Symposium on Surgical Techniques
Technique for Repair and Replacement of the Mitral Valve Floyd D. Loop, M.D.
Extraordinary advances in valve surgery have occurred since the first ball valve replacement by Starr in 1961.1 9 The caged ball prosthesis has been used more than any other model. In the last 2 years, however, emphasis has shifted to the low profile disc valve for aortic and mitral replacement. Reduced operative risk and increased longevity have come about largely through greater surgical experience and a favorable evolution in prosthetic manufacture. The timing of valve repair or replacement profoundly affects both early and late survival. Fortunately, most patients with symptomatic mitral valve disease do not experience the rapid downhill course of those with disabling aortic valve disease. However, this slower, albeit progressive natural history can unduly prolong conservative management and jeopardize the surgical result. When the valve architecture is still preserved, repair by commissurotomy or annuloplasty can restore normal hemodynamic function and provide nearly normal survival during the subsequent 5- to 10-year period. The performance ascribed to the latest ball and disc valves substantiates the concept that earlier operation can now be advised for many patients with cardiac valve dysfunction. Patients often die postoperatively because their cardiac impairment has reached irreversible proportions and cannot be improved by successful valve replacement. This report describes our operative technique for mitral valve procedures. We focus on methods of valve insertion, open commissurotomy, and annuloplasty. Basically, our approach and method have undergone little modification during the past decade.
ANATOMY The mitral apparatus is composed of six anatomic elements: (1) posterior left atrial wall, (2) annulus, (3) leaflets, (4) chordae tendineae, (5) papillary muscles, and (6) left ventricular wall. Left atrial From the Department of Thoracic and Cardiovascular Surgery, The Cleveland Clinic Foundation and The Cleveland Clinic Educational Foundation, Cleveland, Ohio
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size may directly contribute to the mitral valve integrity. Enlargement of the left atrium displaces the posterior wall downward and posteriorly, exerting tension on the posterior leaflet. Similarly, by its size and shape, the left ventricular wall controls the valve competence. Not only.does left ventricular enlargement contribute to annular dilatation but, also, the altered ventricular shape may direct the axes of papillary muscle tension from a vertical to a lateral orientation. This lateral tension opposes leaflet closure, especially for the anterior leaflet, and promotes regurgitation. 14 The anterolateral and posteromedial papillary muscles are firmly embedded almost to their tips in the left atrial wall. The anterolateral papillary muscle arises as a single head in about 75 per cent of the cases in contrast to the posteromedial muscle, which has multiple heads in about two thirds of the patients. The posteromedial papillary muscle arises near the junction of the posterior free left ventricular wall and the interventricular septum. The apices of the muscles usually lie directly under the corresponding commissures. Since the papillary muscles are part of the endocardium, they are particularly vulnerable to ischemia resulting from coronary atherosclerosis and also to perfusion changes caused by hypotension following acute myocardial infarction or severe angina. The blood supply to the anterolateral papillary muscle is largely from the circumflex and anterior descending distribution, whereas the posteromedial supply is more variable. 6 When the right coronary artery is dominant, usually the right coronary artery, via the posterior descending, supplies the posterior papillary muscle. When the left coronary artery is dominant (about 10 per cent of the cases), the circumflex vessels perfuse the posterior muscle. Because both papillary muscles receive arterial blood from multiple sources, occlusion of a single vessel rarely deprives the muscle of all its circulation. Chordae tendineae from each papillary muscle are attached to both leaflets. The chordae tendineae do not change in length appreciably during the left ventricular contraction. They simply anchor the leaflet to the muscular element by multiple fixation points at the leaflet edges. Three varieties of chordae tendineae exist: (1) first order chordae arise from the apices of the papillary muscle and insert into the free edge of the leaflet as fine strands; (2) second order chordae, usually thicker and less numerous than the first order, insert into the ventricular side of the leaflet a short distance from the free edge; (3) third order chordae, which sometimes contain muscle, originate from the ventricular wall and insert near the line of closure or along the basal area of the leaflet. The average diameter of the mitral orifice is 2.5 em, and the circumference ranges from 8 to 11.5 em in the adult, with 9 and 10 em the average circumference for females and males respectively. 5 The anterolateral and posteromedial commissures do not extend out to the valve ring, so that leaflet tissue is actually continuous around the whole circumference of the ring. Both leaflets are trapezoidal, and the anterior (septal or aortic) leaflet is roughly twice the size of the posterior or mural leaflet. The mitral valve annulus is a poorly defined, thin ring of fibrous tissue that surrounds the valve like a horseshoe. The ring is not complete in an area filled by most of the anterior leaflet.
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The fibrous trigone of the cardiac skeleton lies adjacent to the anterior aspect of the mitral ring. This trigone represents a confluence of fibrous tissue from the mitral and tricuspid valves, membranous septum, and posterior aspect of the aortic root. The left coronary and noncoronary cusps of the aortic valve are attached at their bases to the aortic annulus which, in this area, is interlaced with the mitral annulus, the base of the anterior mitral leaflet, the aortic root, and the left atrial myocardium.• Sutures can damage the conduction system in the region of the right fibrous trigone (12 to 4 o'clock when viewed from the left atrium). Conduction beyond this point is related more to the membranous and muscular ventricular septum, and is relatively far from the mitral valve. The left coronary artery arises from the left sinus of Valsalva and passes between the left auricular appendage and the pulmonary artery. The atrioventricular segment of the main circumflex coronary artery begins above the left atrial appendage and therefore lies adjacent to the left side of the mitral ring when viewed from above. The anterior commissure lies behind the circumflex coronary artery about 1 em distal to its origin from the left coronary artery. The variations in the course of the circumflex can bring the artery close to the mitral annulus, and deeply placed sutures can injure or ligate the circumflex coronary artery as it courses through this area.
VALVE REPAIR
Mitral Commissurotomy Rheumatic mitral stenosis results from chordal fusion, leaflet thickening, calcification, and commissural fusion. Eventually, the fibrous reaction extends to the papillary muscle, and the chordae may be so shortened that the papillary muscles are almost fused with the valve leaflet. Severe valvulitis does not always affect the whole valve, and one frequently finds an asymmetrical distribution of the anatomic deformity. Commissural fusion on one side may be manifest by dense calcification and chordal shortening while the other commissure is still only mildly affected. Regardless of the valvular architecture, the pathophysiology does not become clinically apparent until the valve area is reduced by half. The orifice in mitral stenosis is typically a small oval, approximately 1.0 x 0.5 em. Left atrial enlargement and hypertrophy that result from mitral stenosis promote a loss of the normal electrical activity and leads to atrial fibrillation. This loss of atrial systole further impairs ventricular filling, making forward flow even more dependent on the duration of diastole. Under these circumstances, mural thrombi are often found in the left atrium and left auricular appendage. Thrombi are almost always associated with mitral stenosis and rarely found in mitral regurgitation. Although systemic emboli occur in 10 to 25 per cent of patients with rheumatic mitral disease, one paradox of cardiac surgery is that in patients operated on because of systemic emboli, the left atrium is often free of clots. 16 Leaflet calcium can erupt through the
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Figure 1. A, Exposure of the mitral valve through an incision behind the interatrial groove. A curved or rightangle retractor exposes the valve which can be brought further into view by aortic cross-clamping. B, Bilateral open mitral commissurotomy performed with a scalpel. The underlying chordae tendineae must be carefully preserved.
A
B surface epithelium to produce false surface ulceration. Thrombotic material may form within the ulcers and, therefore, the valvular surface, rather than the atrium, may be the source of arterial emboli. 23 For at least 10 years, we have preferred open mitral commissurotomy to the closed method, except in the pregnant woman with mitral stenosis. The open procedure allows a bilateral commissurotomy under direct vision and eliminates the technical errors inherent in a blind approach. The valve can be clearly inspected and, if replacement is necessary, the decision is made immediately. Any thrombi contained within the left atrium are removed, and the risk of embolization is reduced by the open method. Open commissurotomies are almost always approached through a midline sternotomy. After routine cannulation (see cannulation technique in this issue), the left atrium is opened behind the interatrial groove (Fig. 1). By establishing a cleavage plane between an adherent clot and the atrial wall, left atrial thrombi can be peeled out, often in one specimen. Routinely, the atrial appendage is everted for inspection. The valve can then be brought into view with a blunt hook passed through the stenotic orifice. When the valve architecture is still fairly well
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preserved, without marked chordal shortening, a bilateral commissurotomy is accomplished using a no. 15 blade scalpel. The surgeon's index finger assesses the width of the commissurotomy and the extent of subvalvular disease. After commissurotomy, valve competency can be tested by injecting saline into the left ventricle. This maneuver produces coaptation of the leaflets and gives a rough index of the valve closure. A more accurate test of mitral competence involves palpation of the valve structure with the heart beating. First, the aortic clamp is slowly released and air evacuated through a needle vent in the ascending aorta and left ventricular apex. The intraatrial suture line is then partially closed with a running stitch and partial cardiopulmonary bypass instituted. The surgeon inserts his index finger through the partially closed atriotomy and assesses the commissurotomy and valve closure while the heart is beating actively.
Annuloplasty In our institution, mitral insufficiency amen~ble to annuloplasty is confined to two forms of mitral regurgitation: (1) ruptured posterior chordae tendineae, and (2) "fishmouth" commissural regurgitation. Results of annuloplasty for other forms of mitral regurgitation have not been highly successful in our experience. Ruptured chordae tendineae is rarely a complication of myocardial infarction in contrast to papillary muscle rupture. Survival is much greater in patients with chordal rupture than in those with infarction and disruption of the papillary muscle. At one time, bacterial endocarditis was probably the major cause of ruptured chordae tendineae; however, more recently, a significant number of cases have been reported in which there has been no demonstrable cause of rupture and, as a rule, the mitral ring is normal. In isolated chordal rupture, detachment almost always occurs near the cusp rather than near the papillary muscleY There is preferential involvement of the chordae supporting the posterior leaflet of the mitral valve, and this loss of support produces a hood-like prolapse of the unsupported leaflet into the left atrium (Fig. 2). The method of annuloplasty described by McGoon 11 was designed originally for either leaflet. Our experience parallels that of Gerbode et al., 8 in that the annuloplasty is applicable only for the posterior leaflet. The sutures join together the two areas of the posterior leaflet with intact chordae, and mitral regurgitation is effectively counteracted. Localized regurgitation, isolated to one or both commissural regions, is also managed successfully by horizontal mattress sutures. Most often, rheumatic carditis is the underlying cause, and the mitral ring is otherwise normal. To prevent cutting through the annular tissue, each suture is usually mounted on a small Teflon pledget.
MITRAL VALVE REPLACEMENT Removal of the mitral valve and prosthetic insertion is reserved strictly for patients whose valve architecture has been irreparably de-
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Figure 2. A, Ruptured posterior chordae tendineae are most amenable to annuloplasty repair. This schematic drawing demonstrates the hood-like flail segment prolapsing into the left atrium during ventricular systole. B, Interrupted simple sutures and horizontal mattress sutures mounted on Teflon pledgets are used to unite the annular defect. This maneuver implicates the flail segment into the ventricular chamber and reestablishes valve integrity. C, The completed repair after the method of McGoon.•
stroyed by rheumatic carditis or for those who suffer from significant mitral failure related to infection, leaflet degeneration, coronary atherosclerosis, cardiomyopathy, or congenital malformation. For optimum results, operation must be performed before the patient reaches the endstage of the disease. McGoon and associatesl 2 reviewed, by stepwise discriminant analysis, a large series of patients who underwent isolated Starr-Edwards mitral valve replacement. Three factors influenced operative mortality: (1) Functional Class IV status, (2) giant left atrium, and (3) previous heart surgery. Late survival was adversely affected by age over 50, multiple valve involvement, and left atrial size. Similarly,
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1199 Litwak et al. found that several factors increased the risk of mitral operations; they concluded that surgical risk for patients in sinus rhythm with a cardiac index above 2.0 L per min per m 2 was related primarily to technique rather than to myocardial dysfunction. In those patients with stenosis and regurgitation, chordal deformity is an important feature, whereas in mitral regurgitation only, chordal shortening is not the major fault. In many cases mitral regurgitation, secondary to coronary artery disease, has no structural abnormality of the mitral valve or chordae tendineae, and the papillary muscles may only show focal scarring. 18 Left atrial dilation is generally greater when regurgitation rather than stenosis is prominent. 22 Ordinarily, the mitral valve is approached from behind the interatrial groove. The longitudinal left atriotomy usually provides excellent exposure. We have not routinely used the superior approach,1 3 and employ the right atrial transseptal exposure 1 only for patients who have an unusually small left atrium or for those who require mitral reoperations. After inspection and palpation of the valve and its subvalvular mechanism, the valve is excised beginning on the anterior leaflet (Fig. 3). The aorta is crossclamped, and this maneuver produces a still field and provides additional exposure through its decompressive effect. The curved anterior leaflet incision is then extended circumferentially with a long scissors. The remaining chordae tendineae are divided at their attachments to the papillary muscles. Posterior chordae tendineae are often densely adherent to the posterior left ventricular wall and their division may prove difficult. Perforation of the ventricular wall or massive left ventricular hematoma and subsequent rupture have been reported. 20 • 24 Several mechanisms for left ventricular rupture have been postulated, and they include (1) annular calcification in the area of the atrioventricular groove, (2) intrinsic myocardial disease of ischemic, rheumatic, or infectious origin, (3) 10
Figure 3. The incision for mitral valve removal begins on the anterior leaflet several millimeters from the imaginary annulus. Approximately 3 to 4 mm. of leaflet tissue are left attached to the annulus to further buttress the annular suture.
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technical injury to the ventricular wall during division of the papillary muscles or chordae tendineae. The diagnosis of ventricular perforation is usually not appreciated until cardiopulmonary bypass is terminated and often the patient has been moved to the Intensive Care Unit. Although rare, this iatrogenic injury is uniformly fatal. To prevent damage to the posterior left ventricular wall, the leaflets and corresponding chordae must be clearly visualized before excision. A blunt hook may be used to elevate the chordae adherent to the left ventricular wall so that the surgeon's scissors tip does not inadvertently penetrate the thin myocardium in this area (Fig. 4). Division of the chordal attachment is necessary to prevent ball or disc malfunction, and division of all these attachments moves the mitral ring closer to the surgeon and thereby aids exposure. The valvular prosthesis of appropriate size is selected and mounted on the valve holder. The prosthesis may be inserted on the atrial side or in subannular position. Advocates of subannular installation21 point out that seating the prosthetic ring on the ventricular side reduces tension on the suture line, since the sewing ring lies beneath the mitral annulus and is compressed against it by the force of ventricular contraction (Fig. 5). When the annulus is judged to be of good quality, we usually perform supraannular mitral valve replacement. Double-armed sutures are placed in vertical mattress fashion so that one limb goes through the prosthetic sewing ring deeply and the other superficially. Therefore, the suture is tied with a knot on the cloth sewing ring, not on the patient's own tissue (Fig. 6). For suture replacement, the valve circumference is divided into quadrants, and sutures in the two upper quadrants are usually inserted first. As each stitch is placed from annulus to sewing
Figure 4. The chordae tendineae are divided, usually at the tip of the papillary muscles. When the chordal mechanism is severely foreshortened, posterior chordae tendineae can be adherent to the thin posterior left ventricular wall. To prevent iatrogenic perforation or hematoma formation in this area, the chordae tendineae can be gently elevated with a blunt hook to provide a clear view before transsection. Division of all chordal attachments further aids exposure by elevating the mitral ring closer to the surgeon.
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Figure 5. A, Subannular mitral valve replacement. Four quadrant sutures are brought up through the prosthetic sewing ring and then inserted through the patient's annulus from the ventricular to the atrial side. They are passed through Teflon pledgets on the atrial wall to prevent them from cutting through the annular tissue after the knot is tied. B, A profile view showing that the prosthetic ring abuts against the mitral valve ring from the ventricular side. C, Prosthetic valve on holder with four quadrant sutures inserted through the annulus. All sutures can be inserted in this manner, or interrupted single sutures can be placed between the four mattress quadrant sutures.
ring, an assistant simply holds them, and then clamps are fixed to the whole quadrant group, separating them from the next series of stitches. After the valve is seated and the sutures are tied, the aortic crossclamp is slowly released while air is evacuated from the ascending aorta. The left atrium is generally closed with a running 2-0 stitch which can be reinforced when necessary with interrupted sutures. Air must be evacuated from the left ventricular apex before the heart resumes an effective beat. Release of one or both caval tourniquets aids in the evacuation of left ventricular air. The problem of tricuspid valve incompetence in patients with either isolated mitral valve disease or aortic and mitral valve disease has not been fully resolved. In one well-known report,2 the authors recommended conservative management since, in their experience, most cases of tricuspid regurgitation reversed spontaneously after the mitral valve operation. Surgeons at the Mayo Clinic 15 concluded that tricuspid incompetence does not always regress under these circumstances. Our philosophy in this dilemma has generally been one of conservatism. We replace the tricuspid valve only when it is intrinsically damaged or
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Figure 6. A, Standard mitral valve replacement with vertical mattress sutures. This method is now called a supraannular replacement in that the prosthesis lies at the valve ring rather than below it. B, Profile of the supraannular prosthesis showing that the sutures are tied on the fabric. C, Completed prosthetic replacement by interrupted vertical mattress sutures. This method is used most often for mitral valve replacement in our institution.
seriously insufficient. When signs of moderate or severe tricuspid valvular incompetence continue after mitral valve replacement and the right atrial pressure is greater than the left atrial pressure, cardiopulmonary bypass is reestablished and the valve is then replaced by a prosthesis. Recent experience with the Carpentier ring, 3 De Vega annuloplasty, 9 and porcine xenograft 25 offers attractive alternatives to the available metallic prostheses. Periprosthetic leakage is found less often today, probably because of the surgeon's greater experience and technical facility in cardiac valve replacement. The chief cause of leakage is related to calcification and infection, and reoperation must be aggressive when signs of cardiac deterioration develop. Since dehiscence of the prosthesis frequently leaves little surrounding support, double-arm sutures mounted on Teflon pledgets are usually required to close the leak. 7 In these reoperations, the left ventricle must be fully mobilized to evacuate air effectively after the valve procedure. As noted above, adhesions may cause difficult exposure in the interatrial groove and, in this situation, the transseptal approach is a good alternative.
SUMMARY Whenever possible, the patient's own mitral valve mechanism should be preserved. Successful mitral valve repair offers excellent
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benefits in terms of hemodynamic function, clinical improvement, and longevity. Open mitral commissurotomy or valvuloplasty for localized defects or ruptured chordae tendineae constitutes our best reparative efforts. Today, mitral valve replacement can be accomplished with less than a 5 per cent operative mortality, but should be reserved for patients who are not in desperate terminal condition. In our experience, aggressive tactics undertaken at the endstage of the disease have had little or no long-term success. At the Cleveland Clinic, isolated mitral valve repair or replacement is performed under normothermic cardiopulmonary bypass and anoxic arrest. Generally, the valve is exposed through an atriotomy behind the interatrial groove. Valvular replacement is accomplished by interrupted suture technique, seating the prosthesis at the level of the annulus or below it. Risk is influenced mainly by the chronicity of the valve dysfunction. Patients who have not yet reached a Functional Class IV status or sustained massive cardiomegaly and low cardiac output fare better in both early and late follow-up periods.
REFERENCES I. Bowman, F. 0., and Maim, J. R.: The transseptal approach to mitral valve repair. Arch.
Surg., 90:329, 1965. 2. Braunwald, N. S., Ross, J., Jr., and Morrow, A. G.: Conservative management of tricuspid regurgitation in patients undergoing mitral valve replacement. Circulation, 35(Suppl. 1):63, 1967. 3. Carpentier, A., Deloche, A., Dauptain, J., Soyer, R., Blondeau, P., Piwnica, A., and Dubost, C.: A new reconstructive operation for correction of mitral and tricuspid insufficiency. J. Thorac. Cardiovasc. Surg., 61:1, 1971. 4. DaVila, J. C., and Palmer, T. E.: The mitral valve; anatomy and pathology for the surgeon. Arch. Surg., 84:174, 1962. 5. Ellis, F. H., Jr.: Surgery for Acquired Mitral Valve Disease. Philadelphia, W. B. Saunders Co., 1967, p. 49. 6. Estes, E. H., Dalton, F. M., Entman, M. L., Dickson, H. B., and Hackel, D. B.: The anatomy and blood supply of the papillary muscles of the left ventricle. Am. Heart J., 71:356, 1966. 7. Favaloro, R. G., Effler, D. B., Groves, L. K., Suarez, E., and Shirey, E. K.: Surgical repair of leaking prosthetic heart valves. Ann. Thorac. Surg., 3:503, 1967. 8. Gerbode, F., Hill, J.D., Kelly, J. J., Jr., Selzer, A., and Kerth, W. J.: Surgical correction of mitral insufficiency due to ruptured chordae tendineae. Circulation, 37 and 38(Suppl. 11):119, 1968. 9. Grondin, P., Meere, C., Limet, R., Delcan-Dominguez, J., and Rivera-Lopez, R.: Carpentier's annulus and DeVega's annuloplasty; the end of the tricuspid challenge. J. Thorac. Cardiovasc. Surg. (in press). 10. Litwak, R. S., Silvay, J., Gadboys, H. L., Lukban, S. B., Sakurai, H., and Castro-Blanco, J.: Factors associated with operative risk in mitral valve replacement. Am. J. Cardiol., 23:335, 1969. 11. McGoon, D. C.: Repair of mitral insufficiency due to ruptured chordae tendineae. J. Thorac. Cardiovasc. Surg., 39:357, 1960. 12. McGoon, D. C., Oxman, H. A., Connolly, D. C., Wallace, R. B., Danielson, G. K., and Pluth, JR.: Isolated Starr-Edwards mitral valve replacement; factors influencing early and late death and late systemic thromboembolism. (Abstr.) Am. J. Cardiol., 31:146, 1973. 13. Meyer, B. W., Verska, J. J., Lindesmith, G. G., and Jones, J. C.: Open repair of mitral valve lesions; the superior approach. Ann. Thorac. Surg., 1:453, 1965. 14. Perloff, J. K., and Roberts, W. C.: The mitral apparatus; functional anatomy of mitral regurgitation. Circulation, 46:227, 1972. 15. Pluth, J. R., and Ellis, F. H., Jr.: Tricuspid insufficiency in patients undergoing mitral replacement; conservative management, annuloplasty, or replacement. J. Thorac. Cardiovasc. Surg., 58:484, 1969. 16. Reichek, N., Shelburne, J. C., and Perloff, J. K.: Clinical aspects of rheumatic valvular disease. Prog. Cardiovasc. Dis., 15:491, 1973.
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17. Selzer, A., and Katayama, F.: Mitral regurgitation; clinical patterns, pathophysiology and natural history. Medicine, 51:337, 1972. 18. Spencer, F. C., Reppert, E. H., and Stertzer, S. H.: Surgical treatment of mitral insufficiency secondary to coronary artery disease. Arch. Surg., 95:853, 1967. 19. Starr, A., and Edwards, M. L.: Mitral replacement; clinical experience with a ball valve prosthesis. Ann. Surg., 154:726, 1961. 20. Treasure, R. L., Rainer, W. G., Strevey, T. E., and Sadler, T. R.: Intraoperative left ventricular rupture associated with mitral valve replacement. Chest, 66:511, 1974. 21. Weldon, C. S., and Ferguson, T. B.: The elimination of periprosthetic leaks as a complication of mitral valve replacement. Ann. Thorac. Surg., 18:447, 1974. 22. Winters, W. L., Jr., Hafer, J., Jr., and Soloff, L.A.: Abnormal mitral valve motion as demonstrated by the ultrasound technique in apparent pure mitral insufficiency. Am. Heart J., 77:196, 1969. 23. Wooley, C. F., Baba, N., Kilman, J. W., and Ryan, J. M.: Thrombotic calcific mitral stenosis; morphology of the calcific mitral valve. Circulation, 49:1167, 1974. 24. Zacharias, A., Groves, L. K., Cheanvechai, C., Loop, F. D., and Efller, D. B.: Rupture of the posterior wall of the left ventricle following mitral valve replacement. J. Thorac. Cardiovasc. Surg., 69:259, 1975. 25. Zuhdi, N., Hawley, W., Voehl, V., Hancock, W., Carey, J., and Greer, A.: Porcine aortic valves as replacements for human heart valves. Ann. Thorac. Surg., 17:479, 1974. Department of Thoracic and Cardiovascular Surgery The Cleveland Clinic Foundation 9500 Euclid Avenue Cleveland, Ohio 44106
Technique for Repair and Replacement of the Mitral Valve Floyd D. Loop, M.D.
Extraordinary advances in valve surgery have occurred since the first ball valve replacement by Starr in 1961.1 9 The caged ball prosthesis has been used more than any other model. In the last 2 years, however, emphasis has shifted to the low profile disc valve for aortic and mitral replacement. Reduced operative risk and increased longevity have come about largely through greater surgical experience and a favorable evolution in prosthetic manufacture. The timing of valve repair or replacement profoundly affects both early and late survival. Fortunately, most patients with symptomatic mitral valve disease do not experience the rapid downhill course of those with disabling aortic valve disease. However, this slower, albeit progressive natural history can unduly prolong conservative management and jeopardize the surgical result. When the valve architecture is still preserved, repair by commissurotomy or annuloplasty can restore normal hemodynamic function and provide nearly normal survival during the subsequent 5- to 10-year period. The performance ascribed to the latest ball and disc valves substantiates the concept that earlier operation can now be advised for many patients with cardiac valve dysfunction. Patients often die postoperatively because their cardiac impairment has reached irreversible proportions and cannot be improved by successful valve replacement. This report describes our operative technique for mitral valve procedures. We focus on methods of valve insertion, open commissurotomy, and annuloplasty. Basically, our approach and method have undergone little modification during the past decade.
ANATOMY The mitral apparatus is composed of six anatomic elements: (1) posterior left atrial wall, (2) annulus, (3) leaflets, (4) chordae tendineae, (5) papillary muscles, and (6) left ventricular wall. Left atrial From the Department of Thoracic and Cardiovascular Surgery, The Cleveland Clinic Foundation and The Cleveland Clinic Educational Foundation, Cleveland, Ohio
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size may directly contribute to the mitral valve integrity. Enlargement of the left atrium displaces the posterior wall downward and posteriorly, exerting tension on the posterior leaflet. Similarly, by its size and shape, the left ventricular wall controls the valve competence. Not only.does left ventricular enlargement contribute to annular dilatation but, also, the altered ventricular shape may direct the axes of papillary muscle tension from a vertical to a lateral orientation. This lateral tension opposes leaflet closure, especially for the anterior leaflet, and promotes regurgitation. 14 The anterolateral and posteromedial papillary muscles are firmly embedded almost to their tips in the left atrial wall. The anterolateral papillary muscle arises as a single head in about 75 per cent of the cases in contrast to the posteromedial muscle, which has multiple heads in about two thirds of the patients. The posteromedial papillary muscle arises near the junction of the posterior free left ventricular wall and the interventricular septum. The apices of the muscles usually lie directly under the corresponding commissures. Since the papillary muscles are part of the endocardium, they are particularly vulnerable to ischemia resulting from coronary atherosclerosis and also to perfusion changes caused by hypotension following acute myocardial infarction or severe angina. The blood supply to the anterolateral papillary muscle is largely from the circumflex and anterior descending distribution, whereas the posteromedial supply is more variable. 6 When the right coronary artery is dominant, usually the right coronary artery, via the posterior descending, supplies the posterior papillary muscle. When the left coronary artery is dominant (about 10 per cent of the cases), the circumflex vessels perfuse the posterior muscle. Because both papillary muscles receive arterial blood from multiple sources, occlusion of a single vessel rarely deprives the muscle of all its circulation. Chordae tendineae from each papillary muscle are attached to both leaflets. The chordae tendineae do not change in length appreciably during the left ventricular contraction. They simply anchor the leaflet to the muscular element by multiple fixation points at the leaflet edges. Three varieties of chordae tendineae exist: (1) first order chordae arise from the apices of the papillary muscle and insert into the free edge of the leaflet as fine strands; (2) second order chordae, usually thicker and less numerous than the first order, insert into the ventricular side of the leaflet a short distance from the free edge; (3) third order chordae, which sometimes contain muscle, originate from the ventricular wall and insert near the line of closure or along the basal area of the leaflet. The average diameter of the mitral orifice is 2.5 em, and the circumference ranges from 8 to 11.5 em in the adult, with 9 and 10 em the average circumference for females and males respectively. 5 The anterolateral and posteromedial commissures do not extend out to the valve ring, so that leaflet tissue is actually continuous around the whole circumference of the ring. Both leaflets are trapezoidal, and the anterior (septal or aortic) leaflet is roughly twice the size of the posterior or mural leaflet. The mitral valve annulus is a poorly defined, thin ring of fibrous tissue that surrounds the valve like a horseshoe. The ring is not complete in an area filled by most of the anterior leaflet.
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The fibrous trigone of the cardiac skeleton lies adjacent to the anterior aspect of the mitral ring. This trigone represents a confluence of fibrous tissue from the mitral and tricuspid valves, membranous septum, and posterior aspect of the aortic root. The left coronary and noncoronary cusps of the aortic valve are attached at their bases to the aortic annulus which, in this area, is interlaced with the mitral annulus, the base of the anterior mitral leaflet, the aortic root, and the left atrial myocardium.• Sutures can damage the conduction system in the region of the right fibrous trigone (12 to 4 o'clock when viewed from the left atrium). Conduction beyond this point is related more to the membranous and muscular ventricular septum, and is relatively far from the mitral valve. The left coronary artery arises from the left sinus of Valsalva and passes between the left auricular appendage and the pulmonary artery. The atrioventricular segment of the main circumflex coronary artery begins above the left atrial appendage and therefore lies adjacent to the left side of the mitral ring when viewed from above. The anterior commissure lies behind the circumflex coronary artery about 1 em distal to its origin from the left coronary artery. The variations in the course of the circumflex can bring the artery close to the mitral annulus, and deeply placed sutures can injure or ligate the circumflex coronary artery as it courses through this area.
VALVE REPAIR
Mitral Commissurotomy Rheumatic mitral stenosis results from chordal fusion, leaflet thickening, calcification, and commissural fusion. Eventually, the fibrous reaction extends to the papillary muscle, and the chordae may be so shortened that the papillary muscles are almost fused with the valve leaflet. Severe valvulitis does not always affect the whole valve, and one frequently finds an asymmetrical distribution of the anatomic deformity. Commissural fusion on one side may be manifest by dense calcification and chordal shortening while the other commissure is still only mildly affected. Regardless of the valvular architecture, the pathophysiology does not become clinically apparent until the valve area is reduced by half. The orifice in mitral stenosis is typically a small oval, approximately 1.0 x 0.5 em. Left atrial enlargement and hypertrophy that result from mitral stenosis promote a loss of the normal electrical activity and leads to atrial fibrillation. This loss of atrial systole further impairs ventricular filling, making forward flow even more dependent on the duration of diastole. Under these circumstances, mural thrombi are often found in the left atrium and left auricular appendage. Thrombi are almost always associated with mitral stenosis and rarely found in mitral regurgitation. Although systemic emboli occur in 10 to 25 per cent of patients with rheumatic mitral disease, one paradox of cardiac surgery is that in patients operated on because of systemic emboli, the left atrium is often free of clots. 16 Leaflet calcium can erupt through the
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Figure 1. A, Exposure of the mitral valve through an incision behind the interatrial groove. A curved or rightangle retractor exposes the valve which can be brought further into view by aortic cross-clamping. B, Bilateral open mitral commissurotomy performed with a scalpel. The underlying chordae tendineae must be carefully preserved.
A
B surface epithelium to produce false surface ulceration. Thrombotic material may form within the ulcers and, therefore, the valvular surface, rather than the atrium, may be the source of arterial emboli. 23 For at least 10 years, we have preferred open mitral commissurotomy to the closed method, except in the pregnant woman with mitral stenosis. The open procedure allows a bilateral commissurotomy under direct vision and eliminates the technical errors inherent in a blind approach. The valve can be clearly inspected and, if replacement is necessary, the decision is made immediately. Any thrombi contained within the left atrium are removed, and the risk of embolization is reduced by the open method. Open commissurotomies are almost always approached through a midline sternotomy. After routine cannulation (see cannulation technique in this issue), the left atrium is opened behind the interatrial groove (Fig. 1). By establishing a cleavage plane between an adherent clot and the atrial wall, left atrial thrombi can be peeled out, often in one specimen. Routinely, the atrial appendage is everted for inspection. The valve can then be brought into view with a blunt hook passed through the stenotic orifice. When the valve architecture is still fairly well
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preserved, without marked chordal shortening, a bilateral commissurotomy is accomplished using a no. 15 blade scalpel. The surgeon's index finger assesses the width of the commissurotomy and the extent of subvalvular disease. After commissurotomy, valve competency can be tested by injecting saline into the left ventricle. This maneuver produces coaptation of the leaflets and gives a rough index of the valve closure. A more accurate test of mitral competence involves palpation of the valve structure with the heart beating. First, the aortic clamp is slowly released and air evacuated through a needle vent in the ascending aorta and left ventricular apex. The intraatrial suture line is then partially closed with a running stitch and partial cardiopulmonary bypass instituted. The surgeon inserts his index finger through the partially closed atriotomy and assesses the commissurotomy and valve closure while the heart is beating actively.
Annuloplasty In our institution, mitral insufficiency amen~ble to annuloplasty is confined to two forms of mitral regurgitation: (1) ruptured posterior chordae tendineae, and (2) "fishmouth" commissural regurgitation. Results of annuloplasty for other forms of mitral regurgitation have not been highly successful in our experience. Ruptured chordae tendineae is rarely a complication of myocardial infarction in contrast to papillary muscle rupture. Survival is much greater in patients with chordal rupture than in those with infarction and disruption of the papillary muscle. At one time, bacterial endocarditis was probably the major cause of ruptured chordae tendineae; however, more recently, a significant number of cases have been reported in which there has been no demonstrable cause of rupture and, as a rule, the mitral ring is normal. In isolated chordal rupture, detachment almost always occurs near the cusp rather than near the papillary muscleY There is preferential involvement of the chordae supporting the posterior leaflet of the mitral valve, and this loss of support produces a hood-like prolapse of the unsupported leaflet into the left atrium (Fig. 2). The method of annuloplasty described by McGoon 11 was designed originally for either leaflet. Our experience parallels that of Gerbode et al., 8 in that the annuloplasty is applicable only for the posterior leaflet. The sutures join together the two areas of the posterior leaflet with intact chordae, and mitral regurgitation is effectively counteracted. Localized regurgitation, isolated to one or both commissural regions, is also managed successfully by horizontal mattress sutures. Most often, rheumatic carditis is the underlying cause, and the mitral ring is otherwise normal. To prevent cutting through the annular tissue, each suture is usually mounted on a small Teflon pledget.
MITRAL VALVE REPLACEMENT Removal of the mitral valve and prosthetic insertion is reserved strictly for patients whose valve architecture has been irreparably de-
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c
Figure 2. A, Ruptured posterior chordae tendineae are most amenable to annuloplasty repair. This schematic drawing demonstrates the hood-like flail segment prolapsing into the left atrium during ventricular systole. B, Interrupted simple sutures and horizontal mattress sutures mounted on Teflon pledgets are used to unite the annular defect. This maneuver implicates the flail segment into the ventricular chamber and reestablishes valve integrity. C, The completed repair after the method of McGoon.•
stroyed by rheumatic carditis or for those who suffer from significant mitral failure related to infection, leaflet degeneration, coronary atherosclerosis, cardiomyopathy, or congenital malformation. For optimum results, operation must be performed before the patient reaches the endstage of the disease. McGoon and associatesl 2 reviewed, by stepwise discriminant analysis, a large series of patients who underwent isolated Starr-Edwards mitral valve replacement. Three factors influenced operative mortality: (1) Functional Class IV status, (2) giant left atrium, and (3) previous heart surgery. Late survival was adversely affected by age over 50, multiple valve involvement, and left atrial size. Similarly,
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1199 Litwak et al. found that several factors increased the risk of mitral operations; they concluded that surgical risk for patients in sinus rhythm with a cardiac index above 2.0 L per min per m 2 was related primarily to technique rather than to myocardial dysfunction. In those patients with stenosis and regurgitation, chordal deformity is an important feature, whereas in mitral regurgitation only, chordal shortening is not the major fault. In many cases mitral regurgitation, secondary to coronary artery disease, has no structural abnormality of the mitral valve or chordae tendineae, and the papillary muscles may only show focal scarring. 18 Left atrial dilation is generally greater when regurgitation rather than stenosis is prominent. 22 Ordinarily, the mitral valve is approached from behind the interatrial groove. The longitudinal left atriotomy usually provides excellent exposure. We have not routinely used the superior approach,1 3 and employ the right atrial transseptal exposure 1 only for patients who have an unusually small left atrium or for those who require mitral reoperations. After inspection and palpation of the valve and its subvalvular mechanism, the valve is excised beginning on the anterior leaflet (Fig. 3). The aorta is crossclamped, and this maneuver produces a still field and provides additional exposure through its decompressive effect. The curved anterior leaflet incision is then extended circumferentially with a long scissors. The remaining chordae tendineae are divided at their attachments to the papillary muscles. Posterior chordae tendineae are often densely adherent to the posterior left ventricular wall and their division may prove difficult. Perforation of the ventricular wall or massive left ventricular hematoma and subsequent rupture have been reported. 20 • 24 Several mechanisms for left ventricular rupture have been postulated, and they include (1) annular calcification in the area of the atrioventricular groove, (2) intrinsic myocardial disease of ischemic, rheumatic, or infectious origin, (3) 10
Figure 3. The incision for mitral valve removal begins on the anterior leaflet several millimeters from the imaginary annulus. Approximately 3 to 4 mm. of leaflet tissue are left attached to the annulus to further buttress the annular suture.
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technical injury to the ventricular wall during division of the papillary muscles or chordae tendineae. The diagnosis of ventricular perforation is usually not appreciated until cardiopulmonary bypass is terminated and often the patient has been moved to the Intensive Care Unit. Although rare, this iatrogenic injury is uniformly fatal. To prevent damage to the posterior left ventricular wall, the leaflets and corresponding chordae must be clearly visualized before excision. A blunt hook may be used to elevate the chordae adherent to the left ventricular wall so that the surgeon's scissors tip does not inadvertently penetrate the thin myocardium in this area (Fig. 4). Division of the chordal attachment is necessary to prevent ball or disc malfunction, and division of all these attachments moves the mitral ring closer to the surgeon and thereby aids exposure. The valvular prosthesis of appropriate size is selected and mounted on the valve holder. The prosthesis may be inserted on the atrial side or in subannular position. Advocates of subannular installation21 point out that seating the prosthetic ring on the ventricular side reduces tension on the suture line, since the sewing ring lies beneath the mitral annulus and is compressed against it by the force of ventricular contraction (Fig. 5). When the annulus is judged to be of good quality, we usually perform supraannular mitral valve replacement. Double-armed sutures are placed in vertical mattress fashion so that one limb goes through the prosthetic sewing ring deeply and the other superficially. Therefore, the suture is tied with a knot on the cloth sewing ring, not on the patient's own tissue (Fig. 6). For suture replacement, the valve circumference is divided into quadrants, and sutures in the two upper quadrants are usually inserted first. As each stitch is placed from annulus to sewing
Figure 4. The chordae tendineae are divided, usually at the tip of the papillary muscles. When the chordal mechanism is severely foreshortened, posterior chordae tendineae can be adherent to the thin posterior left ventricular wall. To prevent iatrogenic perforation or hematoma formation in this area, the chordae tendineae can be gently elevated with a blunt hook to provide a clear view before transsection. Division of all chordal attachments further aids exposure by elevating the mitral ring closer to the surgeon.
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Figure 5. A, Subannular mitral valve replacement. Four quadrant sutures are brought up through the prosthetic sewing ring and then inserted through the patient's annulus from the ventricular to the atrial side. They are passed through Teflon pledgets on the atrial wall to prevent them from cutting through the annular tissue after the knot is tied. B, A profile view showing that the prosthetic ring abuts against the mitral valve ring from the ventricular side. C, Prosthetic valve on holder with four quadrant sutures inserted through the annulus. All sutures can be inserted in this manner, or interrupted single sutures can be placed between the four mattress quadrant sutures.
ring, an assistant simply holds them, and then clamps are fixed to the whole quadrant group, separating them from the next series of stitches. After the valve is seated and the sutures are tied, the aortic crossclamp is slowly released while air is evacuated from the ascending aorta. The left atrium is generally closed with a running 2-0 stitch which can be reinforced when necessary with interrupted sutures. Air must be evacuated from the left ventricular apex before the heart resumes an effective beat. Release of one or both caval tourniquets aids in the evacuation of left ventricular air. The problem of tricuspid valve incompetence in patients with either isolated mitral valve disease or aortic and mitral valve disease has not been fully resolved. In one well-known report,2 the authors recommended conservative management since, in their experience, most cases of tricuspid regurgitation reversed spontaneously after the mitral valve operation. Surgeons at the Mayo Clinic 15 concluded that tricuspid incompetence does not always regress under these circumstances. Our philosophy in this dilemma has generally been one of conservatism. We replace the tricuspid valve only when it is intrinsically damaged or
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Figure 6. A, Standard mitral valve replacement with vertical mattress sutures. This method is now called a supraannular replacement in that the prosthesis lies at the valve ring rather than below it. B, Profile of the supraannular prosthesis showing that the sutures are tied on the fabric. C, Completed prosthetic replacement by interrupted vertical mattress sutures. This method is used most often for mitral valve replacement in our institution.
seriously insufficient. When signs of moderate or severe tricuspid valvular incompetence continue after mitral valve replacement and the right atrial pressure is greater than the left atrial pressure, cardiopulmonary bypass is reestablished and the valve is then replaced by a prosthesis. Recent experience with the Carpentier ring, 3 De Vega annuloplasty, 9 and porcine xenograft 25 offers attractive alternatives to the available metallic prostheses. Periprosthetic leakage is found less often today, probably because of the surgeon's greater experience and technical facility in cardiac valve replacement. The chief cause of leakage is related to calcification and infection, and reoperation must be aggressive when signs of cardiac deterioration develop. Since dehiscence of the prosthesis frequently leaves little surrounding support, double-arm sutures mounted on Teflon pledgets are usually required to close the leak. 7 In these reoperations, the left ventricle must be fully mobilized to evacuate air effectively after the valve procedure. As noted above, adhesions may cause difficult exposure in the interatrial groove and, in this situation, the transseptal approach is a good alternative.
SUMMARY Whenever possible, the patient's own mitral valve mechanism should be preserved. Successful mitral valve repair offers excellent
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benefits in terms of hemodynamic function, clinical improvement, and longevity. Open mitral commissurotomy or valvuloplasty for localized defects or ruptured chordae tendineae constitutes our best reparative efforts. Today, mitral valve replacement can be accomplished with less than a 5 per cent operative mortality, but should be reserved for patients who are not in desperate terminal condition. In our experience, aggressive tactics undertaken at the endstage of the disease have had little or no long-term success. At the Cleveland Clinic, isolated mitral valve repair or replacement is performed under normothermic cardiopulmonary bypass and anoxic arrest. Generally, the valve is exposed through an atriotomy behind the interatrial groove. Valvular replacement is accomplished by interrupted suture technique, seating the prosthesis at the level of the annulus or below it. Risk is influenced mainly by the chronicity of the valve dysfunction. Patients who have not yet reached a Functional Class IV status or sustained massive cardiomegaly and low cardiac output fare better in both early and late follow-up periods.
REFERENCES I. Bowman, F. 0., and Maim, J. R.: The transseptal approach to mitral valve repair. Arch.
Surg., 90:329, 1965. 2. Braunwald, N. S., Ross, J., Jr., and Morrow, A. G.: Conservative management of tricuspid regurgitation in patients undergoing mitral valve replacement. Circulation, 35(Suppl. 1):63, 1967. 3. Carpentier, A., Deloche, A., Dauptain, J., Soyer, R., Blondeau, P., Piwnica, A., and Dubost, C.: A new reconstructive operation for correction of mitral and tricuspid insufficiency. J. Thorac. Cardiovasc. Surg., 61:1, 1971. 4. DaVila, J. C., and Palmer, T. E.: The mitral valve; anatomy and pathology for the surgeon. Arch. Surg., 84:174, 1962. 5. Ellis, F. H., Jr.: Surgery for Acquired Mitral Valve Disease. Philadelphia, W. B. Saunders Co., 1967, p. 49. 6. Estes, E. H., Dalton, F. M., Entman, M. L., Dickson, H. B., and Hackel, D. B.: The anatomy and blood supply of the papillary muscles of the left ventricle. Am. Heart J., 71:356, 1966. 7. Favaloro, R. G., Effler, D. B., Groves, L. K., Suarez, E., and Shirey, E. K.: Surgical repair of leaking prosthetic heart valves. Ann. Thorac. Surg., 3:503, 1967. 8. Gerbode, F., Hill, J.D., Kelly, J. J., Jr., Selzer, A., and Kerth, W. J.: Surgical correction of mitral insufficiency due to ruptured chordae tendineae. Circulation, 37 and 38(Suppl. 11):119, 1968. 9. Grondin, P., Meere, C., Limet, R., Delcan-Dominguez, J., and Rivera-Lopez, R.: Carpentier's annulus and DeVega's annuloplasty; the end of the tricuspid challenge. J. Thorac. Cardiovasc. Surg. (in press). 10. Litwak, R. S., Silvay, J., Gadboys, H. L., Lukban, S. B., Sakurai, H., and Castro-Blanco, J.: Factors associated with operative risk in mitral valve replacement. Am. J. Cardiol., 23:335, 1969. 11. McGoon, D. C.: Repair of mitral insufficiency due to ruptured chordae tendineae. J. Thorac. Cardiovasc. Surg., 39:357, 1960. 12. McGoon, D. C., Oxman, H. A., Connolly, D. C., Wallace, R. B., Danielson, G. K., and Pluth, JR.: Isolated Starr-Edwards mitral valve replacement; factors influencing early and late death and late systemic thromboembolism. (Abstr.) Am. J. Cardiol., 31:146, 1973. 13. Meyer, B. W., Verska, J. J., Lindesmith, G. G., and Jones, J. C.: Open repair of mitral valve lesions; the superior approach. Ann. Thorac. Surg., 1:453, 1965. 14. Perloff, J. K., and Roberts, W. C.: The mitral apparatus; functional anatomy of mitral regurgitation. Circulation, 46:227, 1972. 15. Pluth, J. R., and Ellis, F. H., Jr.: Tricuspid insufficiency in patients undergoing mitral replacement; conservative management, annuloplasty, or replacement. J. Thorac. Cardiovasc. Surg., 58:484, 1969. 16. Reichek, N., Shelburne, J. C., and Perloff, J. K.: Clinical aspects of rheumatic valvular disease. Prog. Cardiovasc. Dis., 15:491, 1973.
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17. Selzer, A., and Katayama, F.: Mitral regurgitation; clinical patterns, pathophysiology and natural history. Medicine, 51:337, 1972. 18. Spencer, F. C., Reppert, E. H., and Stertzer, S. H.: Surgical treatment of mitral insufficiency secondary to coronary artery disease. Arch. Surg., 95:853, 1967. 19. Starr, A., and Edwards, M. L.: Mitral replacement; clinical experience with a ball valve prosthesis. Ann. Surg., 154:726, 1961. 20. Treasure, R. L., Rainer, W. G., Strevey, T. E., and Sadler, T. R.: Intraoperative left ventricular rupture associated with mitral valve replacement. Chest, 66:511, 1974. 21. Weldon, C. S., and Ferguson, T. B.: The elimination of periprosthetic leaks as a complication of mitral valve replacement. Ann. Thorac. Surg., 18:447, 1974. 22. Winters, W. L., Jr., Hafer, J., Jr., and Soloff, L.A.: Abnormal mitral valve motion as demonstrated by the ultrasound technique in apparent pure mitral insufficiency. Am. Heart J., 77:196, 1969. 23. Wooley, C. F., Baba, N., Kilman, J. W., and Ryan, J. M.: Thrombotic calcific mitral stenosis; morphology of the calcific mitral valve. Circulation, 49:1167, 1974. 24. Zacharias, A., Groves, L. K., Cheanvechai, C., Loop, F. D., and Efller, D. B.: Rupture of the posterior wall of the left ventricle following mitral valve replacement. J. Thorac. Cardiovasc. Surg., 69:259, 1975. 25. Zuhdi, N., Hawley, W., Voehl, V., Hancock, W., Carey, J., and Greer, A.: Porcine aortic valves as replacements for human heart valves. Ann. Thorac. Surg., 17:479, 1974. Department of Thoracic and Cardiovascular Surgery The Cleveland Clinic Foundation 9500 Euclid Avenue Cleveland, Ohio 44106
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