Open mitral commissurotomy

Open mitral commissurotomy

J THoRAc CARDIOVASC SURG 80:842-848, 1980 Open mitral commissurotomy A modern re-evaluation Familiarity with replacement of the mitral valve (MVR) ...

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J

THoRAc CARDIOVASC SURG

80:842-848, 1980

Open mitral commissurotomy A modern re-evaluation Familiarity with replacement of the mitral valve (MVR) with prosthetic and tissue valves has dimmed awareness of the usefulness of open mitral commissurotomy (OMC). This is a review of a 10 year experience ending in December, 1978, of 222 consecutive patients operated upon with a clinical diagnosis of pure mitral stenosis. MVR was necessary in 25 patients (11.3%), primarily because of severe deformity of valvular and sub valvular structures. No closed commissurotomies were performed, as that operation is now considered passe. Of the 197 patients undergoing OMC, 12 had additional cardiac procedures. Of the three patients who died (1.52%), two were operated upon on an emergency basis because of rapidly progressive cardiac failure. Follow-up data were obtained on 191 (97%) of the 197 OMC patients. There were 18 late deaths, of which 14 were related to cardiac disease. Following OMC, 76% (146) of the patients had improved by at least one New York Heart Association class. Fourteen (7%) of the 191 OMC patients had subsequent MVR at times varying from 2 to 92 months after OMC (mean 41.6 months). Ten-year survival for the 197 OMC patients was 81 %. This clinical experience emphasizes that open commissurotomy rather than valve replacement is the best initial treatment for most patients with mitral stenosis.

William L. Halseth, M.D. (by invitation), Donald P. Elliott, M.D. (by invitation), E. L. Walker, M.D. (by invitation), and E. A. Smith, R.N. (by invitation), Denver, Colo. Sponsored by Ben Eiseman, M.D., Denver, Colo.

A s the technology of prosthetic valves improves it is constantly necessary to re-evaluate the relative indications for mitral valve repair and replacement. The magnitude of the problem is appreciated by realizing that approximately 13,000 mechanical and tissue valves were implanted in the mitral position in 1979. * Modem mechanical valves are durable but their insertion involves complications of thromboembolism, valve thrombosis, paravalvular leak, and infection.!":' Postoperative anticoagulation inevitably involves additional risk."? Ultimate deterioration of porcine heterografts casts suspicion on the long-term durability of tissue valves.v !' These factors and the lesser mortality of valve repair compared to replacement dictate a From the Departments of Cardiovascular Surgery of St. Anthony Hospital and Rose Medical Center, Denver, Colo. Read at the Sixtieth Annual Meeting of The American Association for Thoracic Surgery, San Francisco, Calif., April 28 to 30, 1980. Address for reprints: William L. Halseth, M.D., 4200 West Conejos Place, Suite 436, Denver, Colo. 80204. *Shiley, Inc., Irvine, Calif.

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policy of valve repair as the initial operation for pure mitral stenosis and increasingly for insufficiency. 12-19

Methods During a 10 year period from January, 1969, through December, 1978, 222 patients with the primary diagnosis of mitral stenosis had open mitral surgical procedures. Patients ranged in age from 15 to 72 years and included 161 females and 61 males. Thirty-two patients had previously undergone closed mitral commissurotomy (CMC). Of the 197 patients (88%) who had open comrnissurotomy (OMC), 38 preoperatively were in New York Heart Association (NYHA) Functional Class II, 153 patients were in Class III, and six patients were in Class IV. Operation was performed with the use of cardiopulmonary bypass with a bubble oxygenator. Moderate systemic hypothermia (24 to 26 C) was used for myocardial protection. The aorta was cross-clamped during commissurotomy. Fused leaflets, chordae tendineae, and papillary muscles were sharply split. 12 Calcium de0

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0022-5223/80/120842+07$00.70/0 © 1980 The C. V. Mosby Co.

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posits and fibrous tissue were debrided from the leaflets where necessary . Left atrial thrombus, if present, was removed. Following removal of the cross-clamp, digital distortion of the aortic root created aortic regurgitation and permitted filling of the left ventricle with the pump perfusion pressure , so that the repaired mitral valve could be assessed. More recently, with the aorta cross-clamped, cold cardioplegia solution injected into the aortic root has been used to test the mitral valve. During the past 6 years, the orifice of the left atrial appendage was oversewn in all patients with a large left atrium or atrial fibrillation. Intraoperative cardioversion was attempted in all patients with atrial fibrillation. Left atrial pressure was monitored for 48 hours postoperatively. Anticoagulants were not routinely given following valve repair. Follow-up data were obtained through examination and interview of the patients and from questionnaires sent to rural referring physicians and their patients. Survival curves were computed by the actuarial or life-table method. The chi square method was used to compare variables in the group having mitral valve replacement (MVR). Results Of these 222 patients operated upon for mitral stenosis, 197 (88.7 %) had a successful OMC and 25 (11.3 %) had an initial MVR (Fig. 1) . Of 32 patients having previous CMC, eight required initial MVR and 24 had successful OMC. Two of the 24 patients subsequently required MVR . The sex distribution of these 197 patients undergoing OMC was 139 women and 58 men. The women ranged in age from 19 to 72 years with a mean of 48.7 years, and the men ranged in age form 27 to 69 years with a mean of 51.2 years. Hospital mortality was 1.52% (three patients) . The three who died included two moribund patients operated upon under emergency conditions. One patient was in septic shock from a staphylococcal infection of a large left atrial thrombus. The other patient was in cardiogenic shock following cardiac arrest and transfer from another hospital. The third patient died 20 days postoperatively from gram-negative sepsis of genitourinary tract origin. Late follow-up was obtained in 191 of the 197 OMC patients (96.6%) . Follow-up ranged from 9 to 120 months with a mean of 52.9 months . Eighteen late deaths were recorded . Fourteen deaths were cardiac related. Two of these late deaths occurred following MVR, five patients died in congestive heart failure, four died as a result of coronary artery disease, and one died of cardiac arrhythmia . Thromboemboli resulted

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88.7% OMC

AVA

AVC TVA

TVA oo.a..E CAB SNG..E CAB

Fig. 1. All patients with mitral stenosis (N = 222). AVR . Aortic valve replacement. AVC. Aortic valve commissurotomy . TVR. Tricuspid valve replacement. TVA. Tricuspid valve annulopla sty. CAB . Coronary artery bypass.

in two deaths . Four unrelated deaths were caused by cancer , emphysema, pancreatitis, and cerebral hemorrhage. Thrombus and embolus. Preoperatively , 10 patients had systemic thromboemboli . Postoperatively, cerebral emboli occurred early in one patient and late in two patients , all in atrial fibrillation. Postoperatively, 55 OMC patients had occasional or persistent atrial fibrillation. Twenty-seven patients were taking anticoagulants at the time of follow-up . At operation, fibrin thrombus was removed from the mitral leaflets in 19 patients. Three patients from this group had recent preoperative episodes of systemic thromboemboli. Left atrial clot was removed in 18 patients, two of whom had experienced transient neurologic problems from cerebral thromboemboli within 10 days prior to OMC. Calcification and subvalvular fusion. Fifty-four OMC patients had mitral valve calcification. There was moderate valvular calcification in 28 patients and necessitated debridement of leaflet calcium and fibrous tissue in 23 patients. Subvalvular dissection of fused chordae tendineae and papillary muscles was performed in 119 patients (60%) . Nineteen of 22 patients with prior CMC successfully treated by OMC required subvalvular dissection. Postoperative complications. In addition to the three patients with cerebral thromboemboli, seven other patients had nonfatal postoperative complications, including one case each of hemorrhage, pulmonary embolus , cardiac tamponade , superficial wound

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YEARS _ _ _ _ ALL PATIENTS WITH PRIMARY Ox. OF MITRAL STENOSIS (N-1971 _._._._._ .. PATENTS WHO HAD OMC ONLY (N-183)

Fig. 2. Actuarial survival. OMC, Open mitral commissurotomy. infection, tracheal stenosis, keloid scar, and respiratory insufficiency. Reoperation. None of the 197 OMC patients have required subsequent operation for restenosis. Reoperation with replacement of the mitral valve (MVR) was required in 14 patients (7.2%). This group included II women and three men ranging in age from 35 to 67 years (mean age 50.8 years). Time between commissurotomy and replacement ranged from 2 to 92 months (mean 41.6 months). Six patients required MVR within 30 months following commissurotomy. Ages of the patients ranged from 35 to 65 years. Two members of this group had other procedures combined with commissurotomy. One patient had valve calcification and another had a left atrial thrombus. One patient had a prior CMC. Four patients in this group were alive at the time of follow-up and two had died. The remaining eight patients who had MVR went considerably longer after commissurotomy before requiring operation. The range was from 38 to 92 months with a mean time of 64.5 months. Ages of the patients ranged from 43 to 67 years. One patient had a tricuspid annuloplasty at the time of OMC. Another patient in this group had valve calcification and a third had an atrial thrombus. CMC had been done in another patient. At the time of follow-up six patients in this group were alive and two were dead. As anticipated, valvular insufficiency created at the time of OMC more frequently dictated early MVR, with a chi square value of 4.40 (I df; P = 0.01). There was no significant correlation (p = 0.05) with early MVR, patient age, prior operation, calcification of the valve, or additional procedures performed at the time of OMC. Functional results. At the time of follow-up 41 pa-

tients were in NYHA Functional Class I, 107 patients were in Class II, 11 were in Class Ill, and one was in Class IV. Actuarial survival rate for the 197 OMC patients ranged from 96.3% the first year to 80.6% after 10 years. Survival rate for the patients who did not require subsequent reoperation for MVR was 86% at 10 years (Figs. 2 and 3). Discussion Since 1969 we have used the open approach for the operative treatment of mitral stenosis, with no intraoperative deaths and with a single perioperative cerebral embolic event which caused temporary aphasia at 4 days. Cardiopulmonary bypass permits visualization of the mitral valve and precise incision of the fused commissures, chordae tendinease, and papillary muscles. The anterior leaflet and commissural area can be meticulously debrided of calcium and fibrous tissue. Left atrial or leaflet thrombus can be safely removed and valvular regurgitation directly observed by creating aortic insufficiency, and MVR or repair then can be performed as necessary. Replacement incidence. Repair (OMC) not replacement (MVR) was possible in 88.7% of 222 patients. We were able to re-repair, not replace, the valve in 22 of 32 patients with prior CMC. These results compared favorably with the results reported by Roe and colleagues 12 in 1971. In this series 25 of 222 patients (11.3%) required initial MVR because of severe valve deformity, heavy calcification, and/or created insufficiency which could not be repaired. Moderate-to-severe valve calcification necessitated MVR in 25% of patients in a series reported by Grantham and co-workers.f" Olinger, Rio, and Maloney" reported success with CMC for moder-

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Fig. 3. New York Heart Association functional classification.

ately heavy valve calcification in a small patient group. Valve calcification was not a cause for early reoperation for MVR in this study. Mortality. Closed commissurotomy, a procedure that we do not perform, had a mortality of 1% to 3 .7 %, which is essentially similar to that of the more precise open procedure. 20- 23 Operative mortality in this series (1. 5%) is comparable to that reported by others. 12-14. 24 Late deaths related to heart disease were due to thromboembolic events, pre-existing or co-existing cardiac disea se , and residual mitral insufficiency necessitating reoperation (MVR) . Embolus. Studies have found no correlation between the incidence of thromboembolism and the presence of left atrial thrombus or atrial fibrillation. 13. 24 In this series, however, fibrin thrombus was removed from mitral leaflets in three patients and left atrial thrombus was removed in two patients , all of whom experienced thromboembolic events within 2 to 3 weeks prior to OMC. Previous studies record an intraoperative embolic rate of 2.6%20 and resultant death in the early postoperative period following CMC. 22 We had no such catastrophes in the 197 open procedures. There were two late deaths and three instances of systemic thromboembolic complications in patients with atrial fibrillation not receiving warfarin sodium. Long-term anticoagulation therapy has been used in an attempt to prevent late systemic emboli in patients with chronic atrial fibrillation and a large left atrium, and for the past 6 years the atrial appendage has been excluded at the time of OMC. Removal of fibrin thrombus from leaflets and left atrial clot in 37 patients may have prevented early postoperative emboli, since there was only one episode of early postoperative thromboembolism .

Restenosis. The incidence of restenosis necessitating reoperation after CMC may be as high as 60 % to 70 % at 10 years ." Glenn and co-workers" stated that all patients undergoing CMC are potential candidates for restenosis. No patient in this OMC series required operation for restenosis. The high rate of restenosis following CMC may result from untreated subvalvular ste nosis. Subvalvular fusion was not relieved in eight of 63 patients undergoing CMC reported by John and associates. " Release of subvalvular stenosis was performed at OMC in 19 of 24 patients in our group who had prior CMC. Mullin's group" reported that 30% of patients had subvalvular dissection and valve debridement at OMC. Fused chordae tendineae and papillary muscles necessitated splitting dissection in 119 of 197 (60%) OMC patients. Reoperation. The need for reoperation (MVR) following OMC in 22 of 314 patients (7.00%) in Mullin's series was similar to that in this series (7.2%) but lower than the 16% rate reported by Hou sman and colleagues.'" Mullin and associates>' reported early reoperation M VR for regurgitation in two of 96 patients following OMC. In this series six of 194 OMC survivors required early MVR for regurgitation . Combined operations did not increase mortality . Coronary arteriography should be performed at catheterization if there is a possibility of coexistent coronary artery and mitral valve disease. Functional improvement. One hundred forty-six patients had improved by at least one NYHA class . The surv ival rate at 10 years for those patients who did not require reoperation for MVR was 86%. The OMC results of Housman's group!" were better, with an actuarial projected survival of 97 % at 10 years.

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Conclusions 1. It is our belief that all patients requiring operation for mitral stenosis should have an open operation. This approach was used in 222 consecutive patients with pure mitral stenosis, and only 22 (11.3%) patients required MVR as the initial procedure. 2. After successful OMC, only a small number of patients will require subsequent MVR. In this series, 14 of 197 (7.2%) patients required reoperation and

MVR.

3. Fused subvalvular structures should be released at OMC to provide adequate leaflet motion and to prevent restenosis. None of the OMC patients have required operation for restenosis during the follow-up period, which has averaged 52.9 months. Sixty percent of 197 patients required subvalvular dissection at OMC. 4. Patients with a large left atrium and those in chronic atrial fibrillation should have the atrial appendage oversewn and be considered for long-term anticoagulation therapy to reduce embolization. 5. Low hospital mortality (1.5%) and a survival rate of 81 % at 10 years following OMC justifies strenuous effort to salvage and save, not replace, a stenotic mitral valve.

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REFERENCES Salomon NW, Stinson EB, Griepp RB, Shumway NE: Mitral valve replacement. Long-term evaluation of prosthesis-related mortality and morbidity. Circulation 56:Suppl 2:94-101, 1977 Edmiston WA, Harrison EC, Duick GF, Parnassus W, Lau FYK: Thromboembolism in mitral porcine valve recipients. Am J CardioI41:508-51I, 1978 Kirklin JW, Pacifico AD: Surgery for acquired valvular heart disease. N Engl J Med 288:194-198, 1973 Herbert DC: Anticoagulant therapy and the acute abdomen. Br J Surg 55:353-357, 1968 Faraci PA, Deterling RA Jr, Stein AM, Rheinlander HF, Cleveland RJ: Warfarin induced necrosis of the skin. Surg Gynecol Obstet 146:695-699, 1978 Shaul WL, Hall JG: Multiple congenital anomalies associated with oral anticoagulants. Am J Obstet Gynecol 127:191-198, 1977 Roberts MH, Johnston FR: Hepatic rupture from anticoagulant therapy. Arch Surg 110:1152, 1975 Geha AS, Laks H, Stansel HC Jr, Cornhill JF, Kilman JW, Buckley MJ, Roberts WC: Late failure of porcine valve heterografts in children. J THORAC CARDIOVASC SURG 78:351-364, 1979 Oyer PE, Stinson EB, Reitz BA, Miller DC, Rossiter SJ, Shumway NE: Long-term evaluation of the porcine xenograft bioprosthesis. J THORAC CARDIOVASC SURG 78:343-350, 1979 Hetzer R, Hill JD, Kerth WJ: Thrombosis and degenera-

Thoracic and Cardiovascular Surgery

tion of Hancock valves. Clinical and pathological findings. Ann Thorac Surg 26:317-321, 1978 II Lewis JW Jr: Discussion of Geha et al" 12 Roe BB, Edmunds LH Jr, Fishman NH, Hutchinson JC: Open mitral valvulotomy. Ann Thorac Surg 12:483-491, 1971 13 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 73:742-745, 1977 14 Finnegan 10, Gray DC, MacVaugh H III, Joyner CR, Johnson J: The open approach to mitral commissurotomy. J THORAC CARDIOVASC SURG 67:75-82, 1974 15 Chaffin JS, Daggett WM: Mitral valve replacement. A nine-year followup of risks and survivals. Ann Thorac Surg 27:312-319, 1979 16 Hammermeister KE, Fisher L, Kennedy JW, Samuels S, Dodge HT: Prediction of late survival in patients with mitral valve disease from clinical, hemodynamic and quantitative angiographic variables. Circulation 57:341349, 1978 17 Reed GE, Pooley RW, Moggio RA: Durability of measured mitral annuloplasty. J THORAC CARDIOVASC SURG 79:321-325, 1980 18 Duran CG, Pomar JL, Revuelta JM, Gallo I, Poveda J, Ochoteco A, Ubago JL: Conservative operation for mitral insufficiency. J THORAC CARDIOVASC SURG 79:326-337, 1980 19 Shore OF, Wong P, Paneth M: Results of mitral valvuloplasty with a suture plication technique. J THORAC CARre D10VASC SURG 79:349-357, 1980 20 Grantham RN, Daggett WM, Cosimi AB, Buckley MJ, Mundth ED, McEnany MT, Scannell JG, Austen WG: Transventricular mitral valvulotomy. Analysis of factors influencing operative and late results. Circulation 49,50: Suppl 2:200-212, 1974 21 Olinger GN, Rio FW, Maloney JV Jr: Closed valvulotomy for calcific mitral stenosis. J THORAC CARre DIOVASC SURG 62:357-365, 1971 22 Glenn WWL, Calabrese C, Goodyear AVN, Hume M, Stansel HC Jr: Mitral valvulotomy. II. Operative results after closed valvulotomy. A report of 500 cases. Am J Surg 117:493-501, 1969 23 Ellis LB, Singh lB, Morales DO, Harken DE: Fifteen to twenty-year study of one thousand patients undergoing closed mitral valvuloplasty. Circulation 48:357-364, 1973 24 Mullin MJ, Engelman RM, Isom OW, Boyd AD, Glassman E, Spencer FC: Experience with open mitral commissurotomy in 100 consecutive patients. Surgery 76:974-982, 1974 25 Logan A, Lowther CP, Turner RWD: Reoperation for mitral stenosis. Lancet 1:443-449, 1962 26 John S, Perianayagam WJ, Abraham KA, Jairaj PS, Krishnaswami S, Sukumar IP, Cherian G: Restenosis of the mitral valve. Surgical considerations and results of operation. Ann Thorac Surg 125:316-321, 1978

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27 Kay EB, Rodriguez P, Haghighi 0, Suzuki A, Zimmerman HA: Mitral stenosis. Comparative analysis for postoperative results following the closed and open operative approach. Am J CardioI14:139-147, 1964 28 Olesen, KH: The natural history of 271 patients with mitral stenosis under medical treatment. Br Heart J 24:349357, 1962

Discussion DR. CARLOS G. DURAN Santander. Spain

Between June, 1974, and December, 1978, 876 open mItral operations were performed at our institution. Three hundred eighty-seven of the patients had isolated mitral disease. In this group of patients 163 commissurotomies were performed, with a 1.2% hospital mortality. In 103 patients the commissurotomy had to be followed by a flexible ring annuloplasty, with a 1.9% mortality. The remaining 121 patients required valve replacement, with a 9.9% hospital mortality. Close to 70% of our isolated mitral operations have been conservative procedures. In this particular group of patients, 103 valves were saved from replacement by an annuloplasty. I think we have to consider open mitral surgery, not just in terms of commissurotomy or replacement, but as a continuum that stretches between simple commissurotomy and replacement, with a large intermediate area of various plastic procedures which will save many valves. DR. CHARLES P. BAILEY New York. N. Y.

I have only two suggestions with respect to this delightful paper. First, an attempt should always be made first to mobilize the stenotic mitral valve by the closed technique. If it fails, the open procedure is then immediately available. Second, it is overly optimistic to say that replacement will never be necessary in 93% of the cases. The stenosis will recur in almost all cases-unless the pathogenetic process is somehow interrupted. And what is that? It is repetitive, and each episode begins with the aggregation of platelets upon the abnormal (inflamed, roughened, or stiffened) surfaces of the diseased valve. This leads to the deposition of fibrin upon all these surfaces, including the chordae tendineae. Frank Magarey, in 1951, described this beautifully in the British Journal of Medicine. This is followed by organization and then by distortion due to contraction of this newIy formed scar tissue. To stop the continuation of this process after surgical mobilization of the valve, one must forever use platelet-dispersing drugs such as aspirin or dipyridamole (Persantine), as suggested by Drs. Sullivan, Gorlin, and myoid adversary, the senior Dr. Harken. DR. BENSON B. ROE San Francisco. Calif.

Dr. Halseth and his colleagues have resurrected an ancient controversy with which I have long been identified, and I am

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delighted to recognize the chalice in the hands of a disciple. Their score of only II % requiring replacement of the mitral valve is certainly commendable, and their long-term results, I believe, vindicate the operative choice over the closed procedure. I do wonder, however, whether the two patients requiring subsequent MVR and the five dying late, in congestive heart failure, represent incorrect intraoperative assessments and should have had replacement. I agree emphatically with the significantly better anatomic result which can be achieved with careful retraction and exposure, as they demonstrated. The subvalvular anatomy is important, and a plane must be developed which will result in complete leaflet mobilization. This is a delicate task which most certainly cannot be duplicated by a blind tearing process. I challenge the concept of "fused" subvalvular structures, despite Dr. Bailey's illustrations, because it has been my observation that the thickened chordae and papillary muscle serving both leaflets seldom have the appearance to suggest previous separation. On this basis I have long believed that mitral stenosis, like bicuspid aortic stenosis, represents a congenital state of tethered leaflets or short chordae which subsequently become thickened and calcified. In the process of assessing the result of open mitral commissurotomy, I must emphasize that an orifice produced by introducing a finger or an obturator is not necessarily the same as that created with atrial hydraulic pressure. For the purposes of follow-up evaluation, I would encourage the authors to grade their operative result according to the orifice presenting in the relaxed state after completion of their commissurotomy. If the valve leaflets fall open so that you are looking into the ventricle, not shoving your finger into it, then the commissurotomy has an A rating; if the orifice is partially or significantly closed but can be totally opened by an instrument or your finger, a B rating; and if little or no significant orifice improvement has been achieved, a Crating. The authors are certainly to be commended for upholding the important skill of valve preservation which has lagged in this country and which has been so well demonstrated by our European colleagues, Carlos Duran and Alain Carpentier, in particular. DR. FRANK C. SPENCER New York. N. Y.

Dr. Cunningham, a member of our faculty at New York University, prepared these slides for me. I was impressed by how similar our data are to Dr. Halseth's. Over a period of 10 years, we have performed an open mitral commissurotomy in 202 patients. [Slide] This slide illustrates the technique for evaluating mitral insufficiency at the time of operation. The technique was published several years ago and consists of manipulating a perforated catheter across the aortic valve, with some perforations remaining above and some below the valve, so that there is controlled aortic insufficiency. This is different from compressing the aortic root with the finger, a suggestion made by Sterling Edwards some years ago. Why this works better

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than a vent, I am not sure. It may be like the wind catching the sail, depending upon the direction in which force is applied, but it has been of great value at the time of operation. The technique enables the surgeon to perform a more aggressive commissurotomy, because the insufficiency can be checked and repaired if it is inadvertently produced. I think the goal with commissurotomy is not to eliminate the gradient, which can be done by obtaining a cross-sectional area between 2.0 and 2.5 em", but to minimize turbulent flow as much as possible. Dr. Duran mentioned that, in about one half of their patients, insufficiency was detected and corrected with an annuloplasty. Hence, there is a great advantage during commissurotomy of having a reliable technique for detecting insufficiency at the time of operation. I am reasonably certain that many commissurotomies in the past were unduly conservative, resulting in incomplete results and restenosis within a few years, because the original valve was not opened sufficiently. We have now used the perforated catheter technique for several years and have found it reliable, although a bit cumbersome. [Slide] This slide illustrates a survival rate up to IOyears of about 97%. The 5 year survival rate is equally good. Hence, the durability of the operation is very similar to that presented by Dr. Halseth. About 85% of the patients were free of complications at 5 years; about 65% at IO years. There were only six emboli in the entire group-3%. [Slide] Again, similar to Dr. Halseth's experience, we have had to replace the valve in only about 6% of the cases. Reoperation was necessary for residual stenosis in a few patients, mitral regurgitation in the majority. Returning to Dr. Halseth's data, the most significant point in his paper is that he had to do a subvalvular operation in about 60% of the cases. We have not tabulated our data as well as his have been done, but this is a key point. This is the main difference between a closed commissurotomy and open commissurotomy and the reason that I consider a closed commissurotomy to be an inferior operation, because the subvalvular mechanism with fused chordae cannot be effectively treated. In nine of IO patients, Dr. Halseth was able to do a commissurotomy; even in patients operated upon for the second time, a total of 32, commissurotomy was possible in three of four. The efficacy of the commissurotomy is clearly shown by the fact that, to date, he has not had to perform a single reoperation for restenosis. It is impressive to remember that 20 years ago commissurotomy was simply stated to be a palliative procedure because the recurrence rate was about 50%. In retrospect, this

simply means that the valves were not opened adequately by the digital commissurotomy technique, a point emphasized by Ben Roe and many others. Hence, to repeat, these data dramatically demonstrate the great value of the open procedure, both to perform a more effective commissurotomy and to protect from emboli. Finally, I have three questions: One concerns the importance of oversewing the orifice of the atrial appendage, a practice we have followed for several years and do routinely. We cannot prove the statistical value because we have had only six emboli in our entire group. I wonder if Dr. Halseth has any data that this procedure significantly protects from emboli. I think it should, but I cannot prove it. We have not had any problems with our technique of closing the atrial appendage from within in more than 200 patients. My second question is whether gradients were measured at operation. In our experience, a residual gradient, as little as 3 or 4 mm, has an ominous prognosis. Three or four such patients have retumed with severe restenosis within 3 or 4 years, in contrast to those in whom the gradient was completely eliminated. My final question is whether you have been completely satisfied with your digital method of inducing aortic insufficiency to evaluate mitral insufficiency? DR. HAL SET H (Closing) I would like to thank the discussers for their kind and thoughtful remarks. Dr. Duran is to be commended for his conservative approach to mitral valve surgery. Dr. Bailey's evangelistic comments on the controversy of open versus closed operation are appreciated. Dr. Roe, the five late deaths which resulted from congestive heart failure did not occur in patients having recurrent mitral stenosis or insufficiency. Dr. Spencer, we have oversewn the atrial appendage during the past 6 years. The two late deaths from cerebral thromboemboli occurred in patients with chronic atrial fibrillation, and the atrial appendage had not been oversewn. We have not had the opportunity to routinely restudy the patients postoperatively by cardiac catheterization to determine mitral valve gradients. The patients have been followed clinically. However, patients requiring reoperation obviously did have repeat cardiac catheterization and they did have mitral insufficiency. Dr. Spencer, we have been pleased with the success in testing mitral valve repair by the simple technique of digital pressure on the aortic root, which creates aortic regurgitation. The left ventricle is filled with systemic perfusion pressure and mitral valve competency can be easily evaluated.