Increase of WBC, CRP, and BSR following cardiac pacemaker implant

Increase of WBC, CRP, and BSR following cardiac pacemaker implant

Appraisal Edited by Arthur and rsappraisa C. DeGrafl A plea for early, and Julian open mitral of cardiac Frieden commissuros:omy Frank C. Spen...

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Appraisal Edited

by Arthur

and rsappraisa C. DeGrafl

A plea for early,

and Julian

open mitral

of cardiac Frieden

commissuros:omy

Frank C. Spencer, M.D. New York, N. Y.

The concept developed in this short report is that technical advances with open mitral commissurotomy have progreased to where operation should be considered at a much earlier stage than is usually done at present. Specifically, available datale5 support the concept that open mitral commissurotomy should be almost routinely performed in a patient with few symptoms, a small gradient at catheterization, and a calculated, cross-sectional valve area decrease to 1.3 to 1.5 square centimeters. It is similar to the recommendation of operation for a healthy, asymptomatic 16-year-old child with a large atria1 septal defect and a pulmonary blood flow three times normal. Even though the child can usually function well for years without operation, the longterm course is well-known; so early operation is routinely advised. A major concept underlying the importance of early operation is that a radical valvulotomy, not only eliminating the gradient but opening the valve as much as possible without producing insufficiency, may prevent progressive fibrosis from turbulent flow of blood, which in turn will require prosthetic replacement rather than reconstruction, when operation becomes necessary months or years later.

rheumatic inflammatory process, leads to progressive fibrosis, thickening and calcification at an unpredicr,able rate. Thii may occur within a few years cr may extend over three or four decades. It is not unusual for a patient in the sixth decade with a distinct rheumatic history in the late “teens” or early “twenties” to remain minimally symptomatic for the next 20 to 30 years, but eventually progress to severe calcific mitral stenosis requiring prosthetic replacement. The process is similar to that now well recognized in congenital aortic stenosis with a biscupid valve, where patients may not develop calcific aortic stenosis unt.il the sixth or seventh decade of life. Hopefully, early radical commissurotomy that decreases the turbulent flow of blood may prevent these late changes. Pathologic

processes

Reprint requests: Frank C. Spencer, M.D., Department of Surgery, New York University Hospital, Bellevue Medical Center, 550 First Ave., New York, N. Y. 10016.

Three basic processes occur with mitral valve disease. The simplest and most common is fusion of the commissures from the rheumatic inflammation. A more advanced injury is fusion and shortening of the underlying chordae, often depressing the fused commissures down to the underlying papillary muscle. The third, most severe injury is thickening and subsequent calcification of the valve leaflets which could result from the initial inflammatory process, but probably more commonly results from longstanding turbulent flow like that with aortic valvular disease. When this occurs, repair is virtually impossible. Serious secondary changes are the inevitable development of left atria1 hypertrophy, soon followed by atria1 fibrillation and the everpresent risk of thromboembolism from thrombi accumulating in the fibrillating appendage. On a few occasions the author has found 3 to 4 mm. thrombi at operation lying freely in the atria1 appendage like peas in a pod. This may be the mechanism of acute embolism in the patient who

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Etiologic

considerations

Two different pathologic processes are probably significant with rheumatic mitral valve disease. Virtually everyone agrees that the basic cause is rheumatic fever. What is not readily recognized is the concept proposed by Selzer and Cohn” that the continuing turbulent flow of blood, produced by the orifice malformed by the Fmm the Department of Surgery, Bellevue Medical Center, 560 First Received

for publication

Jan.

New York University Ave., New York, N. Y.

Hospital,

30,1978

May, 1978, Vol. 95, No. 5

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The

C. V. Mosby

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Plea for early open mitral commissurotomy

suddenly changes from atria1 fibrillation to a sinus rhythm. Another tragedy from thromboembolism is the occasional occurrence of a devastating cerebral embolus in a patient who previously has had minimal symptoms from his mitral stenosis, Other common secondary changes are the development of pulmonary hypertension and tricuspid insufficiency. The insidious, slowly progressive nature of mitral valve disease invites continued medical therapy, for the disease is primarily one of restriction of blood flow from the lungs; so the left ventricle is not injured, as occurs in mitral insufficiency or aortic valve disease. Hence by restricting physical activity and using diuretics, patients may be treated medically for decades with reasonably good results. Ultimately, however, operation is usually required, and also there is the ever-present risk of thromboembolism. Unfortunately when operation is done, prosthetic replacement is often necessary and atria1 fibrillation often remains permanent. Operative

techniques

Open mitral commissurotomy at New York University has been routinely performed for several years using cardiopulmonary bypass, using a standard technique with hemodilution, a bubble oxygenator and roller pumps. At a temperature of 25” C. the aorta is intermittently clamped for 10 to 15 minutes, intermittently unclamping the aorta, with a large catheter vent in the root of the aorta to remove air, after which the heart is defibrillated. This combination of intermittent unclamping and periodically defibrillating the heart has proved a very reliable technique, for resulting cardiac complications have been negligible. The tricuspid valve is routinely explored for insufficiency and, when found, corrected with a posterior leaflet annuloplasty in over 95 per cent of cases. The only exception is when true organic tricuspid valve disease is present. The atria1 appendage is carefully checked for thrombi, after which the orifice is routinely closed from within with a continuous suture of Prolene. This is placed carefully with superficial bites to avoid injury to the adjacent circumflex coronary artery, but has now been routinely done for over 4 to 5 years with only one instance of injury to the coronary artery occurring several years ago, clearly from a technical error. It is surprising that

American Heart Journal

the technique of routine closure of the atria1 appendage has not been widely adopted because of the well-known problem of continued fibrillation in patients who have been fibrillating for a long time before operation is performed. In patients with a prosthetic valve replacement who remain in atria1 fibrillation, it of course is impossible to tell whether a subsequent episode of thromboembolism originated from the prosthetic valve or the fibrillating appendage. Commissurotomy is performed by incising the fused commissures throughout their length, stopping a short distance from the annulus, usually only a few millimeters, where the commissure ends. The commissurotomy is never carried completely to the annulus, because a true commissure does not extend to the annulus, as small accessory leaflets are present. The change from a thickened fused commissure to a thin area is a clear technical guide to indicate where the commissurotomy should be stopped. In some patients commissurotomy is extremely simple, while in others it is complex and difficult. Several techniques of exposure are crucial, including cardiac arrest, a wide atria1 incision, and proper positioning of a malleable retractor to expose the mitral valve. Shifting the retractor as little as 2 cm. can greatly impair visualization. The key guide in commissurotomy is being certain that the mobilized leaflets are attached to the underlying chordae. In some instances the chordae actually lie close to the under surface of the fused commissure and can be readily severed if the anatomy is not clearly visualized. The “triple right angle” technique, emphasized by Mullin and associates2 in 1974, has been routinely used and remains very valuable. A more difficult technical problem, which well illustrates the advantage of open over closed commissurotomy, is found when chordae are fused, and often shortened to approximate the fused commissure to the underlying papillary muscle. By carefully separating the commissure, the underlying papillary muscle can be split and also the fused chordae separated, obtaining a functional valve that would normally be replaced, and certainly could not be adequately opened with a closed digital commissurotomy. A technique that has greatly facilitated radical commissurotomy is the ability to detect mitral insufficiency at the time of operation and correct this with sutures or an annuloplasty if necessary.

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Spencer

This is done by retrograde insertion of a catheter with multiple perforations across the aortic valve, as described by Mullin and colleagues.’ Rarely debridement of calcium may be feasible, for annuloplasty may be combined with commissurotomy.z Clearly techniques of mitral reconstruction rather than replacement are still evolving, evidenced by the work of Carpentier in Paris,* Reed” at New York University, and Rumel” in Salt Lake City. An important concept is that reconstruction is probably far more feasible and durable than has been considered possible in the past. This aggressive, radical commissurotomy has now been performed at New York University for several years. The technique has a very low mortality rate, in the range of 1 to 3 per cent. Recurrent stenosis has not been seen in any patient operated on by the author in the last ten years and the only late complication observed has been the development of insufficiency in patients in whom fibrosis and distortion of the leaflets were already present, undoubtedly the result of continued turbulent flow of blood and fibrotic contraction. Recurrent emboli have also been virtually unknown since the policy of routinely closing the atria1 appendage was adopted several years ago.

Copyright

It is well recognized that this concept may never be proved statistically because of the long, progressive course of mitral valve disease, often extending over three to five decades, and also because the relative frequency of reconstruction versus replacement will vary not only with the experience and attitude of the surgeon but with the type of valve pathology seen by him. For example, a surgeon experienced and enthusiastic about reconstruction might perform commissurotomy in 95 per cent of cases if patients are referred for operation with relatively early disease, while a similar surgeon might find it necessary to perform replacement in over 30 per cent of casesif patients are referred only with far advanced disease and extensive calcification. REFERENCES 1.

2.

3. 4.

5. 6.

Gerami, S., Messmer, B. J., Hallman, G. L., and Cooley, D. A.: Open mitral commissurotomy, J. Thorac. Cardiovast. Surg. 62:366, 1971. Mullin, M. J., Engelman, R. M., Isom, 0. W., Boyd, A. D., Glassman, E., and Spencer, F. C.: Experience with open mitral commissurotomy in 190 consecutive patients, Surgery 76:974, 1974. Reed, G. E.: The repair of mitral regurgitation: An 11 year experience, Am. J. Cardiol. 31:496, 1973. Carpentier, A.: Material presented at the Annual Meeting of the American College of Surgeons, Dallas, Texas, October, 1977. Rumel, W. R.: Personal communication. Selzer, A., and Cohn, K. E.: Natural history of mitral stenosis: A review, Circulation 45:878, 1972.

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