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Eur J Cardiothorac Surg 2004;26:1112-1117
© 2004 Elsevier Science NL

Ischemic mitral valve prolapse: mechanisms and implications for valve repair

Department of Cardiovascular Surgery, Hôpital de la Salpétrière, 50-52 Bd Vincent Auriol, 75013 Paris, France

Received 16 April 2004; received in revised form 6 July 2004; accepted 13 July 2004.

^* Corresponding author. Tel.: +33 1 42 16 56 85; fax: +33 1 42 16 56 78. (E-mail: c.acar{at}psl.ap-hop-paris.fr).

	Abstract

Top Abstract 1. Introduction 2. Patients and methods 3. Results 4. Discussion References

 
Objective: The aim of this study was to assess the mechanisms of prolapse in ischemic mitral valve regurgitation (MR) and the techniques of valve repair. Methods: Out of 121 patients operated upon for ischemic MR, a prolapse was present in 44 patients (36.4%). The operation was performed emergently in four cases (9.1%) and electively in 40 patients (90.9%). Fifteen patients (34.1%) were operated upon within 60 days following acute myocardial infarction. Results: The diagnosis of prolapse had been overlooked by echography in five cases (11.4%). A commissural area was involved as the site of prolapse in 31 cases (70.4%). The mechanism of prolapse was a papillary muscle (PM) lesion in 38 cases (86.4%) (anterior PM: n=8, posterior PM n=36) or a chordal lesion in six cases (13.6%). PM injury was elongation (n=16), or rupture (total n=1, partial n=21, incomplete n=4). The operative technique was mitral valve repair with Carpentier's techniques in 42 cases (95.5%) or replacement in two cases (4.5%). Hospital mortality was 11.4% (n=4). The mean follow-up was to 44.7±29.6 months. Overall survival and freedom from reoperation were 68.3±9.0 and 89.9±5.7% at 5 years, respectively. Freedom from MR equal or > grade 2 was 69.7±9.5% at 5 years. Conclusions: The mechanisms of ischemic mitral valve prolapse were variable and tightly linked to the PM anatomy. A reliable mitral valve repair could be achieved in most cases with acceptable mid-term results.

	1. Introduction

Top Abstract 1. Introduction 2. Patients and methods 3. Results 4. Discussion References

 
The results of valve repair for ischemic mitral insufficiency are still suboptimal with a relatively high rate of death and reoperation [1–3]. Valve restriction with annular dilatation is the most frequent functional abnormality; however, the recognition of prolapse in ischemic mitral insufficiency has remained difficult [4] and in our experience, can be overlooked. The objective of this study was to describe the surgical findings in a subgroup of patients with ischemic mitral insufficiency resulting from valve prolapse. The mechanisms of papillary muscle lesions were studied as well as their impact on mitral repair.

	2. Patients and methods

Top Abstract 1. Introduction 2. Patients and methods 3. Results 4. Discussion References

 
From March 1994 to January 2004, 121 patients underwent surgery for ischemic mitral valve insufficiency. Inclusion criteria for asserting the ischemic origin of mitral insufficiency were the presence of coronary artery disease with evidence of recent or healed ischemic injury to a papillary muscle or to the surrounding myocardium. Patients with coronary disease whose mitral valve showed typical myxomatous or rheumatic lesions were excluded. Out of these 121 patients, intraoperative inspection of the valve revealed ischemic mitral valve prolapse in 44 patients (36.4%) who represent the study population group.

There were 35 men (79.5%) and nine women (20.5%), whose mean age was 66.8±10 years. The clinical characteristics are shown on Table 1. The operation was performed emergently in four patients (9.1%) and electively in 40 patients (90.9%). Sixteen patients (36.4%) had a recent (<30 days) pulmonary edema and three patients (6.8%) were in cardiogenic shock. Fifteen patients (34.1%) were operated upon within 60 days following acute myocardial infarction. The degree of mitral regurgitation assessed by echocardiography was variable according to the time of examination. The maximum amount of regurgitation was grade 2 in four cases (9.1%), grade 3 in 18 cases (40.9%) and grade 4 in 22 cases (50%). The mean ejection fraction was 54.9±13.8% and end diastolic left ventricular diameter was 60.9±8.9mm. The coronary arteries involved (stenosis>60% or occlusion) were: left anterior descending (n=21 (47.7%)), diagonal (n=16 (36.4%)), circumflex (n=31 (70.5%)) and right coronary artery (n=30 (68.2%)).

2.1. Statistical analysis
Continuous variables were expressed as mean±SD. Statistical comparisons between means were made using unpaired two-tailed student's t-test. Categorial variables were presented as absolute numbers of patients and percentages. Curves were presented according to the method described by Kaplan and Meier. A Cox regression analysis was used to determine multivariate independant predictors of all-cause mortality.

	3. Results

Top Abstract 1. Introduction 2. Patients and methods 3. Results 4. Discussion References

 
3.1. Mechanisms of ischemic mitral valve prolapse
Intraoperative observation revealed leaflet prolapse (functional type II) in all cases. The sites of prolapse are shown on Fig. 1. A commissural area was involved in 31 cases (70.4%). Evidence of acute/healed necrosis of a papillary muscle was found in 38 cases (86.4%). The anterior papillary muscle was involved in eight cases, and the posterior papillary muscle in 30 cases. In six cases (13.6%), necrosis was restricted to the adjacent myocardium.

View larger version (24K): [in this window] [in a new window]   Fig. 1. Site of ischemic mitral valve prolapse (n=44). The posteromedial commissure was involved in the majority of cases. The A3 portion of the anterior leaflet was prolapsed in one-third of the cases.

View larger version (40K): [in this window] [in a new window]   Fig. 2. Segmentation of the papillary muscle. Five steps toward division can be individualized: I, single uniform unit; II, groove with two apexes; III, fenestrations with muscular bridges; IV, complete separation in two adjacent heads; V, complete separation with two distant heads. Division can occur according to two directions: (A) division in a sagittal plane leading to a separate posterior leaflet head. (B) Division in a coronal plane leading to a separate commissural head. A, anterior leaflet; C, commissure; P, posterior leaflet.

View larger version (28K): [in this window] [in a new window]   Fig. 3. Mechanisms of ischemic mitral valve prolapse. (A) Necrosis of a separate commissural head (inserted close to the annulus) with rupture of the anchorage of the commissural chord. (B) Necrosis of a single head papillary muscle subdivided in multiple heads with partial rupture. (C) Necrosis of a fenestrated papillary muscle with detachment of its main insertion: ‘incomplete’ rupture. With time, incomplete rupture mimics papillary muscle elongation. (D) Single papillary muscle with complete and total rupture.

3.2. Operative technique
Mitral valve replacement was performed in two emergency cases (4.5%) including the only case of total and complete papillary muscle rupture. The other patient had a partial rupture in whom a repair was first attempted using chordal transposition. The chordae selected for transposition had been inserted on the freshly necrosed papillary muscle and intraoperative rupture of the papillary head supporting the transferred chordae occurred requiring valve replacement.

Mitral valve repair was performed in 42 cases (95.5%). Carpentier techniques of mitral valve repair were used [5]. Commissural prolapse was treated using a commissuroplasty consisting of closing the commissural area using interrupted sutures (n=23, 54.8%). Anterior leaflet prolapse was treated using chordal transposition from the posterior to the anterior leaflet (n=23, 54.8%) and posterior leaflet prolapse was treated using the quadrangular resection technique (n=4, 9.5%). Papillary muscle head reimplantation was achieved in one case with chronic mitral regurgitation. In all cases, a downsized annuloplasty was performed. A flexible Duiran ring was used in 33 cases (mean size: 27.3±1.6) and a Carpentier physioring was implanted in 10 cases (mean size: 30.8±1.9). Associated procedures were: coronary artery bypass n=34 (77.3%), LV aneurysm exclusion n=2 (4.5%), aortic valve replacement n=4 (9%), Bentall operation n=1 (2.4%), ASD closure n=1 (2.4%). The mean number of coronary bypass grafts was 1.9±0.4. Mean cardiopulmonary bypass time was 89±24min, and mean ischemic time was 73±21min.

3.3. Clinical results
Five patients died for an hospital mortality of 11.4% (emergency valve replacement with total papillary muscle rupture (n=1) and repair (n=4)), four deaths were related to heart failure and one patient died from pulmonary infection. Inotropic support was required for more than 2 days in 10 patients (22.7%) and intraaortic counterpulsation was used in five patients (11.4%). Surviving patients remained in the ICU for 4.4±5.5 days. Postoperative complications were: pulmonary infection (n=5), sternal wound infection (n=3), atrioventricular block requiring permanent pace maker (n=1).

Transthoracic echography at discharge showed no or grade 1 residual mitral insufficiency in 34 cases and grade 2 insufficiency in four cases.

The follow-up period extended from 2 to 119 months (mean: 44.7±29.6 months). Overall survival was 85.8±5.4 and 68.3±9.0% at 1 and 5 years, respectively (Fig. 4). Survival free from cardiac death was 76.8±7.8% at 5 years (Fig. 4). Three patients required a reoperation and freedom from reoperation was 89.9±5.7% at 5 years (Fig. 5). The causes for repair failure were persistent restricted leaflet motion (n=2) and dehiscence of a papillary muscle reimplantation suture (n=1).

View larger version (14K): [in this window] [in a new window]   Fig. 4. Survival following surgery for ischemic mitral valve prolapse. Overall survival and survival free from cardiac death were 68.8±9 and 86.6±7.4% at 5 years, respectively.

View larger version (17K): [in this window] [in a new window]   Fig. 5. Mitral valve function following repair for ischemic mitral valve prolapse. Freedom from reoperation and freedom from significant mitral regurgitation were 89.9±5.7 and 69.7±9.5% at 5 years, respectively.

	4. Discussion

Top Abstract 1. Introduction 2. Patients and methods 3. Results 4. Discussion References

 
Ischemic mitral insufficiency is one of the rare situations in which the three Carpentier functional types of regurgitation can be more or less associated [5]. Restricted leaflet motion is invariably present (type IIIb) due to the segmental akinetic/dyskinetic motion of the ventricle, which results in an increased distance between the papillary muscle and the plane of the mitral annulus. Excess traction on the chordae prevents leaflet coaptation in the area supplied by the ischemic papillary muscle, which comprises the commissure and the adjacent parts of the leaflets (hemivalve). Frequently, a mild or moderate annular dilatation (type I) is associated. Mitral valve prolapse (type II) is more unusual in ischemic mitral insufficiency. However, its occurrence has probably remained underestimated and it represents as much as one-third of the cases in our series. The ischemic injury to the papillary muscle responsible for the prolapse can take multiple forms because of the variability of the coronary vascular distribution and the diversity in papillary muscle anatomy. It is known that the anterior papillary muscle is rarely involved (9% of the cases in this series) because its blood supply is provided both by the left anterior descending coronary artery and a diagonal branch [6,7]. In addition, the tension exerted by the chordae on this papillary muscle is relatively low due to its superficial location with regard to the annulus. Conversely, the posterior papillary muscle is more sensitive to ischemia (91% of the cases) because its blood supply relies on distal branches exclusively furnished by either the right coronary or the circumflex artery [6,7]; furthermore, its location deep in the left ventricle subjects this muscle to a higher shear force.

Studies of the microcirculation of the papillary muscles have demonstrated two different types of distribution modes: an independent blood supply provided by a well-identified arterial trunc perforating the papillary muscle from base to apex (Kügel's artery) and a segmental distribution [6,7] (Fig. 6). The importance of the truncal irrigation mode increases as the papillary muscle is more individualized from the ventricular wall. The apex of the papillary muscle is mainly supplied by a truncal distribution, the presence of muscular bridges between the papillary muscle and the ventricular wall provides as many penetration points for segmental arterial branches [6]. Finally, at the base of papillary muscle, the segmental blood supply is predominant [7]. It is uncertain whether the vascular distribution as described above plays an important role in the pathogenesis of papillary muscle ischemia because it is usually related to disease of the large epicardial coronary arteries rather than to an impairment of the microcirculation. Nevertheless, it appears clear that a well individualized papillary muscle and particularly its apex is more prone to rupture due to the fragility of its truncal blood supply, and to the extent of the physical stress. In contrast, the presence of multiple muscular bridges or even a complete tethering of the papillary muscle to the wall seems to protect it from rupture.

In this series, the ischemic origin of the mitral insufficiency was identified when both coronary artery lesions and a recent/healed ischemic injury involving part or the whole papillary muscle were present. Patients with Barlow disease presenting with coronary lesions were easily excluded in view of grossly myxomatous leaflets and chordae. However, significant difficulties in clarifying the pathogenesis were found in patients with coronary disease and isolated chordae rupture of the posterior leaflet with an otherwise normal valve and papillary muscle. These cases seem to be related to a preexisting fibroelastic deficiency, with rupture of chordae being facilitated by the stress generated by the geometrical systolic modifications of the left ventricle induced by ischemia.

Beside the insertion mode, the morphology of the papillary muscle in itself can vary. There are multiple intermediary forms between a single unit and a papillary muscle split into separate heads (Fig. 2). The morphology of the posterior papillary muscle, which is the usual site of ischemic injury, is as a rule more complex than the anterior papillary muscle and its subdivision into several heads is very frequent. Thus, it is not surprising to observe that ischemic mitral prolapse is frequently caused by a lesion limited to a single head (defined as a ‘partial’ injury Fig. 4). In the autopsy series, rupture of the papillary muscle is partial in 2/3 of the cases [8,9] and has also been frequently reported in the surgical series [10,11]. Prolapse was caused by a partial papillary muscle rupture in half of the cases in the present series (Fig. 3). The separate heads resulting from papillary muscle subdivision support specific portions of the valve; therefore, in case of a partial rupture or elongation, the extent of the leaflet prolapse varies according to the territory supplied by the ischemic head. Our results showed that the most frequent sites of prolapse were the posteromedial commissural area and the A3 of the anterior leaflet (Fig. 1). Total rupture of the papillary muscle produces a prolapse of the whole hemivalve. Whatever the mechanism of prolapse, the remaining portion of the valve is subjected to the restrictive process described above, and this must be considered when sizing the valve for prosthetic ring annuloplasty. An undersized ring should be selected so as to compensate for the incomplete closure of the valve.

Recently, we identified an intermediary form in which an incomplete detachment of a head due to a rupture of its main insertion occurred while it still remained fixed to the ventricle via muscular bridges (‘incomplete’ papillary muscle rupture). We hypothetized that with time this type of lesion could mimic papillary muscle elongation as found in a few cases in this series. Whether papillary elongation invariably represents a late sequellae of an incomplete rupture or whether it can be a primary lesion due to a distension of a scarred papillary muscle submitted to excess tension remains debatable. Complete and total papillary muscle rupture is easily recognized because it creates massive intractable mitral insufficiency requiring emergency surgery and the ruptured muscle is clearly visible on echography. Conversely, in partial or incomplete papillary muscle rupture, the regurgitation can be well tolerated; its quantification is more difficult because of its commissural site and patients are often operated upon later when the papillary muscle head has become the site of fibrosis and involution making it hardly distinguishable on echography.

Intraoperative analysis of the mechanism of prolapse can have important implications for valve repair. It is frequently made more difficult by the small left atrium size often encountered in ischemic mitral insufficiency. If the lesion is overlooked leading to the false conclusion of an isolated type III regurgitation, a residual insufficiency may ensue. Furthermore, a segmental prolapse secondary to a partial papillary muscle injury is often accessible to a reliable valve repair. In our experience, the feasibility of valve repair for ischemic mitral valve prolapse was 95%. Isolated prolapse of a commissure was not uncommon and was treated according to a commissuroplasty (commissural Alfieri technique [12]). Anterior leaflet prolapse was corrected by chordal transposition from the posterior leaflet. Chordae inserted on the same papillary muscle are usually harvested for transposition; however, in case of an acute papillary muscle infarction chordae inserted on a healthy papillary muscle should be used in order to avoid excess tension on the freshly necrosed papillary muscle that could result in recurrent rupture (one case in this series). Posterior leaflet prolapse was treated using the classical quadrangular resection. In our hands, reimplantation of a papillary muscle remnant did not offer a reliable result. Because of retraction and involution of the edges of the remnants, reimplantation resulted in a shorter papillary muscle exposed to superior traction forces that could have been responsible for the recurrence of dehiscence as shown in one case. In the case of an elongation, although not used in this series, the papillary muscle shortening technique or plication [5] represents an alternative to chordal transposition [13,14]. Irrespective to the mechanism of the prolapse prosthetic ring annuloplasty has remained a fundamental step of the repair aiming at (1) treating annular dilatation, (2) releasing traction forces on the suture line and (3) counteracting the restrictive component of the regurgitation by choosing an undersized ring in order to force leaflet coaptation. Rarely, in case of a complete and total papillary muscle rupture, mitral valve replacement was required.

In conclusion, careful inspection of the valve revealed that leaflet prolapse was present in one-third of patients with ischemic mitral valve insufficiency. The causative lesions were variable and tightly linked to the papillary muscle anatomy. A reliable mitral valve repair could be achieved in the vast majority of cases with acceptable mid-term results.

	References

Top Abstract 1. Introduction 2. Patients and methods 3. Results 4. Discussion References

 

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