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Mitral valve repair in cardiomyopathy
Mitral Valve Repair in Cardiomyopathy Gilles Dreyfus, MD, and Sherban Milaiheanu, MD
R
egardless of the etiology, when end-stage heart disease results in congestive heart failure, the primary treatment is heart transplantation. However, donor shortage and side effects of immunosuppressive therapy allow successful transplantation for very few patients. Therefore, alternative therapies have emerged, such as coronary artery revascularization,1 cardiomyoplasty,2 and more recently isolated mitral valve repair,3 or mitral valve repair associated with left ventricular reduction known as the Batista procedure.4,5 Until recently, secondary mitral regurgitation was not considered by itself to be an indication for surgical intervention when occurring as a consequence of dilated cardiomyopathy. The mitral valve plays a key role in left ventricular function and creates a highly dynamic inner supporting structure that optimizes contraction as well as relaxation. Papillary muscles, as components of the ventricular wall, through the chordae tendineae and valve leaflets are linked to the mitral annulus, thereby maintaining the integrity of a complex functional geometry. Primary or acquired myocardial disease can induce mitral dysfunction; mitral regurgitation worsens left ventricular dysfunction when it occurs in end-stage cardiomyopathy. Moreover, mitral regurgitation increases volume overload in an already dilated left ventricle, which further worsens mitral regurgitation, thus establishing a vicious cycle, and is known to predict poor survival when present. We will discuss the pathophysiologic justification for mitral valve repair in heart failure patients, current indications, and incorporation of related surgical procedures.
From the Ho ˆpital Foch, Universite´ de Paris V, Suresnes, France. Submitted March 1, 1999; accepted March 23, 2000. Reprint requests: Gilles Dreyfus, MD, Ho ˆpital Foch, Universite´ de Paris V, Service de Chirurgie Cardiaque, 40 rue Worth, 92151 Suresnes, France. Telephone: 33-1-4625-2487. J Heart Lung Transplant 2000;19:S73–S76. Copyright © 2000 by the International Society for Heart and Lung Transplantation. 1053-2498/00/$–see front matter PII S1053-2498(00)00106-6
RATIONALE FOR MITRAL VALVE REPAIR Mitral valve repair, when feasible, is clearly superior to mitral valve replacement. Many authors have confirmed this, including Carpentier,6 who for 16 years has found a lower incidence of reoperation on the mitral valve following repair. Mitral valve repair not only yields better surgical results than mitral valve replacement but also better preserves left ventricular function. This fact was well documented by Hauser and Sarris. They demonstrated that division of chordae tendineae reduced maximum left ventricular contractile velocity by 50%. Interaction of the mitral annulus and the sub-valvular apparatus with left ventricular function and geometry are essential to preserve left ventricular function and are probably more obvious in patients with severely impaired left ventricular function than in others. Finally, mitral valve repair may improve left ventricular function after surgery.3,6 This is well known for patients who have symptoms of dilated left ventricles before surgery. We have also shown that, even in patients with moderate left ventricular dilatation who are asymptomatic, ventricular size after mitral repair could be decreased.7 In summary, mitral valve repair is superior to mitral valve replacement, as it better preserves and may even improve left ventricular function following surgery.
MITRAL VALVE REPAIR Physiologic consequences of mitral valve repair are shown in Figure 1. The ultimate goal, in thermodynamic terms, for correction of mitral valve regurgitation is to decrease energy loss for the left ventricle by creating a more efficient workload. Mitral valve repair would decrease left ventricular overload, thereby decreasing wall tension and ultimately oxygen consumption. In addition, reduction in mitral insufficiency helps to restore normal ventricular geometry, which provides backing for left ventricular shortening and torque motion. By creating more efficient forward flow, mitral valve repair also contributes to decreased energy loss. S73
S74
Dreyfus and Milaiheanu
The Journal of Heart and Lung Transplantation August (Suppl) 2000
attracted downward. We and others have used this technique as an integral part of left ventricular reduction procedures.
MITRAL VALVE REPAIR ACCORDING TO ETIOLOGY Patients with mitral regurgitation can be divided into 3 distinct groups, which we will discuss below.
Primary Mitral Valve Disease
FIGURE 1 Physiological consequences of mitral valve repair. LV, left ventricular.
ROLE OF THE MITRAL ANNULUS The goal of mitral valve repair is to restore leaflet coaptation. When the left ventricle is dilated, the mitral valve annulus dilates, allowing valvular regurgitation. The role of prosthetic ring placement is to recreate normal mitral annular geometry, thus reapproximating the anterior and posterior leaflets and allowing effective coaptation. When left ventricular dilation occurs, it occurs in all dimensions, resulting not only in increased chamber volume but also sphericity. As the ventricle dilates, papillary muscles are pulled downward, away from the mitral annulus, creating tension on the chordae. As a result, the free edge of both leaflets cannot coapt. Because placement of a prosthetic mitral ring does not influence longitudinal dimension, this intervention by itself may be inadequate to restore normal systolic mitral coaptation. Two things may overcome this problem. The first is to dramatically undersize the mitral ring.3 By doing so, leaflet competence can sometimes be achieved, but this method places increased tension on the base of the left ventricle and therefore impedes contraction. However, Bolling and associates3 have described clinical application of this technique with good preliminary results. A second possibility would be to suture together the free edges of the anterior and posterior leaflet as described by Alfieri and colleagues.8 This technique creates a double orifice or a figure-eight mitral orifice, which no longer allows the coapting portion of both leaflets to be
This group predominantly includes patients with either rheumatic or degenerative mitral disease, often with relatively preserved left ventricular systolic function. In the case of rheumatic valvular disease, repair gives the worst results. Therefore surgical intervention should be late, and prosthetic replacement is the treatment of choice. Conversely, repair of mitral regurgitation of degenerative etiology has excellent immediate and long-term results and therefore should always be considered as the procedure of choice.6 With increasing durability of surgical success, indications have continued to evolve. Current guidelines for surgical indications, based upon end-systolic dimensions of the left ventricle, support intervention when the degree of regurgitation reaches grade 3 to 4⫹ and left ventricular end-systolic diameter reaches 40 mm.7
Intermediate Mitral Valve Disease This group is typically represented by mitral valve lesions associated with coronary artery disease and myocardial ischemia. Ischemic mitral valve disease can assume a variety of forms including papillary muscle elongation or rupture, or acute regional ventricular dysfunction, which creates mitral regurgitation. Regardless of the mechanism for ischemic mitral valve regurgitation, the likelihood of successful repair is excellent.9,10 In most cases surgical correction is easy and can be achieved by inserting a prosthetic ring. Long-term results in such instances can be less certain because of the interaction between the mitral valve and the underlying left ventricular pathology. Ventricular recovery is not easily predictable because ischemic heart disease combines functional and scarred myocardium in a nonhomogenous manner to produce distorted patterns of contraction. At our institution, mitral valve repair is performed when the degree of mitral regurgitation is greater than 2⫹, and when myocardial scarring is seen on echocardiography. Dobutamine stress echocardiography is frequently helpful, mitral repair being considered more strongly if mitral regurgitation increases with stress. In a previous report from our institution, we described revascu-
The Journal of Heart and Lung Transplantation Volume 19, Number 8S
larization outcome in more than 100 patients with ischemic cardiomyopathy and viable myocardium.1 Coronary artery bypass grafting was performed as an alternative to heart transplantation to improve functional class and ejection fraction. In this group of patients, only 3 required concomitant mitral valve repair. We therefore believe that in this specific population, severe mitral regurgitation is less common.
Secondary Mitral Valve Disease This heterogeneous group of patients represents a potentially enormous population which has, until recently, been largely overlooked as candidates for mitral valve surgery. It includes a large proportion of patients with dilated cardiomyopathy who historically have been managed exclusively with medical therapy and, eventually, with transplantation. Traditional views held that because the valve apparatus itself was undamaged, valve-directed intervention was not indicated. Two new surgical options have emerged in the mid-1990s that have challenged this paradigm: isolated mitral valve repair3 and left ventricular volume reduction.11 Bolling and associates3 recently studied 48 patients with chronic New York Heart Association (NYHA) class IV heart failure, all of whom had severe left ventricular dysfunction and severe mitral regurgitation, evenly divided between ischemic and non-ischemic cardiomyopathy. Surgery in all instances consisted of mitral annuloplasty using a flexible ring. The mean size of the ring was 26 mm. In addition, 7 patients had coronary artery bypass grafting and 11 patients had an additional triscupid annuloplasty using the DeVega technique. They observed only one post-operative death (right ventricular failure) and minimal post-operative mitral gradient. Actuarial survival after 1 and 2 years was 82% and 72%, respectively. All patients improved functionally and left ventricular ejection fraction increased from 16% to 26%. Peak exercise oxygen capacity increased from 14.5 to 18.6 ml/kg/min. There were 8 early cardiac deaths but no late deaths. The number of patients in this series precludes meaningful sub-group analysis. However, these promising results suggest that this approach should be considered in patients with severe heart failure complicated by secondary mitral regurgitation. Although these observations are encouraging, several points merit discussion. Although the reported hemodynamic results were excellent with an increase in cardiac output and associated with a low
Dreyfus and Milaiheanu
S75
transmitral gradient, such procedures as described have the potential to decrease left ventricular contractility. Undersizing the mitral ring may increase tension on the base of the left ventricle, stretching myocardial fibers and decreasing what is often the best contracting portion of the failing left ventricle. An alternative intermediate approach would be to size the mitral ring according to Carpentier’s principles,6 which consider the distance in between anterior and posterior commissures. The Alfieri stitch,8 placed at the middle of the free edge of the anterior and posterior mitral leaflets, may address the lack of coaptation of both mitral leaflets when longitudinal shortening is altered. This approach should prevent excessive traction on the base of the left ventricle. As is often the case with innovative surgical procedures, patient selection is critical. In the case of mitral valve repair, the primary issue concerns the degree of left ventricular dilatation and how it should guide operative candidacy. A related procedure, the so-called Batista procedure, consists of combination mitral repair and surgical ventricular remodeling,4,11 the largest well-documented series of which is from the Cleveland Clinic.5 The latest report by McCarthy and coworkers,5 described 52 patients with idiopathic cardiomyopathy. All patients were NYHA class IV patients with idiopathic dilated cardiomyopathy with left ventricular enddiastolic diameter ⬎70 mm and concomitant mitral regurgitation of at least a moderate degree. Mean cardiac output was 2.2 liter/min, and many patients had pulmonary hypertension. All patients received a mitral valve repair using a Cosgrove ring annuloplasty, along with left ventricular volume reduction by resection of the anterolateral wall of the left ventricle from the apex, in between papillary muscles down to the atrioventricular groove. In one third of the patients, 1 papillary muscle was displaced to increase the resection and to preserve the mitral valve. Only 1 patient died post-operatively, but 8 patients required left ventricular assist device in the early post-operative period and were bridged to transplantation. Ten other patients were listed for transplantation more than 14 months follow-up. All other patients improved functionally and, as in Bolling’s experience, have increased their peak oxygen consumption from 12 to 18 ml/kg/min. However, minimal change appeared in hemodynamic status with surgery. Although this innovative technique is intriguing, appropriate patient selection criteria remain to be established. The current paucity of data and lack of estab-
S76
Dreyfus and Milaiheanu
lished guidelines do not allow clear discrimination between isolated mitral valve repair and combination mitral repair/left ventricular reduction. Could some patients undergoing a Batista procedure have enjoyed better results with isolated mitral valve repair? Conversely, could patients who died after isolated mitral valve repair have survived if they had undergone a Batista procedure? In conclusion, prospective randomized studies are clearly indicated, although the requisite large sample sizes will render this a daunting enterprise. Intuitively, isolated repair is probably the best option in the case of severe regurgitation in a moderately dilated left ventricle. Surgical ventricular remodeling can be considered when the left ventricle is extremely dilated and when pre-operative assessment demonstrates potential for recovery. However, many questions concerning left ventricular volume reduction remain unanswered, and further results and larger series may provide answers. However, mitral insufficiency is, if not the key component, certainly a major contributor to progression of disease in patients with chronic heart failure and should be viewed as a potential target of intervention to improve functional status and to avoid or delay heart transplantation.
The Journal of Heart and Lung Transplantation August (Suppl) 2000
3.
4.
5.
6. 7.
8.
9.
10.
11.
REFERENCES 1. Dreyfus GD, Duboc D, Blasco A, et al. Myocardial viability assessment in ischemic cardiomyopathy: benefits of coronary revascularization. Ann Thorac Surg 1994;57:1402– 8. 2. Carpentier A, Chachques JC, Carteaux JP. Dynamic cardio-
12.
myoplasty at eleven years. In: Carpentier A, Chachques JC, Grandjean PA, eds. Cardiac bioassist. Armonk, New York: Futura, 1997, pp. 3–23. Bolling SF, Deeb GM, Brunstring LA, Bach DS. Early outcome of mitral valve reconstruction in patients with end-stage cardiomyopathy. J Thorac Cardiovasc Surg 1995; 109:676 – 83. Batista RV, Santos JL, Takeshina N, Bocchino L, Lima PN, Cunha MA. Partial left ventriculectomy to improve left ventricular function in end-stage heart disease. J Cardiac Surg 1996;11:96 –7. McCarthy PM, Starling RC, Wong J, et al. Early results with partial left ventriculectomy. J Thorac Cardiovasc Surg 1997; 114:755– 65. Carpentier A. Cardiac valve surgery. The French connection. J Thorac Cardiovasc Surg 1983;86:323–37. Sousa Uva M, Dreyfus G, Rescigno G, Al Ayle N, et al. Surgical treatment of asymptomatic and mildly symptomatic mitral regurgitation. J Thorac Cardiovasc Surg 1996;112: 1240 –9. Fucci C, Sandrelli L, Pardini A, Torraca L, Ferrari M, Alfieri O. Improved results with mitral valve repair using new surgical techniques. Eur J Cardiothorac Surg 1995;9: 621–7. Lytle BW, Loop FD, Cosgrove DM, et al. Mitral valve repair for ischemic mitral insufficiency. Ann Thorac Surg 1991;52: 1246 –52. David TE, Komeda M, Pollick C, Burns RJ. Mitral valve annuloplasty: the effect of type on left ventricular function. Ann Thorac Surg 1989;47:524 – 8. Batista RV, Verde J, Nery P, et al. Partial left ventriculectomy to treat end-stage heart disease. Ann Thorac Surg 1997;64:634 – 8. Bach DS, Bolling SF. Early improvement in congestive heart failure after correction of secondary mitral regurgitation in end-stage cardiomyopathy. Am Heart J 1995;129: 1165–70.
R
egardless of the etiology, when end-stage heart disease results in congestive heart failure, the primary treatment is heart transplantation. However, donor shortage and side effects of immunosuppressive therapy allow successful transplantation for very few patients. Therefore, alternative therapies have emerged, such as coronary artery revascularization,1 cardiomyoplasty,2 and more recently isolated mitral valve repair,3 or mitral valve repair associated with left ventricular reduction known as the Batista procedure.4,5 Until recently, secondary mitral regurgitation was not considered by itself to be an indication for surgical intervention when occurring as a consequence of dilated cardiomyopathy. The mitral valve plays a key role in left ventricular function and creates a highly dynamic inner supporting structure that optimizes contraction as well as relaxation. Papillary muscles, as components of the ventricular wall, through the chordae tendineae and valve leaflets are linked to the mitral annulus, thereby maintaining the integrity of a complex functional geometry. Primary or acquired myocardial disease can induce mitral dysfunction; mitral regurgitation worsens left ventricular dysfunction when it occurs in end-stage cardiomyopathy. Moreover, mitral regurgitation increases volume overload in an already dilated left ventricle, which further worsens mitral regurgitation, thus establishing a vicious cycle, and is known to predict poor survival when present. We will discuss the pathophysiologic justification for mitral valve repair in heart failure patients, current indications, and incorporation of related surgical procedures.
From the Ho ˆpital Foch, Universite´ de Paris V, Suresnes, France. Submitted March 1, 1999; accepted March 23, 2000. Reprint requests: Gilles Dreyfus, MD, Ho ˆpital Foch, Universite´ de Paris V, Service de Chirurgie Cardiaque, 40 rue Worth, 92151 Suresnes, France. Telephone: 33-1-4625-2487. J Heart Lung Transplant 2000;19:S73–S76. Copyright © 2000 by the International Society for Heart and Lung Transplantation. 1053-2498/00/$–see front matter PII S1053-2498(00)00106-6
RATIONALE FOR MITRAL VALVE REPAIR Mitral valve repair, when feasible, is clearly superior to mitral valve replacement. Many authors have confirmed this, including Carpentier,6 who for 16 years has found a lower incidence of reoperation on the mitral valve following repair. Mitral valve repair not only yields better surgical results than mitral valve replacement but also better preserves left ventricular function. This fact was well documented by Hauser and Sarris. They demonstrated that division of chordae tendineae reduced maximum left ventricular contractile velocity by 50%. Interaction of the mitral annulus and the sub-valvular apparatus with left ventricular function and geometry are essential to preserve left ventricular function and are probably more obvious in patients with severely impaired left ventricular function than in others. Finally, mitral valve repair may improve left ventricular function after surgery.3,6 This is well known for patients who have symptoms of dilated left ventricles before surgery. We have also shown that, even in patients with moderate left ventricular dilatation who are asymptomatic, ventricular size after mitral repair could be decreased.7 In summary, mitral valve repair is superior to mitral valve replacement, as it better preserves and may even improve left ventricular function following surgery.
MITRAL VALVE REPAIR Physiologic consequences of mitral valve repair are shown in Figure 1. The ultimate goal, in thermodynamic terms, for correction of mitral valve regurgitation is to decrease energy loss for the left ventricle by creating a more efficient workload. Mitral valve repair would decrease left ventricular overload, thereby decreasing wall tension and ultimately oxygen consumption. In addition, reduction in mitral insufficiency helps to restore normal ventricular geometry, which provides backing for left ventricular shortening and torque motion. By creating more efficient forward flow, mitral valve repair also contributes to decreased energy loss. S73
S74
Dreyfus and Milaiheanu
The Journal of Heart and Lung Transplantation August (Suppl) 2000
attracted downward. We and others have used this technique as an integral part of left ventricular reduction procedures.
MITRAL VALVE REPAIR ACCORDING TO ETIOLOGY Patients with mitral regurgitation can be divided into 3 distinct groups, which we will discuss below.
Primary Mitral Valve Disease
FIGURE 1 Physiological consequences of mitral valve repair. LV, left ventricular.
ROLE OF THE MITRAL ANNULUS The goal of mitral valve repair is to restore leaflet coaptation. When the left ventricle is dilated, the mitral valve annulus dilates, allowing valvular regurgitation. The role of prosthetic ring placement is to recreate normal mitral annular geometry, thus reapproximating the anterior and posterior leaflets and allowing effective coaptation. When left ventricular dilation occurs, it occurs in all dimensions, resulting not only in increased chamber volume but also sphericity. As the ventricle dilates, papillary muscles are pulled downward, away from the mitral annulus, creating tension on the chordae. As a result, the free edge of both leaflets cannot coapt. Because placement of a prosthetic mitral ring does not influence longitudinal dimension, this intervention by itself may be inadequate to restore normal systolic mitral coaptation. Two things may overcome this problem. The first is to dramatically undersize the mitral ring.3 By doing so, leaflet competence can sometimes be achieved, but this method places increased tension on the base of the left ventricle and therefore impedes contraction. However, Bolling and associates3 have described clinical application of this technique with good preliminary results. A second possibility would be to suture together the free edges of the anterior and posterior leaflet as described by Alfieri and colleagues.8 This technique creates a double orifice or a figure-eight mitral orifice, which no longer allows the coapting portion of both leaflets to be
This group predominantly includes patients with either rheumatic or degenerative mitral disease, often with relatively preserved left ventricular systolic function. In the case of rheumatic valvular disease, repair gives the worst results. Therefore surgical intervention should be late, and prosthetic replacement is the treatment of choice. Conversely, repair of mitral regurgitation of degenerative etiology has excellent immediate and long-term results and therefore should always be considered as the procedure of choice.6 With increasing durability of surgical success, indications have continued to evolve. Current guidelines for surgical indications, based upon end-systolic dimensions of the left ventricle, support intervention when the degree of regurgitation reaches grade 3 to 4⫹ and left ventricular end-systolic diameter reaches 40 mm.7
Intermediate Mitral Valve Disease This group is typically represented by mitral valve lesions associated with coronary artery disease and myocardial ischemia. Ischemic mitral valve disease can assume a variety of forms including papillary muscle elongation or rupture, or acute regional ventricular dysfunction, which creates mitral regurgitation. Regardless of the mechanism for ischemic mitral valve regurgitation, the likelihood of successful repair is excellent.9,10 In most cases surgical correction is easy and can be achieved by inserting a prosthetic ring. Long-term results in such instances can be less certain because of the interaction between the mitral valve and the underlying left ventricular pathology. Ventricular recovery is not easily predictable because ischemic heart disease combines functional and scarred myocardium in a nonhomogenous manner to produce distorted patterns of contraction. At our institution, mitral valve repair is performed when the degree of mitral regurgitation is greater than 2⫹, and when myocardial scarring is seen on echocardiography. Dobutamine stress echocardiography is frequently helpful, mitral repair being considered more strongly if mitral regurgitation increases with stress. In a previous report from our institution, we described revascu-
The Journal of Heart and Lung Transplantation Volume 19, Number 8S
larization outcome in more than 100 patients with ischemic cardiomyopathy and viable myocardium.1 Coronary artery bypass grafting was performed as an alternative to heart transplantation to improve functional class and ejection fraction. In this group of patients, only 3 required concomitant mitral valve repair. We therefore believe that in this specific population, severe mitral regurgitation is less common.
Secondary Mitral Valve Disease This heterogeneous group of patients represents a potentially enormous population which has, until recently, been largely overlooked as candidates for mitral valve surgery. It includes a large proportion of patients with dilated cardiomyopathy who historically have been managed exclusively with medical therapy and, eventually, with transplantation. Traditional views held that because the valve apparatus itself was undamaged, valve-directed intervention was not indicated. Two new surgical options have emerged in the mid-1990s that have challenged this paradigm: isolated mitral valve repair3 and left ventricular volume reduction.11 Bolling and associates3 recently studied 48 patients with chronic New York Heart Association (NYHA) class IV heart failure, all of whom had severe left ventricular dysfunction and severe mitral regurgitation, evenly divided between ischemic and non-ischemic cardiomyopathy. Surgery in all instances consisted of mitral annuloplasty using a flexible ring. The mean size of the ring was 26 mm. In addition, 7 patients had coronary artery bypass grafting and 11 patients had an additional triscupid annuloplasty using the DeVega technique. They observed only one post-operative death (right ventricular failure) and minimal post-operative mitral gradient. Actuarial survival after 1 and 2 years was 82% and 72%, respectively. All patients improved functionally and left ventricular ejection fraction increased from 16% to 26%. Peak exercise oxygen capacity increased from 14.5 to 18.6 ml/kg/min. There were 8 early cardiac deaths but no late deaths. The number of patients in this series precludes meaningful sub-group analysis. However, these promising results suggest that this approach should be considered in patients with severe heart failure complicated by secondary mitral regurgitation. Although these observations are encouraging, several points merit discussion. Although the reported hemodynamic results were excellent with an increase in cardiac output and associated with a low
Dreyfus and Milaiheanu
S75
transmitral gradient, such procedures as described have the potential to decrease left ventricular contractility. Undersizing the mitral ring may increase tension on the base of the left ventricle, stretching myocardial fibers and decreasing what is often the best contracting portion of the failing left ventricle. An alternative intermediate approach would be to size the mitral ring according to Carpentier’s principles,6 which consider the distance in between anterior and posterior commissures. The Alfieri stitch,8 placed at the middle of the free edge of the anterior and posterior mitral leaflets, may address the lack of coaptation of both mitral leaflets when longitudinal shortening is altered. This approach should prevent excessive traction on the base of the left ventricle. As is often the case with innovative surgical procedures, patient selection is critical. In the case of mitral valve repair, the primary issue concerns the degree of left ventricular dilatation and how it should guide operative candidacy. A related procedure, the so-called Batista procedure, consists of combination mitral repair and surgical ventricular remodeling,4,11 the largest well-documented series of which is from the Cleveland Clinic.5 The latest report by McCarthy and coworkers,5 described 52 patients with idiopathic cardiomyopathy. All patients were NYHA class IV patients with idiopathic dilated cardiomyopathy with left ventricular enddiastolic diameter ⬎70 mm and concomitant mitral regurgitation of at least a moderate degree. Mean cardiac output was 2.2 liter/min, and many patients had pulmonary hypertension. All patients received a mitral valve repair using a Cosgrove ring annuloplasty, along with left ventricular volume reduction by resection of the anterolateral wall of the left ventricle from the apex, in between papillary muscles down to the atrioventricular groove. In one third of the patients, 1 papillary muscle was displaced to increase the resection and to preserve the mitral valve. Only 1 patient died post-operatively, but 8 patients required left ventricular assist device in the early post-operative period and were bridged to transplantation. Ten other patients were listed for transplantation more than 14 months follow-up. All other patients improved functionally and, as in Bolling’s experience, have increased their peak oxygen consumption from 12 to 18 ml/kg/min. However, minimal change appeared in hemodynamic status with surgery. Although this innovative technique is intriguing, appropriate patient selection criteria remain to be established. The current paucity of data and lack of estab-
S76
Dreyfus and Milaiheanu
lished guidelines do not allow clear discrimination between isolated mitral valve repair and combination mitral repair/left ventricular reduction. Could some patients undergoing a Batista procedure have enjoyed better results with isolated mitral valve repair? Conversely, could patients who died after isolated mitral valve repair have survived if they had undergone a Batista procedure? In conclusion, prospective randomized studies are clearly indicated, although the requisite large sample sizes will render this a daunting enterprise. Intuitively, isolated repair is probably the best option in the case of severe regurgitation in a moderately dilated left ventricle. Surgical ventricular remodeling can be considered when the left ventricle is extremely dilated and when pre-operative assessment demonstrates potential for recovery. However, many questions concerning left ventricular volume reduction remain unanswered, and further results and larger series may provide answers. However, mitral insufficiency is, if not the key component, certainly a major contributor to progression of disease in patients with chronic heart failure and should be viewed as a potential target of intervention to improve functional status and to avoid or delay heart transplantation.
The Journal of Heart and Lung Transplantation August (Suppl) 2000
3.
4.
5.
6. 7.
8.
9.
10.
11.
REFERENCES 1. Dreyfus GD, Duboc D, Blasco A, et al. Myocardial viability assessment in ischemic cardiomyopathy: benefits of coronary revascularization. Ann Thorac Surg 1994;57:1402– 8. 2. Carpentier A, Chachques JC, Carteaux JP. Dynamic cardio-
12.
myoplasty at eleven years. In: Carpentier A, Chachques JC, Grandjean PA, eds. Cardiac bioassist. Armonk, New York: Futura, 1997, pp. 3–23. Bolling SF, Deeb GM, Brunstring LA, Bach DS. Early outcome of mitral valve reconstruction in patients with end-stage cardiomyopathy. J Thorac Cardiovasc Surg 1995; 109:676 – 83. Batista RV, Santos JL, Takeshina N, Bocchino L, Lima PN, Cunha MA. Partial left ventriculectomy to improve left ventricular function in end-stage heart disease. J Cardiac Surg 1996;11:96 –7. McCarthy PM, Starling RC, Wong J, et al. Early results with partial left ventriculectomy. J Thorac Cardiovasc Surg 1997; 114:755– 65. Carpentier A. Cardiac valve surgery. The French connection. J Thorac Cardiovasc Surg 1983;86:323–37. Sousa Uva M, Dreyfus G, Rescigno G, Al Ayle N, et al. Surgical treatment of asymptomatic and mildly symptomatic mitral regurgitation. J Thorac Cardiovasc Surg 1996;112: 1240 –9. Fucci C, Sandrelli L, Pardini A, Torraca L, Ferrari M, Alfieri O. Improved results with mitral valve repair using new surgical techniques. Eur J Cardiothorac Surg 1995;9: 621–7. Lytle BW, Loop FD, Cosgrove DM, et al. Mitral valve repair for ischemic mitral insufficiency. Ann Thorac Surg 1991;52: 1246 –52. David TE, Komeda M, Pollick C, Burns RJ. Mitral valve annuloplasty: the effect of type on left ventricular function. Ann Thorac Surg 1989;47:524 – 8. Batista RV, Verde J, Nery P, et al. Partial left ventriculectomy to treat end-stage heart disease. Ann Thorac Surg 1997;64:634 – 8. Bach DS, Bolling SF. Early improvement in congestive heart failure after correction of secondary mitral regurgitation in end-stage cardiomyopathy. Am Heart J 1995;129: 1165–70.