970 to 1984. Shaded and cross-hatched areas represent reconstruction and replacement operations, respectively, performed for mitral regurgitation secondary to mitral valve prolapse.
FIGURE 2. Technique of reconstruction of the mitral valve. A, appearance of valve with ruptured chordae tendineae to midpoint of posterior leaflet (PL). 8, initial plicating suture has been placed. AL = anterior leaflet.
March 1, 1985 THE AMERICAN JOURNAL OF CARDIOLOGY Volume 55
Discussion Mitral valve prolapse is the leading cause of isolated MR and accounts for 10 to 20%5of all open operations on the mitral valve. Since first described in 1958,6the billowing or floppy valve syndrome has been the subject of numerous attempts to characterize the defect or defects leading to it. The primary pathologic process in this condition, according to Guthrie and Edwards,7 is not degeneration but an actual increase in thickness of the spongiosa with acid mucopolysaccharide deposition and focal infiltration of the fibrosa that lead to weakness of this central core. The leaflets increase initially in width and length, especially between sites of chordal attachment, and this gives them a hooded appearance. In addition to chordal elongation, actual rupture of the chordae tendineae is a frequent complication and occurred in 19 of our 31 patients. The chordae attached to the prolapsing portion of the valve are those susceptible to exposure. Congenital clefts of the posterior leaflet, which were present in one-third of our patients, also contribute to incompetence of the mitral valve.8 With few exceptions,s-l4 little enthusiasm is expressed in the U.S. for valve reconstruction in the management of MR in contrast to the wide experience reported from England and Europe.15-20The effort of Carpentier et al 21-24to classify and treat diseasesof the mitral valve has led the field in technical inventiveness and number of patients treated. The experience that we describe is modest in number of patients, but it does emphasize some of the advantages of valve reconstruction over replacement when applied to patients with MVP. The technique is accompanied by a low hospital mortality rate and a low late mortality rate when only deaths caused by cardiac-related factors are considered. Such events as thromboembolic complications and warfarin-related problems are minimal. The major complication of the technique we use is persistent or recurrent MR occurring in 5 of the 30 patients surviving operation. However, only 2 of these 5 patients were among the 6 late
737
deaths. Three are currently well after valve replacement or repair. Persistent or recurrent MR can be reduced by ensuring correction of anular dilatation at the time of operation. The degree of anular dilatation was not appreciated in 4 patients in this series, and posteromedial anuloplasty was not used. In 3 of these patients, persistent or recurrent MR developed. The Carpentier2i ring or excision of the prolapsing portion of the posterior leaflet and placement of anuloplasty sutures at the site of the suture approximation of the surgically produced defect in the leaflet have been used to abolish anular dilatation.14 We have not had experience with such techniques. Although comparison of the results of reconstruction with those of replacement for MVP in our hospital is tempting, the groups are not entirely similar because almost all of the replacement operations were performed by different surgeons and conceivably on patients with different clinical presentations. However, the crude hospital and late mortality rates were higher among the replacement group than among the reconstruction group, and thromboembolic and warfarinrelated complications were more numerous. When the overall actuarial survival rates and complication-free survival rates were compared the differences did not reach statistical significance because of the small size of the reconstruction series. Other workers17p20,25 have performed such comparative studies, and the results favoring replacement over reconstruction are impressive. We believe that valve reconstruction has demonstrable advantages over replacement in the management of MR secondary to MVP. When proper techniques are applied to properly selected patients the risk of the operation is low, and long-term uncomplicated survival rates are high. Acknowledgment: We are grateful to Gerald J. Heatley of the Sias Surgical Research Unit, Lahey Clinic Medical Center, for statistical computations, and to members of the Overholt Thoracic Clinic, New England Deaconess Hospital,
Survival %
,
‘j!g!g[
i,,,,,,,~------~~--~~--~~~ I I 73.0?8.8%
I
60 i
0
I 0
2
I
I 4
I
I 6
I
I 8
I
I 10
ti
I
I
I
12
Time (years)
FIGURE 3. Technique of reconstruction of the mitral valve. A, completion of plication of redundant everting portion of posterior leaflet and placement of figure-eight posteromedial anuloplasty suture. B, completed procedure showing exclusion of the everting redundant portion of posterior leaflet and narrowing of the dilated mitral ring.
FIGURE 4. Actuarial survival after mitral valve reconstruction for mitral regurgitation in the years 1970 to 1984. Adjusted survival excluding non-cardiac-related deaths (dotted line), overall survival (solid line) and survival free of .cardiac-related complications (broken line). SEM = standard error of the mean.
738
VALVE
RECONSTRUCTION
FOR MITRAL
REGURGITATION
and Peter R. Maggs, MD, for permission to include patients operated on by them. References 1. Wailer BF, Morrow AG, Maron BJ, Del Negro AA, Kent KM, McGrath FJ, Wallace RB, McIntosh CL, Roberts WC. Etiology of clinically isolated, Severe, chronic, pure mitral regurgitation: analysis of 97 patients over 30 years of age having mitral valve replacement. Am Heart J 1982;104: 276-288. 2. McGoon DC. Repair of mitral insufficiency due to ruptured chordae tendineae. J Thorac Cardiovasc Surg 1960;39:357-362. 3. Rothman KJ, Boice JD Jr. Epidemiologic Analysis with a Programmable Calculator. 1st ed. Boston: Epidemiology Resources Inc, 1982. efficient rank invariant test procedures. J 4. Pet0 FL Pet0 J. ASVt?WtOtiCallV R Stat Sot 1972; i&A: 185-267. 5. McKay R, Yacoub MH. Clinical and pathological findings in patients with “flooov” valves treated suraicallv. ” _ Circulation 1973:47.48:suool., lll:lll63-id-73. Fernex M, Fernex C. La degenerescence mucoide des valvules mitrales: ses repercussions fonctionnelles. Helv Med Acta 1958;25:694-705. Guthrie RB, Edwards JE. Pathology of the myxomatous mitral valve: nature, secondary changes and complications, Minn Med 1976;59:637-647. McEnany MT, English TA, Ross DN. The congenitally cleft posterior mitral valve leaflet. Ann Thorac Surg 1973;16:281-292. Ellis FH Jr, Frye RL, McGoon DC. Results of reconstructive operations for mitral insufficiency due to ruptured chord ae tendineae. Surgery 1966;59: 165-172. IO. Wychulis AR, Connolly DC, Ellis FH Jr. Open mitral valve reconstruction: review of 232 operations. Arch Surg 1970;101:332-337. 11. Kay JH, Zubiate P, Mendez MA, Vanstrom N, Yokoyama T. Mitral valve repair for siqnificant mitral insufficiency. Am Heart J 1978;96:253-262. 12. Bdnchek LI.-Correction of mitral valve disease without valve replacement. Am Heart J 1982:104:865-868. 13. Frater RWM, Gabbay S, Shore D, Factor S, Strom J. Reproducible re-
14. 15.
16. 17. 18. 19. 20. 21. 22. 23.
24. 25.
placement of elongated or ruptured mitral valve chordae. Ann Thorac Surg 1983;35:14-28. Nunley DL, Starr A. The evolution of reparative techniques for the mitral valve. Ann Thorac Surg 1984;37:393-397. Duran CG, Pomar JL, Revuelta JM, Gallo I, Poveda J, Ochoteco A, Ubago JL. Conservative operation for mitral insufficiency: critical analysis supported by postoperative hemodynamic studies of 72 patients. J Thor& Cardiovasc Sura 1980:79:326-337. Shore DF, Wong P, Paneth M. Results of mitral valvuloplasty with a suture plication technique. J Thorac Cardiovasc Surg 1980;79:349-357. Perier PM, DeLoche A, Carpentier AF. Comparative evaluation of mitral valve repair and mitral valve replacement using Starr, Bjork and porcine valve prostheses (abstr). Circulation 1983;68:suppl lll:lll-319. Lessana A, Viet TT, Ades F, Kara SM, Ameur A, Ruftenach A, Guerin F, Herreman F, DeGeorges M. Mitral reconstructive operations: a series of 130 consecutive cases. J Thorac Cardiovasc Surg 1983;86:553-561. Adebo OA, Ross JK. Conservative surgery for mitral valve disease: clinical and echocardiographic analysis of results. Thorax 1983;38:565-571. Yacoub M, Halim M, Radley-Smith R, McKay R, Nijveld A, Towers M. Surgical treatment of mitral regurgitation caused by floppy valves: repair versus replacement. Circulation 1981;64:suppl ll:ll-210-11-216. Carpentier A, Deloche A, Dauptain J, Soyer R, Blondeau P, Piwnica A, Dubost C. A new reconstructive operation for correction of mitral and tricuspid insufficiency. J Thorac Cardiovasc Surg 1971;61:1-13. Carpentier A, Relland J, Deloche A, Fabiani J-N, d’Allaines C, Blondeau P, Piwnica A, Chauvaud S, Dubost C. Conservative management of the prolapsed mitral valve. Ann Thorac Surg 1978;26:294-302. Carpentier A, Chauvaud S, Fabiani JN, Deloche A, Relland J, Lessana A, d’Allaines C, Blondeau P, Piwnica A, Dubost C. Reconstructive surgery of mitral valve incompetence: ten-year appraisal. J Thorac Cardiovasc Surg 1980;79:338-348. Carpentier A. Cardiac valve surgery: the “French correction.” J Thorac Cardiovasc Surg 1983;86:323-337. Adebo OA, Ross JK. Surgical treatment of ruptured mitral valve chordae: a comparison between valve replacement and valve repair. J Thorac Cardiovasc Surg 1984;32:139-142.
MD,
Jr., MD
Mitral valve prolapse (MVP), often the result of myxomatous degeneration of the mitral valve, is the most commonly known pathologic entity leading to pure mitral regurgitation (MR). Reconstruction of the mitral valve rather than replacement is particularly applicable to this pathologic defect, but is not often used in the U.S. Experience with reconstruction of the mitral valve for MR secondary to MVP during the period January 1970 to January 1984 was reviewed. A total of 479 patients with mitral valve disease underwent operation during this period, 82 (17 % ) of whom had MR secondary to MVP. Thirty-one patients (6%) had valve reconstruction by a technique of leaflet plication and posteromedial anuloplasty. Eleven of these patients had associated cardiac disease requiring correction: 2 requiring
aortic valve replacement and 9 requiring coronary artery bypass grafting procedures. One hospital death (3%) and 6 late deaths (19%) occurred, of which only 3 were related to cardiac factors. Major complications included recurrent MR in 5 patients and cerebral embolus in 1 patient. The adjusted 5-year survival rate was 89 ZIZ6 (mean ZJZ standard error of the mean), and the overall survival rate of patients free of cardiac-related complications was 73 f 9%. Thus, reconstruction of the mitral valve is a highly effective surgical approach to the management of symptomatic patients with MR secondary to MVP, and its use is favored over replacement in the management of these patients.
Mitral valve prolapse (MVP), often the result of myxomatous degeneration of the mitral valve and sometimes described as the floppy valve, is the most usual pathologic entity that leads to pure mitral regurgitation (MR).l Although replacement of the valve is the technique most frequently used in the U.S. for surgical correction of this defect, its pathology is such that reconstruction of the valve is often technically feasible. Many surgeons, particularly those from England and Europe, prefer reconstruction to replacement to minimize the threat of thromboembolicand warfarin-related complications that accompany the use of prosthetic valves. We present our experience with valve reconstruction for pure MR in patients with MVP with and without ruptured chordae tendineae.
Methods
(Am J Cardiol 1985;55:735-738)
Case material: From January 1970 to January 1984,479 patients with disease of the mitral valve were operated on at the New England Deaconess Hospital, Boston. Of these patients, 82 (17%) had MR secondary to MVP, and in 31 patients (6%) valve reconstruction was performed (Fig. 1). Clidical characteristics: The median age of patients was 63 years, and 17 were men and 14 were women. Twenty-seven
patients were in New York Heart Association (NYHA) class III, 2 were in class II and 2 were in class IV. At presentation, 18 patients had atria1 fibrillation, and the others had normal sinus rhythm. Eleven had associated cardiac disease requiring correction at the time of valve reconstruction: 2 requiring aortic valve replacement and 9 having coronary artery bypass grafting procedures. Pathology: Appearance of the mitral valve was similar in all patients. The surface area of the valve leaflets was increased. The chordae tendineae were lengthened and thinned and the interchordal spaces widened, resulting in ballooning of the tissue of the leaflets and giving them a hooded appearance. The posterior leaflet was involved more frequently (22 patients) than the anterior leaflet (8 patients); in only 1 patient were both leaflets involved. Chordal rupture was present in 19 of the 31 patients and usually involved 1 to 3 chordae. Anular dilatation was present in most patients. No patient had mitral stenosis.
From the Section of Thoracic and Cardiovascular Surgery, Section of Cardiology, and Sias Surgical Research Unit, Lahey Clinic Medical Center, Burlington, Massachusetts, and the Division of Thoracic and Cardiovascular Surgery, New England Deaconess Hospital, and Harvard Medical School, Boston, Massachusetts. Manuscript received May 23, 1984; revised manuscript received November 19, 1994, accepted November 20, 1984. Address for reprints: F. Henry Ellis, Jr., MD, PhD, Section of Thoracic and Cardiovascular Surgery, Lahey Clinic Medical Center, 41 Mall Road, Box 541, Burlington, Massachusetts 01805. 735
736
VALVE
RECONSTRUCTION
FOR MITRAL
REGURGITATION
Surgical techniques: The reconstructive procedures were performed by one of us (FHE). When reconstructive attempts failed because of valve distortion, the valve was replaced. Competence was restored by the technique originally described by McGoon,2 which essentially excludes the flail portion of the leaflet by plication with sutures of fine nonabsorbable material that approximate the points on the leading edge of the involved leaflet to which normal chordae remain attached (Fig. 2). The procedure serves the dual purpose of stabilizing the flail segment and decreasing the surface area of the leaflet. To assure coaptation of the 2 leaflets, anuloplasty was performed by the figure-eight suture technique when anular dilatation was recognized (Fig. 3). One figureeight anuloplasty suture was used posteromedially in 14 patients. Additional sutures were needed posteromedially in 4 patients, and 9 patients also required an anuloplasty suture placed anterolaterally. Clefts identified in the leading edge of the posterior leaflet were approximated with interrupted sutures of fine nonabsorbable material in 3 patients. Narrowing of the mitral anulus is an essential part of the reconstructive procedure. The goal is to achieve a degree of overcorrection in anticipation of possible subsequent loosening of the anuloplasty stitch. An opening of 2 fingerbreadths is considered ideal, and competence is tested intraoperatively by intraventricular injection of saline solution under pressure using a handheld syringe. Follow-up data: All surviving patients were available for follow-up evaluation either by personal interview or~by letter within the past 6 months. The mean follow-up interval was 44 months. Factors considered in analysis of results included NYHA classification, cardiac rhythm, presence or absence of apical systolic murmur, thromboembolic and warfarin-related complications, valvular dysfunction, need for repeat operation and death. Statistical methods: Survival patterns and actuarial analysis of complication-free periods were determined by life-table analysis with calculation of standard error values.3 The significance of differences between life-table or complication-incidence plots was determined by logrank analysis.4 Results Complications:
Mortality:
One (3%) of the patients
died in the hospital. This patient with combined aortic and mitral disease was in NYHA class IV. Death occurred 12 days after replacement of the aortic valve and reconstruction of the mitral valve from complications of a cerebrovascular accident. during the perioperative period.
q
Reumstmctim
Six late deaths (19%) occurred, of which only 3 were related to cardiac factors. One patient. died after valve replacement that was undertaken because of persistent MR 2 months after reconstruction. One patient died suddenly at home 4 months after operation, presumably of an arrhythmia before which he was well, and 1 patient. who refused repeat surgery despite residual MR died from heart failure 2 months after reconstruction. The other 3 late deaths were caused by noncardiac factors: 1 patient died after closure of a colostomy 28 months postoperatively, 1 died from a ruptured abdominal aneurysm 9 months after valve reconstruction, and 1 died from unspecified causes 2 years after operation. The actuarial overall 5-year survival rate was 78 f 8% (mean f standard error of the mean), and the adjusted figure excluding non-cardiac-related deaths was 89 f 6% (Fig. 4). Persistent or recurrent mitral regurgitation: Five patients (16%) had either persistent or recurrent MR postoperatively. One of these was the patient who refused to undergo repeat operation and later died from cardiac failure. Another patient had successful repeat operation and repeat valvuloplasty 4 months after the original operation and is well 3 years later. Three patients with recurrent MR required replacement of the mitral valve at 6,11 and 20 months, respectively, after reconstruction. One of these patients died postoperatively and the other 2 are well. Of the 21 surviving patients who did not require repeat operation, 1 has a residual systolic murmur of significance (greater than grade 2 on the basis of 1 to 6), and she is well 12 years after valve reconstruction. Thromboembolic or warfarin-related complications: One patient who had atria1 fibrillation but was not taking anticoagulant medication had a cerebrovascular accident 6 days after operation.
All patients
now receive anticoagulant drugs for at least 6 weeks postoperatively. No bleeding problem was identified in any patient. Cardiac status: All 24 surviving patients are in NYHA class I or II. Twenty patients remained free of cardiac-related complication for an average of 33/4follow-up years. Actuarial curves of survival free of cardiac-related complication are displayed in Figure 4.
(31)
FIGURE 1. Distribution of operations on the mitral valve at the New England Deaconess Hospital by years 1970 to 1984. Shaded and cross-hatched areas represent reconstruction and replacement operations, respectively, performed for mitral regurgitation secondary to mitral valve prolapse.
FIGURE 2. Technique of reconstruction of the mitral valve. A, appearance of valve with ruptured chordae tendineae to midpoint of posterior leaflet (PL). 8, initial plicating suture has been placed. AL = anterior leaflet.
March 1, 1985 THE AMERICAN JOURNAL OF CARDIOLOGY Volume 55
Discussion Mitral valve prolapse is the leading cause of isolated MR and accounts for 10 to 20%5of all open operations on the mitral valve. Since first described in 1958,6the billowing or floppy valve syndrome has been the subject of numerous attempts to characterize the defect or defects leading to it. The primary pathologic process in this condition, according to Guthrie and Edwards,7 is not degeneration but an actual increase in thickness of the spongiosa with acid mucopolysaccharide deposition and focal infiltration of the fibrosa that lead to weakness of this central core. The leaflets increase initially in width and length, especially between sites of chordal attachment, and this gives them a hooded appearance. In addition to chordal elongation, actual rupture of the chordae tendineae is a frequent complication and occurred in 19 of our 31 patients. The chordae attached to the prolapsing portion of the valve are those susceptible to exposure. Congenital clefts of the posterior leaflet, which were present in one-third of our patients, also contribute to incompetence of the mitral valve.8 With few exceptions,s-l4 little enthusiasm is expressed in the U.S. for valve reconstruction in the management of MR in contrast to the wide experience reported from England and Europe.15-20The effort of Carpentier et al 21-24to classify and treat diseasesof the mitral valve has led the field in technical inventiveness and number of patients treated. The experience that we describe is modest in number of patients, but it does emphasize some of the advantages of valve reconstruction over replacement when applied to patients with MVP. The technique is accompanied by a low hospital mortality rate and a low late mortality rate when only deaths caused by cardiac-related factors are considered. Such events as thromboembolic complications and warfarin-related problems are minimal. The major complication of the technique we use is persistent or recurrent MR occurring in 5 of the 30 patients surviving operation. However, only 2 of these 5 patients were among the 6 late
737
deaths. Three are currently well after valve replacement or repair. Persistent or recurrent MR can be reduced by ensuring correction of anular dilatation at the time of operation. The degree of anular dilatation was not appreciated in 4 patients in this series, and posteromedial anuloplasty was not used. In 3 of these patients, persistent or recurrent MR developed. The Carpentier2i ring or excision of the prolapsing portion of the posterior leaflet and placement of anuloplasty sutures at the site of the suture approximation of the surgically produced defect in the leaflet have been used to abolish anular dilatation.14 We have not had experience with such techniques. Although comparison of the results of reconstruction with those of replacement for MVP in our hospital is tempting, the groups are not entirely similar because almost all of the replacement operations were performed by different surgeons and conceivably on patients with different clinical presentations. However, the crude hospital and late mortality rates were higher among the replacement group than among the reconstruction group, and thromboembolic and warfarinrelated complications were more numerous. When the overall actuarial survival rates and complication-free survival rates were compared the differences did not reach statistical significance because of the small size of the reconstruction series. Other workers17p20,25 have performed such comparative studies, and the results favoring replacement over reconstruction are impressive. We believe that valve reconstruction has demonstrable advantages over replacement in the management of MR secondary to MVP. When proper techniques are applied to properly selected patients the risk of the operation is low, and long-term uncomplicated survival rates are high. Acknowledgment: We are grateful to Gerald J. Heatley of the Sias Surgical Research Unit, Lahey Clinic Medical Center, for statistical computations, and to members of the Overholt Thoracic Clinic, New England Deaconess Hospital,
Survival %
,
‘j!g!g[
i,,,,,,,~------~~--~~--~~~ I I 73.0?8.8%
I
60 i
0
I 0
2
I
I 4
I
I 6
I
I 8
I
I 10
ti
I
I
I
12
Time (years)
FIGURE 3. Technique of reconstruction of the mitral valve. A, completion of plication of redundant everting portion of posterior leaflet and placement of figure-eight posteromedial anuloplasty suture. B, completed procedure showing exclusion of the everting redundant portion of posterior leaflet and narrowing of the dilated mitral ring.
FIGURE 4. Actuarial survival after mitral valve reconstruction for mitral regurgitation in the years 1970 to 1984. Adjusted survival excluding non-cardiac-related deaths (dotted line), overall survival (solid line) and survival free of .cardiac-related complications (broken line). SEM = standard error of the mean.
738
VALVE
RECONSTRUCTION
FOR MITRAL
REGURGITATION
and Peter R. Maggs, MD, for permission to include patients operated on by them. References 1. Wailer BF, Morrow AG, Maron BJ, Del Negro AA, Kent KM, McGrath FJ, Wallace RB, McIntosh CL, Roberts WC. Etiology of clinically isolated, Severe, chronic, pure mitral regurgitation: analysis of 97 patients over 30 years of age having mitral valve replacement. Am Heart J 1982;104: 276-288. 2. McGoon DC. Repair of mitral insufficiency due to ruptured chordae tendineae. J Thorac Cardiovasc Surg 1960;39:357-362. 3. Rothman KJ, Boice JD Jr. Epidemiologic Analysis with a Programmable Calculator. 1st ed. Boston: Epidemiology Resources Inc, 1982. efficient rank invariant test procedures. J 4. Pet0 FL Pet0 J. ASVt?WtOtiCallV R Stat Sot 1972; i&A: 185-267. 5. McKay R, Yacoub MH. Clinical and pathological findings in patients with “flooov” valves treated suraicallv. ” _ Circulation 1973:47.48:suool., lll:lll63-id-73. Fernex M, Fernex C. La degenerescence mucoide des valvules mitrales: ses repercussions fonctionnelles. Helv Med Acta 1958;25:694-705. Guthrie RB, Edwards JE. Pathology of the myxomatous mitral valve: nature, secondary changes and complications, Minn Med 1976;59:637-647. McEnany MT, English TA, Ross DN. The congenitally cleft posterior mitral valve leaflet. Ann Thorac Surg 1973;16:281-292. Ellis FH Jr, Frye RL, McGoon DC. Results of reconstructive operations for mitral insufficiency due to ruptured chord ae tendineae. Surgery 1966;59: 165-172. IO. Wychulis AR, Connolly DC, Ellis FH Jr. Open mitral valve reconstruction: review of 232 operations. Arch Surg 1970;101:332-337. 11. Kay JH, Zubiate P, Mendez MA, Vanstrom N, Yokoyama T. Mitral valve repair for siqnificant mitral insufficiency. Am Heart J 1978;96:253-262. 12. Bdnchek LI.-Correction of mitral valve disease without valve replacement. Am Heart J 1982:104:865-868. 13. Frater RWM, Gabbay S, Shore D, Factor S, Strom J. Reproducible re-
14. 15.
16. 17. 18. 19. 20. 21. 22. 23.
24. 25.
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