564
JACC Vol. 15, No. 3 March 1, 1990:564-5
Editorial Comment
Preservation of Left Ventricular Function in Patients With Mitral Regurgitation: A Realistic Goal For the Nineties* BLASE Charleston,
A. CARABELLO,
MD, FACC
South Carolina
Reasons for poor outcome after valve replacement for mitral regurgitation. Currently, correction of mitral regurgitation has a higher operative mortality and a worse outcome than surgery for other valve lesions of the left side of the heart. Recent statistics indicate a survival rate of only 50%at 10 years after mitral valve replacement for mitral regurgitation (1,2). This is in sharp contrast to the results for correction of the other left-sided regurgitant lesion, aortic regurgitation, in which operative mortality has decreased from 11% in the 1960sand early 1970sto 6% in recent years, and 10 year survival rate approaches 80% (3,4). Correction of mitral regurgitation is attended by a poor outcome for several reasons: 1) concealed preoperative left ventricular dysfunction predisposes the patient to poor postoperative ventricular function; 2) creation of unfavorable preoperative geometry aggravates the potential for reduced postoperative ventricular performance; 3) frequent coexistence of coronary artery disease as a cause of mitral regurgitation increases the risk of an intraoperative or subsequent myocardial infarction; and 4) severance of chordae tendineae during mitral valve replacement has an adverse effect on ventricular function. Concealed left ventricular dysfunction. Mitral regurgitation affords an additional low pressure pathway for ejection of blood from the left ventricle. This pathway acts to reduce overall resistance to ejection, thereby reducing left ventricular afterload, while the volume overload resulting from the lesion increases preload. Reduced afterload and increased preload in mitral regurgitation augment ejection performance. Although much has been written about the need for
*Editorials published in Journal of the American College of Cardiology reflect the views of the authors and do not necessarily represent the views of JACC or the American College of Cardiology. From the Cardiology Division and the Gazes Cardiac Research Institute, Medical University of South Carolina, Charleston, South Carolina and the Veterans Affairs Medical Center, Charleston. Address for reorints: Blase A. Carabello, MD, Cardiology Division, Medical University of South Carolina, 171Ashley Avenue, Charleston, South Carolina 29425. 01990 by the American College of Cardiology
a load-independent tool to assess clinical left ventricular function, load-dependent indexes of ejection performance are still by far the most commonly used tools to evaluate contractile function. In mitral regurgitation the favorable loading conditions cause these indexes to overestimate ventricular function. In this regard, ejection fraction in the range of 0.55 to 0.60 or echocardiographic shortening fraction in the range of 0.25 to 0.30 is frequently coexistent with significant muscle dysfunction (5,6). Unfavorablepreoperativegeometry and its effect on postoperative loading conditions. The left ventricle in mitral regurgitation dilates with little increase in wall thickness, resulting in a high left ventricular radius (r) to thickness (h) ration (r/h) (7). Afterload estimated by wall stress is derived from the Laplace relation, where wall stress = (pressure x r) + 2h. Thus, as r/h increases, stress increases, increasing afterload despite the unloading effect of the lesion itself. Wall stress is typically normal (rather than subnormal) in compensated mitral regurgitation and actually higher than normal in decompensated mitral regurgitation (8). In this setting of normal or increased afterload, mitral valve replacement or repair, which closes off the low impedance pathway into the left atrium, results in an immediate further increase in afterload (9). This increase in postoperative afterload together with decreased preload (as the volume overload is removed) invariably causes a decrease in ejection performance (6,lO). If some contractile reserve remains, the ventricle may be able to compensate for the imposition of these unfavorable loading conditions; in this case, the decrease in ejection performance is only mild. If all contractile reserve has been exhausted, the unfavorable loading canditions imposed by mitral valve replacement cause a precipitous, uncompensated decrease in ejection performance, which persists for years after mitral valve replacement (11). Coronary artery disease. Mitral regurgitation is the only left-sided valve lesion that can have coronary artery disease as its primary etiology. An estimated 25% of patients undergoing mitral valve repair or replacement have coronary disease as the primary etiologic factor (12,13). If the mitral regurgitation is coincidentally present with myocardial infarction or if myocardial infarction develops consequent to the coronary disease, ventricular function will be worse than that created by the valve lesion itself. Interactionof the valve apparatus in the ventricle: impact of the current study. Early studies by Rushmer et al. (14) and Lillihei et al. (15) demonstrated that the mitral valve apparatus and its attachments to the papillary muscles do more than prevent systolic mitral regurgitation. These attachments enhance long-axis contraction, “priming” the short axis of the left ventricle for its major role in ventricular ejection by causing a shape change toward spherical in early 0735-1097/90/$3.50
CARABELLO EDITORIAL COMMENT
JACC Vol. 15, No. 3 March 1, 1990:.564-5
systole. Thus, the interaction of the mitral valve with the papillary muscles enhances left ventricular performance. The current study in the Journal by Pitarys et al. (16) demonstrates the results of chordal severance on regional myocardial function. Radial shortening in the region of the insertion of the posteromedial papillary muscle decreased sharply after mitral valve replacement with chordal resection. Although this decrease did not produce a statistically significant decrease in global ventricular ejection performance, there was a correlation between postoperative ejection performance and regional dysfunction. Because considerable data indicate that global ejection fraction usually decreases after mitral valve replacement (6,10,1 l), it is likely that the relatively small sample size of the current study (16) is the source of its inability to detect such a decrease. The importance of the current study is not that it failed to detect this decrease, but rather that the regional dysfunction it demonstrated helps to explain why other studies did find a significant decline in ejection performance after mitral valve replacement. This clinical study (16) adds to previous experimental work (17), demonstrating a reduction in chamber elastance caused by the severance of the chordae tendineae. Conversely, clinical studies (1819) demonstrate that preservation of the chordae tendineae helps maintain ventricular performance. The difference in ventricular performance between operations in which the chordae tendineae were preserved versus severed can probably be explained; whereas unfavorable postoperative loading conditions are imposed in both valve repair and valve replacement, replacement with chordal severance further impairs the ventricle’s ability to overcome these unfavorable loading conditions and this results in reduced ejection performance. It is most likely the preservation of ventricular function combined with the obvious advantage of avoiding implantation of a prosthetic valve that explains valve repair has a substantially better result than does replacement (2,18-21). Conclusions. With knowledge gained about the interaction between the left ventricle in mitral regurgitation and the mitral valve apparatus, it is reasonable to expect that mortality can be reduced and long-term outcome for patients with mitral regurgitation improved in the 1990s. As cardiologists recognize the concealed left ventricular dysfunction in this disease and as surgeons improve the art of valve repair, better candidates for surgery will undergo a better operation. Even for those patients who have neglected their disease until ventricular dysfunction is advanced, repair may offer a reasonable outcome by helping to preserve function without causing further depression.
References 1. Cohn LH, Allred EN, Cohn LA, et al. Early and late risk of mitral valve replacement: a 12 year concomitant comparison of the porcine biopros-
565
thetic and prosthetic disc mitral valves. J Thorac Cardiovasc Surg 1985X1:872-81. 2. Angel1 WW. Oury JH, Shah P. A comparison of replacement and reconstruction in patients and mitral regurgitation. J Thorac Cardiovasc Surg 1987;93:665-74. 3. Bonow RO, Picone AL, McIntosh CL, et al. Survival and functional results after valve replacement for aortic regurgitation from 1976to 1983: impact of preoperative left ventricular function. Circulation 1985:72: 1244-56. 4. Taniguchi K, Nakano S, Hirose H, et al. Preoperative left ventricular function: minimal requirement for successful late results of valve replacement for aortic regurgitation. J Am COBCardiol 1987:10:510-8. 5. Zile MR, Gaasch WH, Levine HJ. Left ventricular stress-dimensionshortening relations before and after correction of chronic aortic and mitral regurgitation. Am J Cardiol 1985;56:99-105. 6. Schuler G, Peterson KL, Johnson A, et al. Temporal response of left ventricular performance to mitral valve surgery. Circulation 1979;59: 1218-31. 7. Kleaveland JP, Kussmaul WG, Vinciguerra T, Diters R, Carabello BA. Volume overload hypertrophy in a closed-chest model of mitral regurgitation Am J Physiol 1988;254(HeartCirc Physiol 23):Hl034-41. 8. Corin WI, Monrad ES, Murakami T. Nonogi H, Hess OM. Krayenbuehl HP. The relationship of afterload to ejection performance in chronic mitral regurgitation. Circulation 1987:76:59-67. 9. Wong CYH, Spotnitz HM. Systolic and diastolic properties of the human left ventricle during valve replacement for chronic mitral regurgitation. Am J Cardiol 1981;47:40-50. IO. Phillips HR, Levine FH. Carter JE, et al. Mitral valve replacement for isolated mitral regurgitation: analysis of clinical course and late postoperative left ventricular ejection fraction. Am J Cardiol 1981;48:647-54.
11.Carabello BA, Williams H, Gash AK, et al. Hemodynamic predictors of outcome in patients undergoing valve replacement. Circulation 1986;74: 1309-16. I?. Scott WC, Miller DC, Haverich A, et al. Operative risk of mitral valve replacement: discriminant analysis of 1329procedures. Circulation 1985; 72(suppl III:II-108-19. 13. Christakis GT, Kormos RL, Weisel RD, et al. Morbidity and mortality in mitral valve surgery. Circulation 1985;72(supplII):Il-120-8. 14. Rushmer RF, Finlayson BL, Nash AA. Movements of the mitral valve. Circ Res 1956;4:337-42. 15. Lillehei CW, Levy MJ, Bonnabeau RC Jr. Mitral valve replacement with preservation of papillary muscles and chordae tendineae. J Thorac Cardiovasc Surg 1964;47:532-43. 16. Pitarys CJ II, Forman MB, Panayiotou H, Hansen DE. Long-term effects of excision of the mitral apparatus on global and regional ventricular function in humans. J Am Coil Cardiol 1990;15:557-63. 17. Sarris GE, Fann Jl, Niczyporuk MA, Derby GC, Handen CE, Miller DC. Global and regional left ventricular systolic performance in the in situ ejecting canine heart: importance of the mitral apparatus. Circulation 1989:8O(suppl I):I-24-42. 18. Goldman ME, Mora F, Guarino T, Fuster V, Mindich BP. Mitral valvuloplasty is superior to valve replacement for preservation of left ventricular function: an intraoperative two-dimensional echocardiographic study. J Am Coil Cardiol 1987;10:568-75. 19. Miki S, Kusuhara K, Ueda Y, Komeda M. Ohkita Y, Tahata T. Mitral valve replacement with preservation of chordae tendineae and papillary muscles. Ann Thorac Surg 1988:45:28-34. 20. Duran CG, Pomar JL, Revuelta JM, et al. Conservative operation for mitral insufficiency: critical analysis supported by postoperative hemodynamic studies of 72 patients. J Thorac Cardiovasc Surg 1980:79:326-37. 21. Cosgrove DM. Mitral valve reconstruction. Cardiol Clin 1985:3:461-9.
JACC Vol. 15, No. 3 March 1, 1990:564-5
Editorial Comment
Preservation of Left Ventricular Function in Patients With Mitral Regurgitation: A Realistic Goal For the Nineties* BLASE Charleston,
A. CARABELLO,
MD, FACC
South Carolina
Reasons for poor outcome after valve replacement for mitral regurgitation. Currently, correction of mitral regurgitation has a higher operative mortality and a worse outcome than surgery for other valve lesions of the left side of the heart. Recent statistics indicate a survival rate of only 50%at 10 years after mitral valve replacement for mitral regurgitation (1,2). This is in sharp contrast to the results for correction of the other left-sided regurgitant lesion, aortic regurgitation, in which operative mortality has decreased from 11% in the 1960sand early 1970sto 6% in recent years, and 10 year survival rate approaches 80% (3,4). Correction of mitral regurgitation is attended by a poor outcome for several reasons: 1) concealed preoperative left ventricular dysfunction predisposes the patient to poor postoperative ventricular function; 2) creation of unfavorable preoperative geometry aggravates the potential for reduced postoperative ventricular performance; 3) frequent coexistence of coronary artery disease as a cause of mitral regurgitation increases the risk of an intraoperative or subsequent myocardial infarction; and 4) severance of chordae tendineae during mitral valve replacement has an adverse effect on ventricular function. Concealed left ventricular dysfunction. Mitral regurgitation affords an additional low pressure pathway for ejection of blood from the left ventricle. This pathway acts to reduce overall resistance to ejection, thereby reducing left ventricular afterload, while the volume overload resulting from the lesion increases preload. Reduced afterload and increased preload in mitral regurgitation augment ejection performance. Although much has been written about the need for
*Editorials published in Journal of the American College of Cardiology reflect the views of the authors and do not necessarily represent the views of JACC or the American College of Cardiology. From the Cardiology Division and the Gazes Cardiac Research Institute, Medical University of South Carolina, Charleston, South Carolina and the Veterans Affairs Medical Center, Charleston. Address for reorints: Blase A. Carabello, MD, Cardiology Division, Medical University of South Carolina, 171Ashley Avenue, Charleston, South Carolina 29425. 01990 by the American College of Cardiology
a load-independent tool to assess clinical left ventricular function, load-dependent indexes of ejection performance are still by far the most commonly used tools to evaluate contractile function. In mitral regurgitation the favorable loading conditions cause these indexes to overestimate ventricular function. In this regard, ejection fraction in the range of 0.55 to 0.60 or echocardiographic shortening fraction in the range of 0.25 to 0.30 is frequently coexistent with significant muscle dysfunction (5,6). Unfavorablepreoperativegeometry and its effect on postoperative loading conditions. The left ventricle in mitral regurgitation dilates with little increase in wall thickness, resulting in a high left ventricular radius (r) to thickness (h) ration (r/h) (7). Afterload estimated by wall stress is derived from the Laplace relation, where wall stress = (pressure x r) + 2h. Thus, as r/h increases, stress increases, increasing afterload despite the unloading effect of the lesion itself. Wall stress is typically normal (rather than subnormal) in compensated mitral regurgitation and actually higher than normal in decompensated mitral regurgitation (8). In this setting of normal or increased afterload, mitral valve replacement or repair, which closes off the low impedance pathway into the left atrium, results in an immediate further increase in afterload (9). This increase in postoperative afterload together with decreased preload (as the volume overload is removed) invariably causes a decrease in ejection performance (6,lO). If some contractile reserve remains, the ventricle may be able to compensate for the imposition of these unfavorable loading conditions; in this case, the decrease in ejection performance is only mild. If all contractile reserve has been exhausted, the unfavorable loading canditions imposed by mitral valve replacement cause a precipitous, uncompensated decrease in ejection performance, which persists for years after mitral valve replacement (11). Coronary artery disease. Mitral regurgitation is the only left-sided valve lesion that can have coronary artery disease as its primary etiology. An estimated 25% of patients undergoing mitral valve repair or replacement have coronary disease as the primary etiologic factor (12,13). If the mitral regurgitation is coincidentally present with myocardial infarction or if myocardial infarction develops consequent to the coronary disease, ventricular function will be worse than that created by the valve lesion itself. Interactionof the valve apparatus in the ventricle: impact of the current study. Early studies by Rushmer et al. (14) and Lillihei et al. (15) demonstrated that the mitral valve apparatus and its attachments to the papillary muscles do more than prevent systolic mitral regurgitation. These attachments enhance long-axis contraction, “priming” the short axis of the left ventricle for its major role in ventricular ejection by causing a shape change toward spherical in early 0735-1097/90/$3.50
CARABELLO EDITORIAL COMMENT
JACC Vol. 15, No. 3 March 1, 1990:.564-5
systole. Thus, the interaction of the mitral valve with the papillary muscles enhances left ventricular performance. The current study in the Journal by Pitarys et al. (16) demonstrates the results of chordal severance on regional myocardial function. Radial shortening in the region of the insertion of the posteromedial papillary muscle decreased sharply after mitral valve replacement with chordal resection. Although this decrease did not produce a statistically significant decrease in global ventricular ejection performance, there was a correlation between postoperative ejection performance and regional dysfunction. Because considerable data indicate that global ejection fraction usually decreases after mitral valve replacement (6,10,1 l), it is likely that the relatively small sample size of the current study (16) is the source of its inability to detect such a decrease. The importance of the current study is not that it failed to detect this decrease, but rather that the regional dysfunction it demonstrated helps to explain why other studies did find a significant decline in ejection performance after mitral valve replacement. This clinical study (16) adds to previous experimental work (17), demonstrating a reduction in chamber elastance caused by the severance of the chordae tendineae. Conversely, clinical studies (1819) demonstrate that preservation of the chordae tendineae helps maintain ventricular performance. The difference in ventricular performance between operations in which the chordae tendineae were preserved versus severed can probably be explained; whereas unfavorable postoperative loading conditions are imposed in both valve repair and valve replacement, replacement with chordal severance further impairs the ventricle’s ability to overcome these unfavorable loading conditions and this results in reduced ejection performance. It is most likely the preservation of ventricular function combined with the obvious advantage of avoiding implantation of a prosthetic valve that explains valve repair has a substantially better result than does replacement (2,18-21). Conclusions. With knowledge gained about the interaction between the left ventricle in mitral regurgitation and the mitral valve apparatus, it is reasonable to expect that mortality can be reduced and long-term outcome for patients with mitral regurgitation improved in the 1990s. As cardiologists recognize the concealed left ventricular dysfunction in this disease and as surgeons improve the art of valve repair, better candidates for surgery will undergo a better operation. Even for those patients who have neglected their disease until ventricular dysfunction is advanced, repair may offer a reasonable outcome by helping to preserve function without causing further depression.
References 1. Cohn LH, Allred EN, Cohn LA, et al. Early and late risk of mitral valve replacement: a 12 year concomitant comparison of the porcine biopros-
565
thetic and prosthetic disc mitral valves. J Thorac Cardiovasc Surg 1985X1:872-81. 2. Angel1 WW. Oury JH, Shah P. A comparison of replacement and reconstruction in patients and mitral regurgitation. J Thorac Cardiovasc Surg 1987;93:665-74. 3. Bonow RO, Picone AL, McIntosh CL, et al. Survival and functional results after valve replacement for aortic regurgitation from 1976to 1983: impact of preoperative left ventricular function. Circulation 1985:72: 1244-56. 4. Taniguchi K, Nakano S, Hirose H, et al. Preoperative left ventricular function: minimal requirement for successful late results of valve replacement for aortic regurgitation. J Am COBCardiol 1987:10:510-8. 5. Zile MR, Gaasch WH, Levine HJ. Left ventricular stress-dimensionshortening relations before and after correction of chronic aortic and mitral regurgitation. Am J Cardiol 1985;56:99-105. 6. Schuler G, Peterson KL, Johnson A, et al. Temporal response of left ventricular performance to mitral valve surgery. Circulation 1979;59: 1218-31. 7. Kleaveland JP, Kussmaul WG, Vinciguerra T, Diters R, Carabello BA. Volume overload hypertrophy in a closed-chest model of mitral regurgitation Am J Physiol 1988;254(HeartCirc Physiol 23):Hl034-41. 8. Corin WI, Monrad ES, Murakami T. Nonogi H, Hess OM. Krayenbuehl HP. The relationship of afterload to ejection performance in chronic mitral regurgitation. Circulation 1987:76:59-67. 9. Wong CYH, Spotnitz HM. Systolic and diastolic properties of the human left ventricle during valve replacement for chronic mitral regurgitation. Am J Cardiol 1981;47:40-50. IO. Phillips HR, Levine FH. Carter JE, et al. Mitral valve replacement for isolated mitral regurgitation: analysis of clinical course and late postoperative left ventricular ejection fraction. Am J Cardiol 1981;48:647-54.
11.Carabello BA, Williams H, Gash AK, et al. Hemodynamic predictors of outcome in patients undergoing valve replacement. Circulation 1986;74: 1309-16. I?. Scott WC, Miller DC, Haverich A, et al. Operative risk of mitral valve replacement: discriminant analysis of 1329procedures. Circulation 1985; 72(suppl III:II-108-19. 13. Christakis GT, Kormos RL, Weisel RD, et al. Morbidity and mortality in mitral valve surgery. Circulation 1985;72(supplII):Il-120-8. 14. Rushmer RF, Finlayson BL, Nash AA. Movements of the mitral valve. Circ Res 1956;4:337-42. 15. Lillehei CW, Levy MJ, Bonnabeau RC Jr. Mitral valve replacement with preservation of papillary muscles and chordae tendineae. J Thorac Cardiovasc Surg 1964;47:532-43. 16. Pitarys CJ II, Forman MB, Panayiotou H, Hansen DE. Long-term effects of excision of the mitral apparatus on global and regional ventricular function in humans. J Am Coil Cardiol 1990;15:557-63. 17. Sarris GE, Fann Jl, Niczyporuk MA, Derby GC, Handen CE, Miller DC. Global and regional left ventricular systolic performance in the in situ ejecting canine heart: importance of the mitral apparatus. Circulation 1989:8O(suppl I):I-24-42. 18. Goldman ME, Mora F, Guarino T, Fuster V, Mindich BP. Mitral valvuloplasty is superior to valve replacement for preservation of left ventricular function: an intraoperative two-dimensional echocardiographic study. J Am Coil Cardiol 1987;10:568-75. 19. Miki S, Kusuhara K, Ueda Y, Komeda M. Ohkita Y, Tahata T. Mitral valve replacement with preservation of chordae tendineae and papillary muscles. Ann Thorac Surg 1988:45:28-34. 20. Duran CG, Pomar JL, Revuelta JM, et al. Conservative operation for mitral insufficiency: critical analysis supported by postoperative hemodynamic studies of 72 patients. J Thorac Cardiovasc Surg 1980:79:326-37. 21. Cosgrove DM. Mitral valve reconstruction. Cardiol Clin 1985:3:461-9.
![[The effect of mitral valve replacement with preservation of mitral complex on left ventricular function in mitral regurgitation].](/assets/img/hold.png)
