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Indications for surgery of the mitral valve
CONTROVERSIESIN CARDIOLOGY-I
Indications for Surgery of the Mitral Valve LAWRENCE
Milwaukee,
I. BONCHEK,
MD,
FACC
Wisconsin
In a recent review of the indications for mitral valve surgery published in this Journal, Fowler and Van Der Bel-Kahn1 suggested that as a general rule, mitral valve replacement. should be “considered only for patients in functional classes III or IV of the New York Heart Association* who do not respond to medical management ” Patients with mitral stenosis, who are often can%&es for mitral commissurotomy, should not have surgical treatment “as long as symptoms can be controlled medically,” since there need be no fear of “progressive left ventricular dysfunction that might become irreversible.” Our practice at the Milwaukee Regional Medical Center of the Medical College of Wisconsin is sufficiently different to warrant exposition, in view of the current results of mitral valve surgery. Mitral Regurgitation Operative Mortality
It is generally agreed that no operation should be offered unless its benefits outweigh its risks. In the article by Fowler and Van Der Bel-Kahn, the principal concerns about mitral valve replacement were the “high” operative mortality and morbidity in patients with mitral insufficiency, and the complications related to prosthetic valves. Reported experience: In support of their concern about operative mortality, the authors cited reports published in 1973 in which the operative mortality rates in patients with mitral insufficiency were 19 and 20 percent, respectively. 3p4They then suggested that “more recent reports” indicate a mortality rate of 7, percent, and cited a report that, although published in 1976, also discussed patients operated on in 1972 and 1973. However, even in that report despite a total early mortality rate of 7 percent, patients in New York Heart Association functional class III preoperatively had a 1.3 percent operative mortality rate for open mitral valve surgery; all but two operative deaths were in patients in functional class IV before operation. Even so, none of those studies reflects the current state of the art for mitral valve replacement. Reports from major cardiac centers of high operative mortality From the Department of Cardiothoracic Surgery,The f4edical College of Wisconsin, Milwaukee, Wisconsin. Manuscript received December 28, 1979, accepted March 12, 1980. Address for reprints: Lawrence I. Bonchek, MD, Department of Cardiothoracic Surgery, The Medical College of Wisconsin, 8700 West Wisconsin Avenue, Milwaukee, Wisconsin 53228.
rates for mitral valve replacement are usually attributable to the inclusion of patients tindergoing emergency valve replacement for cardiogenic shock due to myocardial infarction with rupture of a papillary muscle, or of patients with chronic ventricular dysfunction due to ischemic heart disease who undergo concomitant coronary bypass surgery. 6,7Published reports must be scrutinized for potentially confusing inclusion of heterogeneous subsets of patients. Results in patients with cardiogenic shock, in neglected patients in functional class IV or in those who require concomitant procedures are simply not relevant to the decision to carry out elective isolated mitral valve replacement in patients in functional class III with chronic mitral valve disease. Such patients can be operated on in large centers with an operative mortality rate of 1 to 3 percent.5,s,g Technical misadventures such as intraoperative atrioventricular disruption that causes uncontrollable hemorrhage are now rare causes of operative death. (This writer has not experienced such a complication.) Most operative deaths (70 to 90 percent.) are now caused by left ventricular failure, arrhythmias or infarction, which occur predominantly in neglected patients with endstage ventricular dysfunction or coronary artery disease, or both.8 As will be discussed further, the sudden increase in left ventricular afterload that accompanies restoration of mitral valve competence can acutely depress left ventricular ejection in some patients, thus unveiling more advanced ventricular dysfunction than had been appreciated preoperatively.1° Personal experience: Our own experience confirms the low mortality of mitral valve replacement. We8 reported a series of 150 consecutive mitral replacements that concluded in 1974 with an operative mortality rate of 2 percent. Although Fowler suggests that low operative mortality rates must be due to inclusion of large numbers of patients with early disease, few symptoms and good ventricular function, or that the definition of hospital mortality in such a report may not have been liberal enough, our publication clearly indicated that only 17 patients were in functional class II, whereas 112 were in class III and 21 in class IV. (Many of the patients in class II had predominant mitral stenosis, and the primary indication for operation was preoperative emboli.) There were two operative deaths (1.8 percent) in the 112 patients in class III, and one death (4.8 percent) in the 21 patients in class IV. All hospital deaths, and all those occurring within 30 days, were included; July 1990
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each was described in detail. The New York Heart Association classifications were assigned in conjunction with the cardiologists at the University of Oregon, whose views on valve disease are well known.‘lJ2 Current results of mitral valve replacement at the Milwaukee Regional Medical Center 07 the Medical College of Wisconsin are consistent with those reported earlier from the University of Oregon. If one excludes patients with preoperative cardiogenic shock due to acute myocardial infarction, there was one operative death (2 percent) in the last 50 consecutive mitral valve replacements performed. The death occurred in a moribund patient in functional class IV with cardiac cirrhosis, hypersplenism, cachexia and left main coronary stenosis that was unrecognized because the patient’s preoperative renal failure and ventricular irritability (including ventricular tachycardia during catheterization) precluded complete coronary angiography. As noted earlier, such results are not unique.5s The recent introduction of hypothermic cardioplegic arrest has been a major advance in intraoperative management. Fowler and Van Der Bel-Kahn suggest that aortic valve replacement has “a lower average surgical mortality rate” than mitral valve replacement. In my personal experience,13 isolated mitral valve replacement has always had an operative mortality rate as low as or lower than that of aortic valve replacement.
Hemorrhagic complications of anticoagulant therapy occurred in six patients in our series (2 percent per patient year), but most of these were trivial (hematuria, leg hematoma, for example). One complication was serious (subarachnoid hemorrhage), but none was fatal. In the series of Bjork and Henze, the incidence rate of serious hemorrhagic complications was 0.4 percent per patient year. It must be emphasized that patients with mitral valve disease who are not treated surgically are at risk of thromboembolic episodes, and often receive anticoagulant therapy. In our series,8 13 patients (9 percent) had preoperative emboli. Although the total preoperative period at risk for all patients was not comparable with the postoperative period of follow-up, the overall incidence of embolism was higher before than after valve replacement. Finally, it is apparent that bacterial endocarditis can also develop in patients who are not operated on, and this, too, can be fatalis It is not statistically meaningful to cite cases of prosthetic endocarditis observed in a particular medical center within a particular time span without knowing the total number of patients with prosthetic heart valves at risk in that population, as well as the number of patients at risk with valvular heart disease who were not operated on in whom endocarditis developed. Such comparative data have not been reported.
Late Prosthesis-Related Complications
Functional Results of Mitral Valve Replacement
In the 1960’s the long-term results of mitral valve replacement were influenced significantly by valverelated complications. Now that cardiac surgical techniques and prosthetic devices have improved considerably, the postoperative prognosis is no longer influenced as significantly by valve-related complications.13 In the report cited earlier8 of experience with the cloth-covered Starr-Edwards prosthesis, there were 15 late deaths (10 percent) from 1 to 35 months postoperatively. Actuarially projected survival at 5 years was 85 percent. Most important, only 3 of the 15 late deaths were related to the prosthesis7; others were of cardiac origin (myocardial failure, for example), and 6 were of noncardiac origin. Overall, in survivors and nonsurvivors, there were two instances of perivalvular leak (1 percent per patient year), three of prosthetic endocarditis (1 percent per patient year) and nine of systemic embolism (3 percent per patient year). The Bjork-Shiley prosthesis has had a similarly low incidence rate of late complications. In the experience of Bjork and Henze14 with 195 patients who had mitral valve replacement, the incidence rate of late complications related to the prosthesis was 1.2 percent per patient year for perivalvular leak or prosthetic thrombosis requiring reoperation and 0.4 percent per patient year for prosthetic endocarditis. Systemic embolism occurred at a rate of 6 percent per patient year. With tissue valves such as the Hancock porcine bioprosthesis, the incidence rate of thromboembolic complications is lower (3 to 5 percent per patient year), even though most patients do not receive long-term anticoagulant therapy unless they have chronic atria1 fibrillation.7J5
Current survival statistics after mitral valve replacement are based on data from patients who had, in most cases, advanced disease before operation. Late survival in patients who undergo operation earlier would undoubtedly be better, because late myocardial failure-the most frequent cause of late death-would be uncommon. Moreover, survival after valve replacement must be compared with natural history studies that begin with the development of symptoms, not with diagnosis, lest an inappropriately long and benign course with medical treatment be inferred. Mortality in medically treated valve disease varies widely (from 25 to 75 percent at 5 years) depending on the nature and site of the valve lesion and the circumstances under which the patient entered the study.i7 Left ventricular function: The left ventricle in mitral regurgitation has a chronic volume overload that is ejected partially through a low impedance path into the left atrium. As a result, patients with mitral regurgitation may have severe hemodynamic abnormalities without striking clinical disability. The left ventricle eventually suffers irreversible damage, and may become so dependent on afterload reduction that mitral valve replacement, which increases afterload, causes further depression of certain variables of left ventricular performance. Schuler and co-workers18 at the University of California, San Diego recently demonstrated that in patients with marked left ventricular enlargement and hypertrophy (defined by quantitative criteria), and ejection fraction at the lower end of the normal range mitral valve replacement was followed (1) by severe impairment of the ejection fraction that continued to worsen 1 year after operation, (2) persistent left ven-
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tricular dilatation and hypertrophy, and (3) increased end-systolic dimensions. In contra&valve replacement in patients with mild to moderate ventricular dilatation and hypertrophy was followed by reduction in left ventricular size and hypertrophy and no deterioration of left ventricular performance. Optimal timing of valve replacement: We8 assessed this problem in a different manner in 1974, and found no correlation between postoperative functional class and 19 preoperative clinical and hemodynamic variables including age, functional class, rhythm, left atria1 pressure, left ventricular end-diastolic pressure, cardiac index or pulmonary vascular resistance. (The patients studied had been evaluated before calculation of cardiac dimensions and ejection fraction became routine.) However, a prognostic classification derived from the duration of symptoms and the response to medical management was highly discriminatory. Patients with clinical symptoms for more than 3 years who did not show improvement by at least one functional class on intensified medical therapy had only a 25 percent chance of achieving New York Heart Association functional class I status postoperatively, whereas those with symptoms for less than 3 years had a 77 percent chance of doing so. We are therefore concerned about delaying operation until symptoms are totally refractory to medical management. It can be argued that these problems in
analysis and comparison of results can be resolved only by a randomized prospective clinical trial of earlier valve replacement. I have discussed elsewherelsJ0 the problems that arise in randomized trials of operations or prosthetic devices that are substantially altered during the course of the trials as a result of continuing technical and engineering advances. At the conclusion of such trials, the original prosthetic device or the operation being assessed no longer exists, and the trial becomes irrelevant to current clinical practice. Regardless of one’s feelings about the merits of such trials, they have not yet been carried out, and practical decisions about patients with chronic mitral regurgitation must be made on the basis of available data. On this basis, we currently follow the plan for management described in the next section. Plan for Management of Patients Wlth Mitral Regurgitation
Patients with chronic mitral regurgitation (pure or predominant) and symptoms that are provoked by less than normal daily activities (light housework, sedentary office work) are in New York Heart Association functional class III and should be offered operation for relief of symptoms alone. Patients who require a more active life-style may find less extreme symptoms intolerable, and are also undeniable candidates for operation to relieve symptoms. Patients with symptoms provoked only by extraordinary activity (functional class II), who are content
with their exercise tolerance, are followed up closely (at 6 month intervals) by a cardiologist with chest X-ray films to assess cardiac size. Increasing heart size is a qualitative but useful and specific indicator of cardiac
decompensation, and heart size correlates closely with survival in patients with heart disease.21 Any significant change in heart size provokes frequent examinations (as often as every 3 months). The patient is clearly told that an operation will inevitably become necessary, but the timing is indefinite. Noninvasive assessment of cardiac performance may be carried out at this point, but progressive cardiac enlargement on two successive examinations, even without a change in symptoms, inevitably provokes more sophisticated noninvasive examination (echocardiography, nuclear imaging) and, if depressed left ventricular function is found (as is usually the case), cardiac catheterization is performed. If substantial hemodynamic abnormalities are found, such as significant elevation of pulmonary arterial or left ventricular end-diastolic pressure or depression of left ventricular ejection fraction, an operation is recommended if the patient is a good operative candidate otherwise. The decision for surgery in such patients is simplified if progressive cardiomegaly and atrial fibrillation (with its attendant risk of systemic emboli) have developed only recently and if the patients otherwise have an active life-style and reasonable expectation of longevity. In such patients the operative risk is approximately 1 percent, and there is a 70 to 90 percent chance of restoring them to an asymptomatic state.8 We find that these considerations are readily understood by the patient of average intelligence. The patient has a right to know that it is possible to carry out an operation at low risk with a good functional result if it is performed before their symptoms are totally refractory, that procrastination can result in irretrievable damage to the myocardium, but that the prosthetic device has hazards as well. Some patients prefer relief from symptoms and drugs and readily accept the risk of a prosthetic device; some do not, and are followed up with medical therapy until symptoms are incapacitating. we select tissue valves for patients over the age of 60 years, those with limited life expectancy for other reasons (for example, end-stage ventricular dysfunction), those with contraindications (including hazardous occupations or avocations) to anticoagulant therapy, and young women who wish to bear children. The latter are advised to have all their children within the ensuing 10 years, because the tissue valve will probably require replacement eventually, after which they will receive a mechanical prosthesis and anticoagulant therapy. (Reoperation is tedious, but can be carried out with mortality no greater than that of the first operation by experienced surgeons.) All other patients receive a mechanical prosthesis because the long-term durability of tissue valves is unknown. Mitral Stenosis
In patients with mitral stenosis, unsuspected deterioration of ventricular function is unlikely, but insidious loss of exercise capacity and the high risk of major systemic emboli are good enough reasons to be aggressive in offering open mitral commissurotomy. (The prolonged technical debate about open versus closed July 1990
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commissurotomy will soon end, because closed commissurotomy is rarely taught now. For the next generation of surgeons in this country, closed commissurotomy will be a rare skill.) Our recommendations about mitral commissurotomy are based on several factors: (1) The mortality rate of open commissurotomy alone in experienced hands is 1 percent or less. In a report by Montoya et a1.,22 one of two deaths in 105 patients was due to myocardial infarction in a patient who had coronary bypass grafting with commissurotomy; in our report from Oregon,23 the only death in 100 consecutive patients was from fulminant hemorrhagic pancreatitis. (2) Nonsurgical therapy imposes substantial risks of embolism (18 percent in the series of Montoya et al. and 13 percent in our report). (3) The occurrence of emboli or the finding of left atria1 thrombus at operation had no correlation with the cardiac rhythm in either report, making it difficult to decide which patients should receive anticoagulant therapy preoperatively. (4) Longterm preoperative anticoagulant therapy poses notable risks, with a 5 year mortality that exceeds the combined surgical and late mortality for commissurotomy. Indications for mitral commissurotomy: Because systemic embolism is quite uncommon after operation, avoidance of all the risks cited and restoration of functional capacity seem well worth the minimal surgical risk to most patients. It is therefore my belief that open mitral commissurotomy can now be reasonably offered
to patients with the catheterization findings of pure mitral stenosis who are unable to function in New York Heart Association class I and who wish to do ~0.~~This means that operation should be offered when cardiac symptoms cause curtailment of normal daily activities and should not be withheld until the patient is incapacitated. In addition, a patient who sustains a major systemic embolus should have cardiac catheterization. If hemodynamically significant mitral stenosis is found, an operation should be offered, because the risk of operation is much less than the risk of another major embolus, and-as noted earlier-postoperative emboli are distinctly uncommon. Indications for valve replacement: If, in a particular patient, there is uncertainty that the valve will be suitable for commissurotomy, the indications for valve replacement discussed should be applied, because the latter are less liberal. If more liberal indications are to be adopted for commissurotomy than for valve replacement, it will once again become essential to ascertain the exact nature of the patient’s valve disease preoperatively, just as it was in the 1950’s before valve replacement was available. Now, with sophisticated hemodynamic, angiographic, and echocardiographic studies, it is possible to predict the likelihood of successful commissurotomy with reasonable precision. Obviously, the cardiac surgeon responsible for such patients must be experienced in reconstructive mitral surgery, not just in valve replacement.
References 1. Fowler NO, Van Der Bel-Kahn JM. Indications for surgical replacement of the mitral valve. Am J Cardiol 1979;44:148-57. 2. Criteria Committee of the New York Heart Association. Nomenclature and Criteria for Diagnosis of Diseases of the Heart and Great Vessels. Boston: Little, Brown, 1973:286. 3. Kouchoukos N. Problems in mitral valve replacement. In: Kirklin JW, ed. Advances in Cardiovascular Surgery. New York: Grune & Stratton, 1973:205. 4 Kirklin JW, Pacifko AD. Surgery for acquired valvular heart disease. N Engl J Med 1973;288: 133-40. 5. Appelbaum A, Kouchoukos NT, Blackstone EH, Klrklln JW. Early risks of open heart surgery for mitral valve disease. Am J Cardiol 1976;37:201-9. 6. Gyer PE, Stlnson EB, Rosaiter SJ, Miller DC, Reltz BA, Shumway NE. Extended experience with the Hancock xenograft bioprosthesis. In: Sebening F, ed. Bioprosthetic Cardiac Valves. Munich: Deutsches Herzzentrum, 1979:47. 7. Cohn LH. Bioprosthetic cardiac valves-anticoagulation or not? In Ref 6: 107. 8. Bonchek LI, Anderson RP, Starr A. Mitral valve replacement with cloth-covered composite-seat prostheses. J Thorac Cardiovasc Surg 1974;67:93-109. 9. Mantles JR, Goudard A, Blln D, et al. 481 bioprosthetic valves. Early and middle term results. In Ref 6: 39. 10. Urschel CW, Covell JW, Sonnenbllck EH, Rosa J Jr, Braunwald E. Myocardiil mechanics in aortic and mitral valvular regurgitation. The concept of instantaneous impedance as a determinant of the performance of the intact heart. J Clin Invest 1968;47:867. 11. Rahlmtoola SH. Early valve replacement for preservation of ventricular function: Am J Cardiol 1977;40:472-5. 12. Murphy ES, Kloster FE. Late results of valve replacement surgery. Mod Concepts Cardiovasc Dis 1979;48:53-8.
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13. Bonchek LI, Starr A. Ball valve prostheses: current appraisal of late results. Am J Cardiol 1975;35:843-54. 14. Bjork VO, Henze A. Prosthetic heati valve replacement. Nine years’ experience with the Bjork-Shiley tilting disc valve. In: lonescu MI, ed. Tissue Heart Valves. London: Butterworths, 1979: 1. 15. Cohn LH, Koster JK, Mee RBB, et al. Long-term follow-up of the Hancock bioprosthetic heart valve. A B-year review. Circulation 1979;60:1-87. 16. Richardson JV, Karp RB, Klrklin JW, et al. Treatment of infective endocarditis. A lo-year comparative analysis. Circulation 1978; 58:589-97. 17. Rapapori E. Natural history of aortic and mitral valve disease. Am J Cardiol 1975:35:221-7. 18. Schuler G, Peterson KL, Johnson A, et al. Temporal response of left ventricular performance to mitral valve surgery. Circulation 1979;59:1218-31. 19. Bonchek LI. Are randomized trials appropriate for evaluating new operations? N Enql J Med 1979:301:44-5. 20. B&chek LI. Correspondence: randomized clinical trials in surgery. N Engl J Med 1979;301:1181-3. 21. Hammermeister KE, Chickos PM, Fisher L, Dodge HT. Relationship of cardiothoracic ratio and plain film heart volume to late survival. Circulation 1979;59:89-95. 22. Montoya A, Mulet J, Plffare R, Moran JM, Sullivan HJ. The advantages of open mitral commissurotomy for mitral stenosis. Chest 1979;75:131-5. 23. Housman LB, Bonchek LI, Lambert L, Grunkemeier G, Starr A. Prognosis of patients after open mitral commissurotomy. J Thorac Cardiovasc Surg 1977;73:742-5. 24. Bonchek LI. Mitral commissurotomy: a perspective. Chest 1979;75:112-3.
Indications for Surgery of the Mitral Valve LAWRENCE
Milwaukee,
I. BONCHEK,
MD,
FACC
Wisconsin
In a recent review of the indications for mitral valve surgery published in this Journal, Fowler and Van Der Bel-Kahn1 suggested that as a general rule, mitral valve replacement. should be “considered only for patients in functional classes III or IV of the New York Heart Association* who do not respond to medical management ” Patients with mitral stenosis, who are often can%&es for mitral commissurotomy, should not have surgical treatment “as long as symptoms can be controlled medically,” since there need be no fear of “progressive left ventricular dysfunction that might become irreversible.” Our practice at the Milwaukee Regional Medical Center of the Medical College of Wisconsin is sufficiently different to warrant exposition, in view of the current results of mitral valve surgery. Mitral Regurgitation Operative Mortality
It is generally agreed that no operation should be offered unless its benefits outweigh its risks. In the article by Fowler and Van Der Bel-Kahn, the principal concerns about mitral valve replacement were the “high” operative mortality and morbidity in patients with mitral insufficiency, and the complications related to prosthetic valves. Reported experience: In support of their concern about operative mortality, the authors cited reports published in 1973 in which the operative mortality rates in patients with mitral insufficiency were 19 and 20 percent, respectively. 3p4They then suggested that “more recent reports” indicate a mortality rate of 7, percent, and cited a report that, although published in 1976, also discussed patients operated on in 1972 and 1973. However, even in that report despite a total early mortality rate of 7 percent, patients in New York Heart Association functional class III preoperatively had a 1.3 percent operative mortality rate for open mitral valve surgery; all but two operative deaths were in patients in functional class IV before operation. Even so, none of those studies reflects the current state of the art for mitral valve replacement. Reports from major cardiac centers of high operative mortality From the Department of Cardiothoracic Surgery,The f4edical College of Wisconsin, Milwaukee, Wisconsin. Manuscript received December 28, 1979, accepted March 12, 1980. Address for reprints: Lawrence I. Bonchek, MD, Department of Cardiothoracic Surgery, The Medical College of Wisconsin, 8700 West Wisconsin Avenue, Milwaukee, Wisconsin 53228.
rates for mitral valve replacement are usually attributable to the inclusion of patients tindergoing emergency valve replacement for cardiogenic shock due to myocardial infarction with rupture of a papillary muscle, or of patients with chronic ventricular dysfunction due to ischemic heart disease who undergo concomitant coronary bypass surgery. 6,7Published reports must be scrutinized for potentially confusing inclusion of heterogeneous subsets of patients. Results in patients with cardiogenic shock, in neglected patients in functional class IV or in those who require concomitant procedures are simply not relevant to the decision to carry out elective isolated mitral valve replacement in patients in functional class III with chronic mitral valve disease. Such patients can be operated on in large centers with an operative mortality rate of 1 to 3 percent.5,s,g Technical misadventures such as intraoperative atrioventricular disruption that causes uncontrollable hemorrhage are now rare causes of operative death. (This writer has not experienced such a complication.) Most operative deaths (70 to 90 percent.) are now caused by left ventricular failure, arrhythmias or infarction, which occur predominantly in neglected patients with endstage ventricular dysfunction or coronary artery disease, or both.8 As will be discussed further, the sudden increase in left ventricular afterload that accompanies restoration of mitral valve competence can acutely depress left ventricular ejection in some patients, thus unveiling more advanced ventricular dysfunction than had been appreciated preoperatively.1° Personal experience: Our own experience confirms the low mortality of mitral valve replacement. We8 reported a series of 150 consecutive mitral replacements that concluded in 1974 with an operative mortality rate of 2 percent. Although Fowler suggests that low operative mortality rates must be due to inclusion of large numbers of patients with early disease, few symptoms and good ventricular function, or that the definition of hospital mortality in such a report may not have been liberal enough, our publication clearly indicated that only 17 patients were in functional class II, whereas 112 were in class III and 21 in class IV. (Many of the patients in class II had predominant mitral stenosis, and the primary indication for operation was preoperative emboli.) There were two operative deaths (1.8 percent) in the 112 patients in class III, and one death (4.8 percent) in the 21 patients in class IV. All hospital deaths, and all those occurring within 30 days, were included; July 1990
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each was described in detail. The New York Heart Association classifications were assigned in conjunction with the cardiologists at the University of Oregon, whose views on valve disease are well known.‘lJ2 Current results of mitral valve replacement at the Milwaukee Regional Medical Center 07 the Medical College of Wisconsin are consistent with those reported earlier from the University of Oregon. If one excludes patients with preoperative cardiogenic shock due to acute myocardial infarction, there was one operative death (2 percent) in the last 50 consecutive mitral valve replacements performed. The death occurred in a moribund patient in functional class IV with cardiac cirrhosis, hypersplenism, cachexia and left main coronary stenosis that was unrecognized because the patient’s preoperative renal failure and ventricular irritability (including ventricular tachycardia during catheterization) precluded complete coronary angiography. As noted earlier, such results are not unique.5s The recent introduction of hypothermic cardioplegic arrest has been a major advance in intraoperative management. Fowler and Van Der Bel-Kahn suggest that aortic valve replacement has “a lower average surgical mortality rate” than mitral valve replacement. In my personal experience,13 isolated mitral valve replacement has always had an operative mortality rate as low as or lower than that of aortic valve replacement.
Hemorrhagic complications of anticoagulant therapy occurred in six patients in our series (2 percent per patient year), but most of these were trivial (hematuria, leg hematoma, for example). One complication was serious (subarachnoid hemorrhage), but none was fatal. In the series of Bjork and Henze, the incidence rate of serious hemorrhagic complications was 0.4 percent per patient year. It must be emphasized that patients with mitral valve disease who are not treated surgically are at risk of thromboembolic episodes, and often receive anticoagulant therapy. In our series,8 13 patients (9 percent) had preoperative emboli. Although the total preoperative period at risk for all patients was not comparable with the postoperative period of follow-up, the overall incidence of embolism was higher before than after valve replacement. Finally, it is apparent that bacterial endocarditis can also develop in patients who are not operated on, and this, too, can be fatalis It is not statistically meaningful to cite cases of prosthetic endocarditis observed in a particular medical center within a particular time span without knowing the total number of patients with prosthetic heart valves at risk in that population, as well as the number of patients at risk with valvular heart disease who were not operated on in whom endocarditis developed. Such comparative data have not been reported.
Late Prosthesis-Related Complications
Functional Results of Mitral Valve Replacement
In the 1960’s the long-term results of mitral valve replacement were influenced significantly by valverelated complications. Now that cardiac surgical techniques and prosthetic devices have improved considerably, the postoperative prognosis is no longer influenced as significantly by valve-related complications.13 In the report cited earlier8 of experience with the cloth-covered Starr-Edwards prosthesis, there were 15 late deaths (10 percent) from 1 to 35 months postoperatively. Actuarially projected survival at 5 years was 85 percent. Most important, only 3 of the 15 late deaths were related to the prosthesis7; others were of cardiac origin (myocardial failure, for example), and 6 were of noncardiac origin. Overall, in survivors and nonsurvivors, there were two instances of perivalvular leak (1 percent per patient year), three of prosthetic endocarditis (1 percent per patient year) and nine of systemic embolism (3 percent per patient year). The Bjork-Shiley prosthesis has had a similarly low incidence rate of late complications. In the experience of Bjork and Henze14 with 195 patients who had mitral valve replacement, the incidence rate of late complications related to the prosthesis was 1.2 percent per patient year for perivalvular leak or prosthetic thrombosis requiring reoperation and 0.4 percent per patient year for prosthetic endocarditis. Systemic embolism occurred at a rate of 6 percent per patient year. With tissue valves such as the Hancock porcine bioprosthesis, the incidence rate of thromboembolic complications is lower (3 to 5 percent per patient year), even though most patients do not receive long-term anticoagulant therapy unless they have chronic atria1 fibrillation.7J5
Current survival statistics after mitral valve replacement are based on data from patients who had, in most cases, advanced disease before operation. Late survival in patients who undergo operation earlier would undoubtedly be better, because late myocardial failure-the most frequent cause of late death-would be uncommon. Moreover, survival after valve replacement must be compared with natural history studies that begin with the development of symptoms, not with diagnosis, lest an inappropriately long and benign course with medical treatment be inferred. Mortality in medically treated valve disease varies widely (from 25 to 75 percent at 5 years) depending on the nature and site of the valve lesion and the circumstances under which the patient entered the study.i7 Left ventricular function: The left ventricle in mitral regurgitation has a chronic volume overload that is ejected partially through a low impedance path into the left atrium. As a result, patients with mitral regurgitation may have severe hemodynamic abnormalities without striking clinical disability. The left ventricle eventually suffers irreversible damage, and may become so dependent on afterload reduction that mitral valve replacement, which increases afterload, causes further depression of certain variables of left ventricular performance. Schuler and co-workers18 at the University of California, San Diego recently demonstrated that in patients with marked left ventricular enlargement and hypertrophy (defined by quantitative criteria), and ejection fraction at the lower end of the normal range mitral valve replacement was followed (1) by severe impairment of the ejection fraction that continued to worsen 1 year after operation, (2) persistent left ven-
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tricular dilatation and hypertrophy, and (3) increased end-systolic dimensions. In contra&valve replacement in patients with mild to moderate ventricular dilatation and hypertrophy was followed by reduction in left ventricular size and hypertrophy and no deterioration of left ventricular performance. Optimal timing of valve replacement: We8 assessed this problem in a different manner in 1974, and found no correlation between postoperative functional class and 19 preoperative clinical and hemodynamic variables including age, functional class, rhythm, left atria1 pressure, left ventricular end-diastolic pressure, cardiac index or pulmonary vascular resistance. (The patients studied had been evaluated before calculation of cardiac dimensions and ejection fraction became routine.) However, a prognostic classification derived from the duration of symptoms and the response to medical management was highly discriminatory. Patients with clinical symptoms for more than 3 years who did not show improvement by at least one functional class on intensified medical therapy had only a 25 percent chance of achieving New York Heart Association functional class I status postoperatively, whereas those with symptoms for less than 3 years had a 77 percent chance of doing so. We are therefore concerned about delaying operation until symptoms are totally refractory to medical management. It can be argued that these problems in
analysis and comparison of results can be resolved only by a randomized prospective clinical trial of earlier valve replacement. I have discussed elsewherelsJ0 the problems that arise in randomized trials of operations or prosthetic devices that are substantially altered during the course of the trials as a result of continuing technical and engineering advances. At the conclusion of such trials, the original prosthetic device or the operation being assessed no longer exists, and the trial becomes irrelevant to current clinical practice. Regardless of one’s feelings about the merits of such trials, they have not yet been carried out, and practical decisions about patients with chronic mitral regurgitation must be made on the basis of available data. On this basis, we currently follow the plan for management described in the next section. Plan for Management of Patients Wlth Mitral Regurgitation
Patients with chronic mitral regurgitation (pure or predominant) and symptoms that are provoked by less than normal daily activities (light housework, sedentary office work) are in New York Heart Association functional class III and should be offered operation for relief of symptoms alone. Patients who require a more active life-style may find less extreme symptoms intolerable, and are also undeniable candidates for operation to relieve symptoms. Patients with symptoms provoked only by extraordinary activity (functional class II), who are content
with their exercise tolerance, are followed up closely (at 6 month intervals) by a cardiologist with chest X-ray films to assess cardiac size. Increasing heart size is a qualitative but useful and specific indicator of cardiac
decompensation, and heart size correlates closely with survival in patients with heart disease.21 Any significant change in heart size provokes frequent examinations (as often as every 3 months). The patient is clearly told that an operation will inevitably become necessary, but the timing is indefinite. Noninvasive assessment of cardiac performance may be carried out at this point, but progressive cardiac enlargement on two successive examinations, even without a change in symptoms, inevitably provokes more sophisticated noninvasive examination (echocardiography, nuclear imaging) and, if depressed left ventricular function is found (as is usually the case), cardiac catheterization is performed. If substantial hemodynamic abnormalities are found, such as significant elevation of pulmonary arterial or left ventricular end-diastolic pressure or depression of left ventricular ejection fraction, an operation is recommended if the patient is a good operative candidate otherwise. The decision for surgery in such patients is simplified if progressive cardiomegaly and atrial fibrillation (with its attendant risk of systemic emboli) have developed only recently and if the patients otherwise have an active life-style and reasonable expectation of longevity. In such patients the operative risk is approximately 1 percent, and there is a 70 to 90 percent chance of restoring them to an asymptomatic state.8 We find that these considerations are readily understood by the patient of average intelligence. The patient has a right to know that it is possible to carry out an operation at low risk with a good functional result if it is performed before their symptoms are totally refractory, that procrastination can result in irretrievable damage to the myocardium, but that the prosthetic device has hazards as well. Some patients prefer relief from symptoms and drugs and readily accept the risk of a prosthetic device; some do not, and are followed up with medical therapy until symptoms are incapacitating. we select tissue valves for patients over the age of 60 years, those with limited life expectancy for other reasons (for example, end-stage ventricular dysfunction), those with contraindications (including hazardous occupations or avocations) to anticoagulant therapy, and young women who wish to bear children. The latter are advised to have all their children within the ensuing 10 years, because the tissue valve will probably require replacement eventually, after which they will receive a mechanical prosthesis and anticoagulant therapy. (Reoperation is tedious, but can be carried out with mortality no greater than that of the first operation by experienced surgeons.) All other patients receive a mechanical prosthesis because the long-term durability of tissue valves is unknown. Mitral Stenosis
In patients with mitral stenosis, unsuspected deterioration of ventricular function is unlikely, but insidious loss of exercise capacity and the high risk of major systemic emboli are good enough reasons to be aggressive in offering open mitral commissurotomy. (The prolonged technical debate about open versus closed July 1990
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commissurotomy will soon end, because closed commissurotomy is rarely taught now. For the next generation of surgeons in this country, closed commissurotomy will be a rare skill.) Our recommendations about mitral commissurotomy are based on several factors: (1) The mortality rate of open commissurotomy alone in experienced hands is 1 percent or less. In a report by Montoya et a1.,22 one of two deaths in 105 patients was due to myocardial infarction in a patient who had coronary bypass grafting with commissurotomy; in our report from Oregon,23 the only death in 100 consecutive patients was from fulminant hemorrhagic pancreatitis. (2) Nonsurgical therapy imposes substantial risks of embolism (18 percent in the series of Montoya et al. and 13 percent in our report). (3) The occurrence of emboli or the finding of left atria1 thrombus at operation had no correlation with the cardiac rhythm in either report, making it difficult to decide which patients should receive anticoagulant therapy preoperatively. (4) Longterm preoperative anticoagulant therapy poses notable risks, with a 5 year mortality that exceeds the combined surgical and late mortality for commissurotomy. Indications for mitral commissurotomy: Because systemic embolism is quite uncommon after operation, avoidance of all the risks cited and restoration of functional capacity seem well worth the minimal surgical risk to most patients. It is therefore my belief that open mitral commissurotomy can now be reasonably offered
to patients with the catheterization findings of pure mitral stenosis who are unable to function in New York Heart Association class I and who wish to do ~0.~~This means that operation should be offered when cardiac symptoms cause curtailment of normal daily activities and should not be withheld until the patient is incapacitated. In addition, a patient who sustains a major systemic embolus should have cardiac catheterization. If hemodynamically significant mitral stenosis is found, an operation should be offered, because the risk of operation is much less than the risk of another major embolus, and-as noted earlier-postoperative emboli are distinctly uncommon. Indications for valve replacement: If, in a particular patient, there is uncertainty that the valve will be suitable for commissurotomy, the indications for valve replacement discussed should be applied, because the latter are less liberal. If more liberal indications are to be adopted for commissurotomy than for valve replacement, it will once again become essential to ascertain the exact nature of the patient’s valve disease preoperatively, just as it was in the 1950’s before valve replacement was available. Now, with sophisticated hemodynamic, angiographic, and echocardiographic studies, it is possible to predict the likelihood of successful commissurotomy with reasonable precision. Obviously, the cardiac surgeon responsible for such patients must be experienced in reconstructive mitral surgery, not just in valve replacement.
References 1. Fowler NO, Van Der Bel-Kahn JM. Indications for surgical replacement of the mitral valve. Am J Cardiol 1979;44:148-57. 2. Criteria Committee of the New York Heart Association. Nomenclature and Criteria for Diagnosis of Diseases of the Heart and Great Vessels. Boston: Little, Brown, 1973:286. 3. Kouchoukos N. Problems in mitral valve replacement. In: Kirklin JW, ed. Advances in Cardiovascular Surgery. New York: Grune & Stratton, 1973:205. 4 Kirklin JW, Pacifko AD. Surgery for acquired valvular heart disease. N Engl J Med 1973;288: 133-40. 5. Appelbaum A, Kouchoukos NT, Blackstone EH, Klrklln JW. Early risks of open heart surgery for mitral valve disease. Am J Cardiol 1976;37:201-9. 6. Gyer PE, Stlnson EB, Rosaiter SJ, Miller DC, Reltz BA, Shumway NE. Extended experience with the Hancock xenograft bioprosthesis. In: Sebening F, ed. Bioprosthetic Cardiac Valves. Munich: Deutsches Herzzentrum, 1979:47. 7. Cohn LH. Bioprosthetic cardiac valves-anticoagulation or not? In Ref 6: 107. 8. Bonchek LI, Anderson RP, Starr A. Mitral valve replacement with cloth-covered composite-seat prostheses. J Thorac Cardiovasc Surg 1974;67:93-109. 9. Mantles JR, Goudard A, Blln D, et al. 481 bioprosthetic valves. Early and middle term results. In Ref 6: 39. 10. Urschel CW, Covell JW, Sonnenbllck EH, Rosa J Jr, Braunwald E. Myocardiil mechanics in aortic and mitral valvular regurgitation. The concept of instantaneous impedance as a determinant of the performance of the intact heart. J Clin Invest 1968;47:867. 11. Rahlmtoola SH. Early valve replacement for preservation of ventricular function: Am J Cardiol 1977;40:472-5. 12. Murphy ES, Kloster FE. Late results of valve replacement surgery. Mod Concepts Cardiovasc Dis 1979;48:53-8.
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13. Bonchek LI, Starr A. Ball valve prostheses: current appraisal of late results. Am J Cardiol 1975;35:843-54. 14. Bjork VO, Henze A. Prosthetic heati valve replacement. Nine years’ experience with the Bjork-Shiley tilting disc valve. In: lonescu MI, ed. Tissue Heart Valves. London: Butterworths, 1979: 1. 15. Cohn LH, Koster JK, Mee RBB, et al. Long-term follow-up of the Hancock bioprosthetic heart valve. A B-year review. Circulation 1979;60:1-87. 16. Richardson JV, Karp RB, Klrklin JW, et al. Treatment of infective endocarditis. A lo-year comparative analysis. Circulation 1978; 58:589-97. 17. Rapapori E. Natural history of aortic and mitral valve disease. Am J Cardiol 1975:35:221-7. 18. Schuler G, Peterson KL, Johnson A, et al. Temporal response of left ventricular performance to mitral valve surgery. Circulation 1979;59:1218-31. 19. Bonchek LI. Are randomized trials appropriate for evaluating new operations? N Enql J Med 1979:301:44-5. 20. B&chek LI. Correspondence: randomized clinical trials in surgery. N Engl J Med 1979;301:1181-3. 21. Hammermeister KE, Chickos PM, Fisher L, Dodge HT. Relationship of cardiothoracic ratio and plain film heart volume to late survival. Circulation 1979;59:89-95. 22. Montoya A, Mulet J, Plffare R, Moran JM, Sullivan HJ. The advantages of open mitral commissurotomy for mitral stenosis. Chest 1979;75:131-5. 23. Housman LB, Bonchek LI, Lambert L, Grunkemeier G, Starr A. Prognosis of patients after open mitral commissurotomy. J Thorac Cardiovasc Surg 1977;73:742-5. 24. Bonchek LI. Mitral commissurotomy: a perspective. Chest 1979;75:112-3.