Ann Thorac Surg 2009;88:1191-1196. doi:10.1016/j.athoracsur.2009.05.086
© 2009 The Society of Thoracic Surgeons
Original Articles: Adult Cardiac
Nonresectional Repair of the Barlow Mitral Valve: Importance of Dynamic Annular Evaluation
Gerald M. Lawrie, MD*,
Elizabeth A. Earle, JD,
Nan R. Earle, MS
The Heart Valve Institute, Methodist DeBakey Heart and Vascular Center, Houston, Texas
Accepted for publication May 28, 2009.
* Address correspondence to Dr Lawrie, 6560 Fannin, #1842, Houston, TX 77030 (Email: gmlawrie{at}att.net).
Presented at the Poster Session of the Forty-fifth Annual Meeting of The Society of Thoracic Surgeons, San Francisco, CA, Jan 26–28, 2009.
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Abstract
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Background: The most extensive form of myxomatous degeneration of the mitral valve causing severe mitral regurgitation is "Barlow disease." Surgical repair of this condition has been considered difficult because of the extent and magnitude of annular, leaflet, and chordal abnormalities and has usually involved partial resection of one or both mitral leaflets.
Methods: A surgical approach has been developed which does not involve leaflet resection. Instead, by means of precise dynamic annular sizing, a predetermined zone of leaflet apposition is achieved. The leaflets are positioned so that their large area is contained within the left ventricle. Normal annular, leaflet, and papillary muscle dynamic function is restored.
Results: This procedure was performed in 61 patients. The repair rate was 100%. The mean age was 57.6 ± 12.7 years. They were 67.2% male. The preoperative anteroposterior annular dimension was 52.1 ± 4.3 mm. The full, flexible complete ring size was 33.4 ± 1.9 mm. There was no perioperative mortality. There was no systolic anterior leaflet motion. All patients were discharged with no or mild mitral regurgitation. At a follow-up interval of 1.2 ± 2.1 years one patient had developed recurrent mitral regurgitation, secondary to marked remodeling to normal left ventricular function.
Conclusions: Initial experience with a nonresectional approach for Barlow disease has produced good early results.
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Introduction
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Since the introduction of clinical echocardiography 30 years ago [1], the dynamic function of the mitral valve apparatus in normal and diseased patients has become more fully appreciated. A substantial amount of experimental work also has been performed in animal models. Based on these data, a technique has been developed which allows the treatment of all forms of myxomatous mitral valve prolapse causing mitral regurgitation without leaflet resection or unusually large annuloplasty rings [2].
The aim of this report is to describe this approach and to document the results of nonresectional mitral valve repair using these techniques in a series of patients with Barlow disease.
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Material and Methods
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This prospective study was approved by our Institutional Review Board. The study was exempted from the need for individual patient consent. For the purpose of this study, Barlow disease was defined as the presence of severe generalized bileaflet myxomatous mitral valve disease. The preoperative mitral annular anteroposterior diameter was 48 mm or greater in all cases. There was generalized marked enlargement and systolic prolapse of all leaflet segments. All such patients were diagnosed by preoperative transthoracic and (or) transesophageal echo, and intraoperatively by transesophageal echo and direct inspection during surgery. Of a series of 1,121 consecutive patients who underwent mitral valve repair, 61 patients were identified by these criteria. These 61 patients were compared with 367 patients with pure myxomatous disease and mitral regurgitation from leaflet prolapse operated upon during the same time interval. Surgery was performed between April 4, 1997 and December 31, 2008. The patients were contacted annually by questionnaire, telephone calls, or information was obtained from physician offices and examination of the Social Security Death Index at Rootsweb.ancestry.com.
Statistical Analysis
The data were recorded prospectively on custom forms and entered into a custom database. The database, which was designed in FileMaker (FileMaker Pro version 7.0v2), resides on a Pentium III Personal Computer running Windows 2000 Professional, version 5.0.2195 with Service Pack 4 (Microsoft Corp, Redmond, WA). Data analyses were carried out in S-Plus version 6.2, Professional Edition (Insightful Corporation, Seattle, WA). The variables of interest were imported into S-Plus by an intermediate Excel file (Microsoft Excel 2003 [11.6560.8036 SP2]). Formal statistical analyses carried out in S-Plus were the following: 
2 analyses for categoric data, analysis of variance for continuous variables, and Cox proportional hazard analysis for predictors of survival and freedom from reoperation, as well as Kaplan-Meier survival analyses and their resulting graphs. Significant statistical differences were considered to exist if p was less than 0.05. There was no adjustment for multiple tests.
Surgical Technique
A brief description of the technique is provided here. A fuller description is contained in reference 2. Further extensive technical details, including narrated videos of this technique by open and robotic approaches are available at www.geraldlawriemd.com.
The chest is entered either through a full median sternotomy, a limited lower sternal incision, or more recently with the DaVinci robotic-assisted approach through the right lateral chest wall using a 20 mm working port. The left atrium is entered through an interatrial incision and the mitral valve is exposed. Stay stitches of 2-0 polypropylene are placed at the following sites: two anterior to the commissures into the right and left fibrous trigones, and two or three into the posterior annulus. The annulus, valve leaflets, chordae, and papillary muscles are examined. The left ventricle is inflated with 75 to 100 mL of saline at a rate of 4 L/minute using a motorized laparoscopic suction irrigator until the aortic root pressure is 80 to 100 mm. The abnormal structures are identified.
If localized, more severe and asymmetric areas of leaflet prolapse are present, which affect leaflet edge alignment; they are corrected by insertion of No. 5 polytetrafluoroethylene (PTFE) sutures. Dots are placed with a marker pen along the upper margins of the rough zones or, if these are not identifiable, 5 to 10 mm from the free edges of the leaflets to mark the desired zone of apposition. Because the radial dimensions ("depth" or "height") of the different segments of the leaflets vary widely, if the upper edge of the rough zone cannot be identified, the dots are placed about half way up the smaller segments (usually about 5 mm) and on the larger segments at about 10 mm. The left ventricle is inflated with saline and chordal length is adjusted to align the free edges of the leaflets to the same plane as the opposite segment. The two or three stay stitches in the posterior annulus are then brought forward to simulate the effect of left atrial contraction on the posterior annulus reducing the dimensions by 25% so as to bring the lines of dots on both leaflets into apposition. Leaflet alignment and apposition are checked and the PTFE chordae are further adjusted as needed. At this point the mitral orifice is sized according to its circumference in this position using standard ring sizers. A fully flexible adjustable ring of a size which will maintain the zone of leaflet apposition which has been simulated is chosen.
The PTFE chordae, if present, are tied down. The annuloplasty ring is secured to the annulus with the previously placed trigonal 2-0 sutures in continuous fashion. The valve is again tested by saline insufflation of the left ventricle. The marking dots and PTFE knots now should be observed to be buried in the line of apposition. These sequential changes are illustrated in Figure 1. The left atrium is closed. The air is evacuated, warm blood cardioplegia given, and the aorta unclamped. The operation is completed and the repair is checked by transesophageal echocardiography (TEE). The postrepair TEE (Fig 2) shows the widely open left ventricular outflow tract seen with this technique.
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Fig 1. Illustration of surgical technique employed. (A) Appearance of Barlow valve intraoperatively. (B) The edges of the desired lines of apposition have been marked with dots and the left ventricle inflated with the annulus unadjusted and still dilated. (C) The posterior annulus is displaced forward with the ventricle inflated, causing the leaflets to develop the zone of apposition marked by the dots. (D) Appearance of the completed repair.
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Fig 2. Echocardiographic findings from a patient who underwent repair of Barlow disease comparing the preoperative (A) and postoperative (B) appearance of the left ventricular outflow tract (LVOT). The presence of large leaflets has not produced a narrow LVOT.
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Results
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The clinical, angiographic, and echocardiographic features of these patients are summarized in Table 1. The surgical techniques employed are summarized in Tables 2 and 3.
In the Barlow group there was no perioperative mortality (30 day) (Table 4). Results of Kaplan-Meier analyses for freedom from reoperation and significant mitral regurgitation are shown in Figures 3 and 4.
The late severity of mitral regurgitation assessed by echocardiography is shown in Figure 5
and Table 5. No patient required reoperation for systolic anterior motion of the anterior leaflet. One patient required reoperation 10 months after surgery for recurrent mitral regurgitation secondary to marked reduction of left ventricular dimensions after operation.
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Fig 3. Kaplan-Meier curve of freedom from reoperation. (--- = 268 Non-Barlow myxomatous patients; — = 48 Barlow patients.)
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Fig 4. Kaplan-Meier curve of freedom from significant mitral regurgitation. (--- = 267 Non-Barlow myxomatous patients; — = 61 Barlow patients.)
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Fig 5. Incidence and severity of preoperative, predischarge, and late mitral regurgitation (A) for Barlow disease and (B) non-Barlow disease patients.
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Comment
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In 1963 Barlow and colleagues [3] reported on the findings in 7 patients with late systolic murmurs who underwent phonocardiography and left ventriculography. They demonstrated that the cause of the murmurs was mild mitral regurgitation. They showed that the mitral regurgitation was maximal in late systole. Later studies further elucidated these initial findings [4–6]. Thus, the term "Barlow disease" is used properly to describe a syndrome of mild late systolic mitral regurgitation due to myxomatous degeneration of the mitral valve with leaflet prolapse. However, in the surgical literature it has commonly been used to describe a subgroup of patients with the most severe form of myxomatous degeneration who have generalized marked enlargement of all segments of both leaflets. During systole there is progressive prolapse of all leaflet segments, which increases during systole to a maximum at end systole. In addition, some patients may have localized segments with more severe prolapse due to asymmetrical chordal elongation or rupture [7]. The mitral annulus is markedly dilated in patients with mitral regurgitation.
Many of these patients have been treated in the past with mitral valve replacement due to the extent of the disease. When mitral repair has been performed, some form of leaflet resection has usually been recommended and large annuloplasty rings have been employed [8].
The complex and dynamic function of the mitral apparatus determines the position of the mitral leaflets during the cardiac cycle. The six components of the mitral apparatus are the left atrium, the mitral leaflets, the mitral annulus, the chordae tendinae, papillary muscles, and the left ventricle [9].
The structures most affected by the Barlow form of myxomatous mitral valve disease are the leaflets, chordae tendineae, and the mitral annulus. The mitral leaflet areas in this condition are markedly enlarged, usually by a factor of two times or more. The chordae and annulus are also enlarged by a similar amount [10]. Because of these changes, leaflet motion in Barlow disease during systole has unique characteristics [11–13]. The changes seen in less severe forms of myxomatous disease, such as failure of leaflet apposition due to leaflet separation by annular dilatation and chordal elongation or rupture causing segmental prolapse, may be seen in Barlow disease. However, the exceptionally large areas of the mitral leaflets in Barlow disease cause them to unfurl progressively during systole so that they act like large sails projecting horizontally across the mitral orifice parallel to the plane of the mitral annulus. This leads to progressive loss of the area of leaflet systolic apposition as the leaflet edges are pulled up and out of the left ventricle at peak systole [11–13].
This loss of apposition is further exacerbated by the failure of the mitral annulus to achieve the normal area reduction of 25% to 30% of the orifice area during the cardiac cycle [11, 14–16]. Patients with myxomatous mitral disease and severe mitral regurgitation experience only a 15% reduction in mitral annular area [16]. This has been shown in mathematical simulation to delay the development of leaflet apposition and reduce the area of the zone of leaflet apposition achieved during systole [11]. This leads to marked increase in systolic stress levels experienced by the leaflets and particularly the chordae tendineae. The marked increase in leaflet chordal loading leads to their progressive systolic elongation. These phenomena exacerbate the degree of prolapse of the leaflets as systole progresses [11].
The phenomenon described as "mitral papillary muscle traction" plays an important role in the leaflet prolapse of Barlow disease [12, 13]. Due to the excessive systolic loading on the chordae, the tips of the papillary muscles move paradoxically upward toward the mitral annulus during systole, rather than downward toward the left ventricular apex. This further exacerbates the severity of the leaflet prolapse as systole progresses. This is well seen in Figure 6
which shows frames from an intraoperative three dimensional echo study of this phenomenon in one of our patients with Barlow disease.
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Fig 6. Three frames taken from an intraoperative three-dimensional echo of a patient with Barlow disease. In early (A) and midsystole (B) the papillary muscle and annulus do not descend toward the apex of the left ventricle. In midsystole (B) and late systole (C), the head of the papillary muscle and leaflet move paradoxically upward markedly toward the left atrium. (A = annulus; ML = mitral leaflet; TP = tip of papillary muscle.)
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Another important phenomenon observed in normal mitral valves at end diastole and early systole is "diastolic locking." Normally, as left ventricular filling is completed at the end of atrial systole, the mitral annulus has been reduced by 25% [15, 16]. The final phase of left ventricular filling during atrial contraction involves elongation of the long axis of the left ventricle with associated upward motion of the mitral annulus [17]. At the onset of systole, the mitral annulus and papillary muscles start moving downward toward the apex of the left ventricle. The curvature of the anterior portion of the mitral annulus steepens along its attachment to the aortic root through the aortic-mitral continuity [18, 19]. The mitral leaflets are drawn downward into the left ventricle, becoming flattened. Leaflet tenting area is now absent in normal patients. The combined effects of all these events is to force the leaflets into the left ventricle and into apposition with each other. This apposition continues to increase until end systole. This locking together of the leaflets produces a remarkable reduction in systolic chordal tension and allows the tips of the papillary muscles to move normally toward the apex [11, 20]. These phenomena together move the free edges of the leaflets as much as 2 cm into the left ventricle.
Mathematical engineering simulation studies [21] have demonstrated clearly the importance of the interaction of progressive annular reduction and leaflet apposition on the patterns of distribution of leaflet and chordal stress. The progressive increase in the zone of leaflet apposition combined with the flattened more vertical position of the leaflets results in minimal stress on the marginal chordae and transfer of load to the very strong strut chordae, and the mitral annulus [21].
The most common ring sizes we have employed in Barlow repair are 33 mm and 35 mm simple flexible circumferential rings. In 4 patients with a preoperative annular size of more than 60 mm, 37 mm rings were used. Despite using a 37 mm ring in only 4 patients and 33 mm or 35 mm in the remainder, we have seen no leaflet SAM (systolic anterior motion). In a small number of cases we have observed transient chordal SAM. The dimensions of the left ventricular outflow tract in systole have always been generous (Fig 2).
In addition to the obvious advantage arising from the simplicity of this procedure we feel that this repair creates the optimal conditions delineated by Kunzelman and colleagues [11], Sokamoto and colleagues [18], Sacks and colleagues [19], and Nazari and colleagues [21] for a procedure associated with minimal levels of postoperative leaflet and chordal stress. This may play an important role in the avoidance of failure of other severely diseased components of the mitral valve over time. We are following these patients closely as the long-term durability of this technique is not yet established.
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Abstract
Introduction
