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Ann Thorac Surg 2007;84:1578-1584. doi:10.1016/j.athoracsur.2007.05.086
© 2007 The Society of Thoracic Surgeons
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Right arrow Valve disease

Original Articles: Cardiovascular

Efficacy of the Edge-to-Edge Repair in the Setting of a Dilated Ventricle: An In Vitro Study

Laura R. Croft, BSa, Jorge H. Jimenez, PhDa, Robert C. Gorman, MDb, Joseph H. Gorman, III, MDb, Ajit P. Yoganathan, PhDa,*

a Wallace H. Coulter Department of Biomedical Engineering, Georgia Institute of Technology and Emory University, Atlanta, Georgia
b Harrison Department of Surgical Research, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania

Accepted for publication May 30, 2007.

* Address correspondence to Dr Yoganathan, Wallace H. Coulter School of Biomedical Engineering, Georgia Institute of Technology and Emory University, Room 2119 U.A. Whitaker Building, 313 Ferst Dr, Atlanta, GA 30332-0535 (Email: ajit.yoganathan{at}bme.gatech.edu).


   Abstract
Top
 Abstract
Introduction
 Material and Methods
 Results
 Comment
 Acknowledgments
 References
 
Background: The edge-to-edge repair to correct mitral regurgitation (MR) has shown substandard results in cases of ischemic MR or dilated cardiomyopathy.

Methods: Ten porcine mitral valves were investigated in a left heart simulator (120 mm Hg, 5 L/min). Pathologic conditions of a dilated ventricle were simulated by using an annular model capable of three levels of dilation (normal, 56%, and 120%) and by displacing papillary muscles (PMs) 10 mm in the apical, lateral, and posterior directions. The edge-to-edge repair was performed; a central stitch was investigated for symmetric and asymmetric PM displacements, and a paracommissural stitch was investigated for asymmetric PM displacements. Left ventricular pressure and mitral flow rate were monitored, and regurgitation fraction was calculated from the mitral flow curve.

Results: Under symmetric PM displacement, the repair reduced MR by 5.1% at dilation level one and by 9.1% at dilation level two. The repair decreased MR by 10.9% (dilation level two) after asymmetric displacement of the anterior-lateral PM, and by 5.4% (dilation level one) and 7.9% (dilation level two) after asymmetric displacement of the posterior-medial PM. The edge-to-edge repair reduced (p < 0.05) MR owing to annular dilation; however, it was unable to completely eliminate the MR. The repair did not significantly reduce MR caused by PM displacement, regardless of the displacement geometry. Stitch location did not affect repair efficacy.

Conclusions: The edge-to-edge repair is not an effective procedure in correcting MR associated with PM displacement, although it is able to partially reduce MR caused by annular dilation.


   Introduction
Top
 Abstract
 Introduction
Material and Methods
 Results
 Comment
 Acknowledgments
 References
 
Ischemic heart disease and dilated cardiomyopathy cause a series of events in which ventricular remodeling or dilation leads to mitral valve (MV) malfunction and subsequent mitral regurgitation (MR). Common alterations to MV geometry can include annular dilation and flattening as well as papillary muscle (PM) repositioning or contractile malfunction [1–7]. Annular dilation expands the mitral orifice and decreases coaptation length of the leaflets, and thus causes malcoaptation and regurgitation [7]. Papillary muscle displacement increases tension on the chordae tendineae, which restricts motion of the leaflets, resulting in regurgitation [1, 8, 9]. Mitral insufficiency associated with topologic alterations of the left ventricle presents a complex condition for which there is still no established standard repair procedure.

Recent clinical studies have shown advantages to performing MV repair to correct MR, as opposed to MV replacement [10]. One such repair technique is the edge-to-edge repair, also known as the Alfieri stitch, in which a few stitches join the tips of the anterior and posterior leaflets to force proper coaptation [11, 12]. The Alfieri stitch is most commonly performed on the center of the main scallop of both leaflets. This placement is the simplest approach and can be performed percutaneously as the main scallop is easily accessible [13, 14]. In cases of lateral regurgitant jets caused by asymmetric PM displacement, surgeons often perform a paracommissural stitch, joining the commissural leaflets on the side of the valve where the center of the orifice is present [15, 16]. As there is a dense distribution of chordae tendineae near the commissures of the MV, this stitch is only possible through an atriotomy. Generally the Alfieri stitch is performed as a secondary procedure to ring annuloplasty. Although some groups have performed edge-to-edge repairs without the annuloplasty, recent studies have shown that the Alfieri stitch acting alone leads to substandard results [16, 17].

The edge-to-edge repair has shown suboptimal results in cases involving ventricular remodeling [16–18]. Therefore, the effectiveness of this repair under these pathologic entities warrants further investigation. Extensive infarctions or cardiomyopathy leads to symmetric PM displacements in which both PMs move away from the annulus and away from the center of the ventricle, whereas more localized infarctions cause asymmetric PM displacements, in which one muscle remains in the native position while the other migrates [1, 2, 7].

The objective of this study is to investigate the efficacy of the edge-to-edge repair in the setting of annular dilation and symmetric or asymmetric PM displacement. The results from this study should provide insight into which ventricular alterations are the main determinants of Alfieri stitch repair failure in patients with enlarged hearts. Additionally, these results may provide understanding of whether concomitant annuloplasty is required in all edge-to-edge repair procedures.


   Material and Methods
Top
 Abstract
 Introduction
 Material and Methods
Results
 Comment
 Acknowledgments
 References
 
Valve Preparation
Ten fresh porcine MVs with normal features and similar orifice areas (5.3 ± 0.3 cm2) were obtained from a local abattoir. Valves were excised as to preserve all chordae tendineae and the entire mitral apparatus and were maintained in a 0.9% saline solution at 13°C. Experiments were completed within 72 hours of the animal’s expiration.

Annular Model
Valves were tested at normal annular size, dilation level one, and dilation level two using an annular model capable of controlling annular size by means of a drawstring mechanism. The annular model was attached to the atrial chamber of the heart simulator. The anatomic D-shape of the valve was maintained in all annular sizes. Mitral annular area (MAA) was calculated from the septal-lateral and commissural diameters of the annulus. Normal annular size had an MAA of 5.3 cm2. Dilation level one had an MAA of 8.29 cm2, which was a 56% increase from the normal MAA. Dilation level two had an MAA of 11.68 cm2, which was an increase of 120% from the normal MAA. A similar annular model has been described in previous publications [7, 19].

Left Heart Simulator
The in vitro experiments were carried out in the modified Georgia Tech left heart simulator (Fig 1), which includes an atrial chamber, ventricular chamber, and systemic circulation. The simulator is composed of a pressure-driven compressible bladder-type pump, which is controlled and synchronized by a pulse-generating computer system. This system is capable of physiologic and pathophysiologic flow and pressure waveforms. In the ventricular chamber of the simulator, PM rods suspend the PMs and chordae in a physiologic position and allow for control of three-dimensional positioning of the PMs. Left ventricular pressure was monitored using a pressure transducer, and mitral flow rate was acquired using an electromagnetic flow transducer. The Georgia Tech left heart simulator and data acquisition hardware and software have been described in previous articles [19, 20].


Figure 1
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  		Fig 1. Schematic of the Georgia Tech left heart simulator and its various components.

 
Experimental Protocol
Valves were sutured to the annular model and placed in the simulator between the atrial and ventricular chambers. Papillary muscle holding disks attached the PMs to PM rods that suspended the chordae tendineae and PMs in a physiologic position within the ventricular chamber. The normal PM position [7] was observed to have proper coaptation and no observed regurgitation. Data were acquired at physiologic conditions: 120 mm Hg, 5 L/min, 70 bpm, and systolic duration of 300 ms. Left ventricular pressure and mitral flow rate were monitored for 10 cardiac cycles and averaged off-line. The experiment was conducted at all three annular sizes. For each annular size, experiments were conducted for four PM displacement positions: normal, symmetric displacement, and two asymmetric displacements. Each PM displacement was achieved through a combined displacement of the muscle 10 mm in the apical direction, 10 mm in the lateral direction, and 10 mm in the posterior direction. The symmetric PM displacement position was simulated by displacing both PMs as seen in Figure 2. The asymmetric anterior-lateral PM displacement was simulated by displacing the anterior-lateral PM from the defined normal position, while the posterior-medial PM stayed in the defined normal position. The asymmetric posterior-medial PM displacement position involved displacement of the posterior-medial PM from the defined normal position, while the anterior-lateral PM stayed in the defined normal position. Symmetric PM displacement positions were performed without a stitch and with a central stitch present. Asymmetric PM displacement positions were performed without a stitch, with a central stitch, and with a paracommissural stitch (Fig 3). Paracommissural stitches were placed in the center of the observed regurgitation orifice. All experimental conditions are summarized in Table 1.


Figure 2
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  		Fig 2. Schematic of normal papillary muscle position and papillary muscles displaced 10 mm in the posterior, lateral, and apical directions.

 

Figure 3
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  		Fig 3. Schematic of the atrial view of the valve showing stitch location and annular dilations.

 

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  		Table 1 Repairs Performed Under All Pathologic Conditions
 
Data Analysis
Regurgitation volumes were calculated by integrating the negative volume from the average mitral flow curve. Stroke volume was obtained by integrating one complete cardiac cycle from the average mitral flow curve. Regurgitation fraction was calculated by dividing the regurgitation volume by the stroke volume.

All data are presented as mean ± standard deviation unless otherwise stated. An Anderson-Darling test showed that the regurgitation data was not normally distributed; therefore a Box-Cox transformation was applied to normalize the data. Regurgitation volumes from the transformed data were compared using paired Student’s t tests with a confidence interval of 95%.


   Results
Top
 Abstract
 Introduction
 Material and Methods
 Results
Comment
 Acknowledgments
 References
 
Baseline Position
The valve in the baseline position was defined as having normal annular size and normal PM position. In this position the valve was observed to have normal leaflet coaptation geometry. A systemic closing volume was present; this value was considered the baseline value as there were no visible regurgitation orifices or jets observed through the atrial chamber.

Pathologic Conditions
The regurgitation of the valve increased as annular dilation increased. As compared with the baseline value, regurgitation volume had a 17.9% increase when the valve was dilated to dilation level one, and had a 59.2% increase when the valve was dilated to dilation level two, which brought the regurgitation to 41.46 ± 4.013 mL corresponding to a regurgitation fraction of 0.575 ± 0.065. Both increases in regurgitation volume were statistically significant (p < 0.05).

Next, PM displacements were applied to the valve under normal annular dilation. The asymmetric displacement of the anterior-lateral PM caused a significant (p < 0.05) increase in regurgitation volume of 25.2%, the asymmetric displacement of the posterior-medial PM caused a significant (p < 0.05) increase of 19.4%, and the symmetric displacement of both PMs caused a significant (p < 0.05) increase of 30.3% (with respect to the baseline). The symmetric PM displacement produced a regurgitation of 33.96 ± 3.999 mL with a corresponding regurgitation fraction of 0.464 ± 0.050.

Annular dilation and PM displacements were then combined, and increases in regurgitation volume were observed. When the valve was dilated to dilation level one and the anterior-lateral PM was displaced, the regurgitation volume increased 51.4% as compared with baseline. When only the posterior-medial PM was displaced at dilation level one, the regurgitation volume increased 42.6%. Symmetric displacement of both PMs under dilation level one increased the regurgitation volume 53.7%. All three PM displacements at dilation level one showed statistically significant increases in regurgitation volume (p < 0.05) with respect to baseline.

The PM displacements were next combined with annular dilation level two. Anterior-lateral PM displacement at this dilation level showed a significant (p < 0.05) increase in regurgitation volume of 100.9% (regurgitation, 52.34 ± 6.882 mL; regurgitation fraction, 0.721 ± 0.101) as compared with the baseline. Posterior-medial PM displacement at dilation level two significantly (p < 0.05) increased regurgitation volume by 82.9% (regurgitation, 47.64 ± 5.694 mL; regurgitation fraction, 0.652 ± 0.087) with respect to the baseline. When both PM muscles were displaced at dilation level two, regurgitation volume increased significantly (p < 0.05) by 99.6% (regurgitation, 52.00 ± 6.814 mL; regurgitation fraction, 0.710 ± 0.101) compared with that of baseline.

Increases in regurgitation volume caused by dilation and PM displacement are depicted in Figures 4 through 6. Go Go


Figure 4
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  		Fig 4. Mitral regurgitation reduction of Alfieri stitch with both papillary muscles displaced (n = 10). Plot of regurgitation volumes before (black bars) and after (gray bars) the Alfieri repair for symmetric papillary muscle displacement of both muscles, shown for all three annular dilation sizes. The Alfieri repair shown was performed using a central stitch. *p < 0.05.

 

Figure 5
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  		Fig 5. Mitral regurgitation reduction of Alfieri stitch with the anterior-lateral papillary muscle displaced (n = 10). Plot of regurgitation volumes before (black bars) and after (gray bars) the Alfieri repair for asymmetric papillary muscle displacement of the anterior-lateral papillary muscle, shown for all three annular dilation sizes. The Alfieri repair shown was performed using a central stitch. *p < 0.05.

 

Figure 6
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  		Fig 6. Mitral regurgitation reduction of Alfieri stitch with the posterior-medial papillary muscle displaced (n = 10). Plot of regurgitation volumes before (black bars) and after (gray bars) the Alfieri repair for asymmetric papillary muscle displacement of the posterior-medial papillary muscle, shown for all three annular dilation sizes. The Alfieri repair shown was performed using a central stitch. *p < 0.05.

 
Alfieri Stitch Repair
For symmetric PM positions, a central Alfieri stitch was used as the edge-to-edge repair. This repair reduced regurgitation volume by 5.1% and 9.1% for dilation levels one and two, respectively (Fig 4). The repair corrected a higher percentage of regurgitation at higher levels of annular dilation. Regurgitation at normal annular size was not significantly corrected, whereas the decreases in regurgitation for dilation levels one and two were significant. After the stitch was performed, regurgitation volumes at annular dilation levels one and two were 37.98 ± 4.341 mL and 47.28 ± 4.426 mL, respectively, with corresponding regurgitation fractions 0.523 ± 0.066 and 0.652 ± 0.073.

For asymmetric PM positions in which only one PM was displaced, two Alfieri stitch locations were tested individually, a central stitch and a paracommissural stitch. For displacement of the anterior-lateral PM after the central stitch was performed, regurgitation volume decreased 10.9% for dilation level two (Fig 5). Once again the repair corrected more regurgitation at increased levels of annular dilation. No significant reduction in regurgitation was seen after the repair was performed at normal annular size or dilation level one. Only the regurgitation reduction at dilation level two was significant; however, a regurgitation volume of 46.62 ± 4.258 mL, which corresponded to a regurgitation fraction of 0.642 ± 0.062, was still present after the repair.

For displacement of the posterior-medial PM, the central stitch induced a decrease in regurgitation volume of 5.4% and 7.9% for dilations levels one and two, respectively (Fig 6). The central stitch corrected a higher percentage of regurgitation as annular dilation levels increased. The decrease in regurgitation associated with normal annular size was not statistically significant, whereas those at dilation levels one and two were significant (p < 0.05). The regurgitation present after repair under the conditions for dilation levels one and two were 35.14 ± 3.515 mL and 43.86 ± 3.287 mL, respectively, with corresponding regurgitation fractions of 0.489 ± 0.047 and 0.599 ± 0.049.

For asymmetric PM displacements, a paracommissural stitch was also performed. This condition was performed last in each experiment and was not completed for 2 of the 10 valves used in this study because of failures in experimental setup. For the displacement of the anterior-lateral PM, this stitch caused a decrease in regurgitation volume of 11.6% for annular dilation level two. Significant correction of regurgitation was not seen after the repair at normal annular size or at annular dilation level one. The decrease in regurgitation for the highest level of annular dilation, level two, was the only statistically significant reduction (p < 0.05).

The paracommissural stitch performed after posterior-medial PM displacement decreased regurgitation volume by 6.5% and 8.7%, respectively, for annular dilation levels one and two. Reduction in regurgitation after the repair was not statistically significant at normal annular size, but was significant for annular dilation levels one and two (p < 0.05).

The corrections of regurgitation for the repairs using the paracommissural stitch were similar to those using the central stitch, as shown in Figure 7 for posterior-medial PM displacement. Each condition that showed statistically significant reduction in regurgitation after the central stitch also showed significant reduction in regurgitation after the paracommissural repair. For all pathologic and repair conditions, the regurgitation volumes of the two stitch locations were not significantly different.


Figure 7
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  		Fig 7. Mitral regurgitation correction comparison for different stitch locations with the posterior-medial papillary muscle displaced (n = 8). Plot of regurgitation volumes after the Alfieri repair for both the central stitch (black bars) and the paracommissural stitch (gray bars), under the condition of asymmetric papillary muscle displacement of the posterior-medial papillary muscle, shown for all three annular sizes.

 

   Comment
Top
 Abstract
 Introduction
 Material and Methods
 Results
 Comment
Acknowledgments
 References
 
The edge-to-edge repair performed alone showed suboptimal results after annular dilation and ventricular enlargement. The repair significantly reduced regurgitation at higher levels of annular dilation; however, regurgitation owing to PM displacement was not corrected by the edge-to-edge repair. For regurgitation caused by asymmetric PM displacement, stitch location did not affect repair efficacy.

The in vitro system used in the study was capable of producing physiologic flow and pressure waveforms and simulating pathologic conditions of annular dilation and PM displacement. The use of 10 mm for the magnitude of PM displacement associated with ventricular enlargement is comparable to magnitudes of displacement found in in vivo studies of chronic ischemic MR [21].

The simulation of pathologic conditions created regurgitation as expected [7]. Mitral regurgitation increased with increased annular dilation, the three geometries of PM displacement, and the combinations of dilation and PM displacement. For normal annular size the edge-to-edge repair did not significantly reduce regurgitation for any of the PM displacement geometries. When comparing the results at the three different PM displacement positions, there was no significant difference in the percentage of regurgitation corrected by the repair at an associated annular size. For asymmetric PM displacements at all annular sizes, performing the paracommissural stitch instead of the center stitch did not significantly decrease regurgitation as compared with the regurgitation present after the center stitch; therefore, stitch placement did not affect repair efficacy. Thus, the edge-to-edge repair does not correct MR associated with PM displacement, independent of the subvalvular geometry.

The edge-to-edge repair significantly reduced MR associated with annular dilation. The repair demonstrated significant reduction at dilation level one for two of the three PM geometries (5.1% and 5.4% for symmetric PM displacement and asymmetric displacement of the posterior-medial PM). The repair significantly reduced MR at dilation level two for all PM conditions (9.1%, 10.9%, and 7.9% for symmetric PM displacement and asymmetric displacements of the anterior-lateral PM and posterior-medial PM, respectively). Therefore, for all PM geometries, as annular dilation increased, an increased percentage of regurgitation was corrected. Although the efficacy of the repair improved with increased annular dilation, sizable regurgitation fractions were still present after most of the repairs. The substantial MR still present after repair in cases of dilation and PM displacement is most likely associated with PM displacement, which as stated is not addressed by this repair.

As the results in this study show, the edge-to-edge repair performed alone shows substandard results in correcting MR after ventricular remodeling as seen in pathologic entities such as ischemic MR and dilated cardiomyopathy. Mitral regurgitation associated with these diseases is caused by two main factors: annular dilation and PM displacement. Annular dilation causes MR by increasing orifice area and decreasing coaptation length, whereas PM displacement tethers the leaflets into the ventricle, restricting proper coaptation of the valve. The edge-to-edge repair addresses the mechanism by which annular dilation contributes to MR by bringing the leaflets together and forcing coaptation on a segment of the leaflets. However, this repair is not sufficient to reduce MR caused by PM displacement. A stitch placed at one point along the coaptation line would not correct tenting along the entire length of the leaflets. Leaflet tethering would still persist along the remainder of the valve, especially among the commissures. As the ventricle continues to expand, the MR remaining as a result of PM displacement will probably worsen and return to its initial levels. The results are consistent with those of in vivo animal studies, which showed that when performed alone the edge-to-edge repair is ineffective against acute ischemic MR [17]. This phenomenon is also supported by clinical results in which the edge-to-edge repair was unable to fully correct MR in patients with enlarged hearts [16].

Results on the efficacy of the edge-to-edge repair performed with concomitant ring annuloplasty remain conflicting. Clinical studies of dilated cardiomyopathy support the use of ring annuloplasty along with the edge-to-edge repair [22], whereas other clinical studies suggest that the edge-to-edge repair may be ineffective even when performed in conjunction with ring annuloplasty for ischemic MR conditions [18]. Repairing such conditions with concomitant annuloplasty reduces the annular area and decreases the septal-lateral axis, bringing the leaflets closer together. Although the annulus after annuloplasty is now fixed, the ventricle will continue to deform and expand, exacerbating PM displacement. In these cases the edge-to-edge repair with concomitant annuloplasty is probably a temporary solution, as MR associated with further PM displacement will increase with time as neither annuloplasty nor the Alfieri stitch address PM displacement. Alternative surgical techniques that aim to directly correct subvalvular remodeling would be more effective methods to reduce MR caused by PM displacement [23].

Other clinical trials have presented procedures for percutaneous MV repair, an attractive option for patients [24]. In these procedures the edge-to-edge repair is performed without ring annuloplasty. The current study has demonstrated that in cases of ventricular remodeling, this percutaneous option will most likely be ineffective because it does not address PM displacement. Therefore, percutaneous edge-to-edge repairs may initially reduce regurgitation by bringing the leaflets together, but levels of MR may recur with continuous ventricular expansion.

Limitations
Although the simulator has been used in several pioneering studies [19, 20], this in vitro system does not fully characterize aspects of the heart such as ventricular wall motion, PM contraction, or the dynamic state of the annulus. Leaflet and chordae tendineae remodeling that occur as a function of time with ventricular remodeling were not simulated; however, limited elongation of the viscoelastic chordae was observed as creep did occur after PM displacement. The current study is a comparative one with the aim of isolating variables; therefore, the limitations of the left heart simulator should not affect the conclusions of this study.

Conclusion
The results of this study demonstrate that the edge-to-edge repair is able to reduce MR caused by annular dilation, but does not reduce regurgitation caused by the displacement of the PMs. For cases of asymmetric regurgitation orifices, repair efficacy was independent of stitch location.


   Acknowledgments
Top
 Abstract
 Introduction
 Material and Methods
 Results
 Comment
 Acknowledgments
References
 
This work was supported by a grant from the National Heart, Lung, and Blood Institute (HL52009).


   References
Top
 Abstract
 Introduction
 Material and Methods
 Results
 Comment
 Acknowledgments
 References
 

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