Correction of mitral valve disease without valve replacement

PROGRESS IN CARDIOLOGY

Correction of mitral valve disease without replacement Lawrence I. Bonchek,

M.D. Milwaukee,

W&c.

Although mitral valve reconstruction has been used extensively in several European centers during the past decade,‘e3 it has been used only sporadically in the United States,dm6 where mitral valve replacement has been the standard operation for mitral regurgitation since the introduction of acceptable prosthetic heart valves in 1961. Mitral repair should be used more widely because all prosthetic valves have inherent disadvantages.7~8 Mechanical valves are noisy and require lifelong anticoagulation with warfarin sodium. Thromboembolic complications still occur in 2 % to 5% of patients per year, and hemorrhagic complications of anticoagulation occur in 1% to 3 % of patients per year.’ Tissue valves are less thrombogenic, but their durability is still uncertain, and some porcine valves fail sporadically within a few years after insertion. In contrast, mitral valve reconstruction preserves the patient’s native tissues, minimizes the risk of thromboembolic complications, and makes anticoagulation with warfarin sodium unnecessary for most patients. There is no risk of sudden, fatal mechanical failure or thrombosis, which can occur with a mechanical prosthesis, and the noise of a prosthesis is avoided. Finally, as discussed below, reconstruction in properly selected patients provides durable restoration of normal hydraulic function. TECHNIQUES

OF MITRAL

VALVE

RECONSTRUCTION

This discussion will focus on mitral reconstruction for mitral regurgitation as pioneered by Carpentier; mitral commissurotomy for mitral stenosis has been discussed elsewhere.s-ll Carpentier et al.’ have pioneered techniques of anatomic repair based on an analysis of mitral valve anatomy. Operative techniques for predictable correction of mitral regurgitation without valve replacement must deal with the From the surgery. Received

Medical

College

for publication

Reprint requests: Surgery, Medical kee, WI 53226.

of Wisconsin, March

11, 1982;

Lawrence I. Bonchek, College of Wisconsin,

0002-8703/82/100865

Department accepted

19, 1982.

M.D., Dept. of Cardiothoracic 8700 W. Wisconsin Ave., Milwau-

+04$00.40/001982

The C.V. M&y

following abnormalities in various combinations: (1) dilatation of the mitral anulus, (2) elongation or rupture of chordae tendineae permitting prolapse of leaflets upward into the atrium;3 redundancy and deformity of valve leaflets, and (4) restricted motion of the leaflets as a result of fusion of commissures and chordae, shortening and thickening of chordae, or both. Dilatation of the anulus is the most consistent finding in mitral regurgitation, because even if not present initially it develops secondarily as the left ventricle (LV) enlarges. Suture anuloplasty can cause eccentric narrowing of the anulus, and may require overcorrection of the anular dilatation with creation of mild stenosis to achieve mitral valve competence. Carpentier et al. therefore use a symmetric semirigid cloth-covered metal ring to restore and maintain the normal configuration and size of the anulus. Since dilatation occurs mainly in the posterior portion of the mitral anulus, the anuloplasty rings are designed to plicate the posterior anulus selectively. Ruptured chordae, which occur spontaneously or secondary to endocarditis, are managed by resecting the flail portion of the leaflet. If the flail segment is too large, the valve must be replaced. Elongated chordae, found in mitral valve prolapse, can also be managed by leaflet resection if the chordae serve a limited portion of the leaflet. If the flail portion of leaf-let is too large to resect, the elongated chordae must be shortened by imbricating the chordae into an incision in the respective papillary muscle and closing the incision over the chordae. Combined leaflet resection and chordal shortening is often necessary. Leaflets with restricted motion are treated by commissurotomy, fenestration of fused chordae, and resection of secondary chordae attached to the ventricular surface of the mural leaflet. CLINICAL RESULTS RECONSTRUCTION

of Cardiothoracic Apr.

valve

Co.

OF MITRAL

VALVE

Carpentier et al.’ have recently reported a summary of 10 years’ experience (1969 to 1978) with mitral reconstruction in 551 patients, of whom 174 665

866

Bonchek

also required tricuspid ring anuloplasty. In the group undergoing mitral repair only, hospital mortality (4.2 % ) and late mortality (18% at 9 years) were lower than in most reviews of mitral valve replacement during that era, but the patients were selected for repair. More pertinent is the fact that the repairs were quite durable. Of 270 patients available for long-term follow-up an average of 4 years after operation, 207 were in New York Heart Association functional class I, 51 were in class II, 10 were in class III, and two were in class IV. Preoperatively, all but 13 had been in class III or IV. Thirty-seven patients (11% ) underwent reoperation (an actuarial probability of 13% at 8 years), but half of these reoperations (18) were necessary within 2 years of the first operation, with a rate of reoperation after that of only 1% per year. The need for early reoperation suggests that the causes were related to avoidable technical factors or to poor case selection. Reoperations were more common in the group with rheumatic valvular disease, and conversely the best results were obtained in patients with prolapsed leaflets. Carpentier et al. have pointed out that better results can be expected with current techniques and with a better understanding of the limitations of these techniques. The incidence of thromboembolic events was only 0.6 % per patient year in the group that had mitral repair without associated procedures (eight events in seven patients). Only half the patients in the series received anticoagulants, and all emboli occurred in patients with rheumatic valve disease, restricted leaflet motion, a small prosthetic ring, or a thrombosed or calcified left atrium. Our experience with mitral valve reconstruction at the Milwaukee Regional Medical Center-Medical College of Wisconsin, was initiated in January, 1981, in patients with mitral prolapse, since they are the most likely to be suitable for reconstruction. Since that time mitral valve replacement has not been necessary for nonrheumatic mitral regurgitation except in one patient with Marfan’s syndrome. With that exception, nine consecutive patients with nonrheumatic mitral regurgitation have undergone mitral valve repair. All nine had severe mitral regurgitation, six had ruptured chordae tendineae, and one had Marfan’s syndrome. Partial leaflet resection was necessary in all nine patients with supplemental chordal shortening in five. One patient died of complications unrelated to the choice of valve repair instead of replacement. He was a frail man of 74 years with long-standing heart failure who developed postoperative renal insufficiency secondary to a hemolytic reaction. Despite normal cardiac

American

October, 1982 Hem Journal

function, he died 3 weeks later of irreversible renal failure and terminal pneumonia. Postoperative echocardiography in all nine patients, including the patient who later died, revealed correction of valve prolapse. All eight survivors are asymptomatic. Postoperative catheterization in all eight surviving patients revealed excellent valve function. Five patients had no mitral regurgitation on angiography and no residual murmurs. Three patients had trivial regurgitation on angiography and had soft late systolic murmurs. HEMODYNAMIC

STUDIES

AFTER VALVE

REPAIR

There have been few hemodynamic studies after valve repair. Carpentier et al. reported a “close correlation” between clinical and catheterization findings in 42 patients. Twenty-one asymptomatic patients with mild-to-moderate or no residual murmur had normal hemodynamics, whereas 21 symptomatic patients with moderate-to-severe murmurs had moderately elevated pulmonary artery and pulmonary capillary wedge pressures. The catheterization findings in seven of our patiental 7 to 11 days postoperatively revealed significant (p < 0.05) declines from preoperative levels in mean values (+S.D.) of the following parameters: LV end-diastolic pressure (16.0 + 3.8 to 9.2 it 3.4 mm Hg), pulmonary artery wedge pressure (21.9 f 8.9 to 10.4 + 3.8 mm Hg), and pulmonary artery mean pressure (30.4 * 11.4 to 19.9 & 6.0 mm Hg). Cardiac index rose from 2.3 i- 0.6 to 3.0 2 0.5 L/min/m2. Although these results were not surprising after correction of severe mitral regurgitation, other measurements were unexpected, as they suggested that LV function may be better preserved after successful mitral valve repair than after valve replacement. Certainly, mitral valve replacement for severe mitral regurgitation is often followed by depressed LV function and persistent LV dilatation that are generally attributed to increased impedance to ejection and increased LV wall stress. Boucher et all3 studied LV function with multigated blood pool imaging before and 2 to 4 weeks after mitral valve replacement in 20 patients, of whom 15 had myxomatous valves and/or ruptured chordae. Although end-diastolic volume index fell significantly 0, < 0.001) from 131 & 40 to 78 +- 30 cc/m2, ejection fraction also fell significantly from 0.66 + 0.09 to 0.48 +- 0.11 and end-systolic volume index was unchanged (45 + 19 vs 42 of: 21 cc/m2). In sharp contrast, there was little or no deterioration of LV function in our patients. As in Boucher’s study, LV end-diastolic volume index fell significantly (p < 0.05) from a mean of 125 + 33 to 73 -t

Volume

104

Number

4, Part

1

20 cc/m* but, unlike Boucher’s findings, there was also a significant fall in end-systolic volume index (45 f 16 to 26 f 8 cc/m2) and ejection fraction was virtually unchanged (0.66 + 0.08 vs 0.63 + 0.11). Although it is not possible to know whether our patients are comparable to Boucher’s patients in all respects, it is noteworthy that mean preoperative ejection fraction, as well as end-diastolic and endsystolic volume indices were comparable in both studies. Similarly, Lessana et al.” studied 26 patients before and 2 to 60 months after mitral reconstruction and also found significant declines in end-systolic as well as in end-diastolic volume indices without a decline in ejection fraction in patients whose regurgitation was completely corrected. It thus seems possible that some of the LV dysfunction seen after mitral valve replacement and formerly attributed entirely to restoration of mitral valve competence may be due simply to excision of the native valve and its attachments, as suggested some years ago by Lillehei et a1.15Mitral valve repair may preserve LV function by retaining the tethering effect of chordal attachments, thus preventing postoperative LV dilatation and moderating LV wall stress. Although it has generally been assumed that Lillehei’s speculation was refuted by experimental studies16 that detected no benefit from preservation of chordae tendineae during mitral valve replacement in dogs, those studies are probably not pertinent, since folding of valve leaflets so they can be “preserved” when the valve is replaced does not retain the anatomical alignment and systolic tension of the chordae that results from mitral valve repair as described herein. ANALYSIS

Mitral valve reconstruction for mitral regurgitation provides reproducible and stable clinical results, and eliminates the complications associated with prosthetic heart valves such as sudden, catastrophic mechanical failure, major emboli, noise, and intraoperative trauma to the LV. In most patients long-term anticoagulation is unnecessary. Furthermore, the likelihood of successful valve repair is reasonably predictable, particularly in patients with nonrheumatic mitral regurgitation. Mitral valve repair is also appropriate in selected patients with rheumatic valve disease. Why then has mitral valve reconstruction been used so sparingly in the United States? The preference for valve replacement seems due to a number of factors. Mitral valve replacement is a common and standardized procedure that offers reproducible

Carpentier anuloplasty for mitral regurgitation

867

results, whereas the techniques of mitral reconstruction are complex. Reconstructive techniques are unfamiliar to most surgeons as they cannot be learned from descriptions, but require repeated personal observation of successful operations before complex valve repairs can be undertaken with predictable results and without a long “learning curve.” Unlike other major technical advances in cardiac surgery such as valve replacement and coronary bypass which originated in the United States and could easily be observed, current techniques of valve reconstruction have been developed and popularized in Europe, particularly by Carpentier in Paris. There is also the psychological factor that failure of a reconstructed valve causes the surgeon to feel guilty, whereas failure of a prosthetic valve is beyond the surgeon’s direct responsibility. Indeed, this rationale may also restrict the use of mitral commissurotomy by some surgeons, since valve replacement is a more predictable operation for mitral stenosis as well. TIMING

OF OPERATION

I have discussed elsewhere the indications for mitral valve replacement and mitral commissurotomy,” and have emphasized the importance of correcting mitral regurgitation before LV function deteriorates irreversibly. Since some physicians postpone valve replacement because of concern not only about operative mortality but also about complications related to the prosthesis, the availability of a safe and effective operation that avoids the use of a prosthesis could influence the timing of operation. When the predictable and durable results of mitral valve repair, especially for patients with nonrheumatic mitral valve disease, become as recognized in the United States as in several European centers, physicians may become increasingly comfortable recommending earlier operative intervention to preserve LV function in patients with mitral regurgitation. REFERENCES

Carpentier A, Fabiani JN, Relland J, d’Allaines C, Piwnica A: Reconstructive surgery of mitral valve incompetence. Tenyear appraisal. J Thorac Cardiovasc Surg 79:338, 1980. Yacoub M, Halim M, Radley-Smith R, McKay R, Nuveld A, Towers M: Surgical treatment of mitral regurgitation caused by floppy valves: Repair versus replacement. Circulation 64 (suppl II):II-210, 1981. 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 Thorac Cardiovasc Surg 79:326, 1980. Kay JH, Zubiate P, Mendez MA, Vanstrom N, Yokoyama T: Mitral valve repair for significant mitral insufficiency. AM HEART J 96:253, 1978.

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5. Reed GE, Pooley RW, Moggio RA: Durability of measured mitral annuloplasty. Seventeen-year study. J Thorac Cardiovast Surg 79:321, 1980. 6. Rouleau CA, Frye RL, Ellis FH Jr: Hemodynamic state after open mitral valve replacement and reconstruction. J Thorac Cardiovasc Surg 58:870, 1969. 7. Bonchek LI: The current status of cardiac valve replacement: Selection of a prosthesis and indications for operation. AM HEART J 101:96, 1981. 8. Bonchek LI, Starr A: Ball-valve prostheses: Current analysis of late results. Am J Cardiol 35:843, 1975. 9. Bonchek LI: Mitral commissurotomy-a perspective (Editorial). Chest 75:112, 1979. 10. Housman LB, Bonchek L, Lambert L, Grunkemeier G, Starr A: Prognosis of patients after open mitral commissurotomy: Actuarial analysis of late results in 100 patients. J Thorac Cardiovasc Surg 73:742, 1977. 11. Bonchek LI: Indications for surgery of the mitral valve. Am J Cardiol 46:155, 1980. 12. Bonchek LI, Siegel R, Olinger GN, Keelan MH, Tresch DT:

American

13.

14.

15. 16.

October, 1982 Heart Journal

Left ventricular function is better after mitral valve repair than after valve replacement (abstr). Am J Cardiol 49:922, 1982. Boucher CA, Bingham JB, Osbakken MD, Okada RD, Strauss HW, Block PC, Levine FH, Phillips HR, Pohost GM: Early changes in left ventricular size and function after correction of left ventricular volume overload. Am J Cardiol 47:991, 1981. Lessana A, Herreman F, Boffety C, Cosma H, Guerin F, Kara M, Degeorges M: Hemodynamic and cineangiographic study before and after mitral valvuloplasty (Carpentier’s technique). Circulation 64(suppl II):II-195, 1981. Lillehei CW, Levy MJ, Bonnabeau RC; Mitral valve replacement with preservation of papillary muscles and chordae tendineae. J Thorac Cardiovasc Surg 47:532, 1964. Rastelli GC, Tsakiris AG, Frye RL, Kirklin JW: Exercise tolerance and hemodynamic studies after replacement and canine mitral valve with and without preservation of chordae tendineae. Circulation 35 and 36(suppl 1):134, 1967.