- Email: [email protected]
Annulus tension of the prolapsed mitral valve corrected by edge-to-edge repair
Journal of Biomechanics 45 (2012) 562–568
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Annulus tension of the prolapsed mitral valve corrected by edge-to-edge repair Shamik Bhattacharya, Zhaoming He n Department of Mechanical Engineering, Texas Tech University, Lubbock, TX 79409, 7th and Boston, PO Box 41021, Lubbock, TX 79409-1021
a r t i c l e i n f o
a b s t r a c t
Article history: Accepted 9 November 2011
Background: Mitral valve (MV) performance after edge-to-edge repair (ETER) without ring annuloplasty is suboptimal. ETER efficacy needs to be evaluated from annulus tension (AT) of a prolapsed MV corrected by ETER to understand annular dilatation. Methods: Ten porcine MVs were harvested and mounted on a MV closure test rig. The MV annulus tissue rested on top of a saddle-shaped plastic ring on which the annulus could slide freely. The annulus was held by strings in the periphery during MV closure under a hydrostatic trans-mitral pressure. String tensions were measured and further divided by string spacing to obtain AT. The MVs were then prolapsed by shifting split papillary muscles to simulate mono-leaflet prolapse due to elongation of chords, which insert into a single leaflet. Last, MV prolapse was corrected by ETER applied in the central leaflet region and AT was measured. Results: AT in both anterior and posterior leaflet prolapse corrected by ETER was less than that of normal MVs. AT in the anterior leaflet prolapse corrected by ETER was less than that in the posterior leaflet prolapse corrected by ETER. Conclusion: ETER does not restore the normal AT and therefore leads potential of annular dilatation. The anterior leaflet prolapse has a greater potential of annular dilatation than the posterior leaflet prolapse after ETER. Annuloplasty is recommended to maintain long-term ETER efficacy. & 2011 Elsevier Ltd. All rights reserved.
Keywords: Mitral valve In vitro study Valve repair Surgical instruments
1. Introduction Mitral valve (MV) prolapse is a typical disease of the MV caused by papillary muscle elongation, chordal elongation or rupture, or enlarged leaflets, and is responsible for mitral regurgitation. A repair technique known as edge-to-edge repair (ETER) has been used extensively to correct MV prolapse (Alfieri et al., 2001; Fucci et al., 1995). ETER is most commonly performed on the center of the main scallop of leaflets with ring annuloplasty, which is required to reshape the annulus and reduce the annular orifice (Alfieri et al., 2001). ETER performed without ring annuloplasty yields suboptimal midterm results when compared to ETER, performed with annuloplasty (Maisano et al., 2003; Timek et al., 2003). Annular dilatation may persist after ETER without annuloplasty. Therefore, the success of ETER largely depends on the use of ring annuloplasty and ETER is thus considered as a secondary procedure. It elicits a question: why does ETER not prevent the MV from annular dilatation in the long run? Therefore we investigated annulus tension (AT) in ETER using a novel system that is able to reveal the mechanism of annular dilatation
n
Corresponding author. Tel.: þ806 742 3563x225; fax: þ 806 742 3540. E-mail address: [email protected] (Z. He).
0021-9290/$ - see front matter & 2011 Elsevier Ltd. All rights reserved. doi:10.1016/j.jbiomech.2011.11.005
(Bhattacharya and He, 2009; He and Bhattacharya, 2008; He and Bhattacharya, 2010). We proposed a mechanism of annulus dilatation that mitral annulus dilatation is a consequence of imbalanced annulus mechanics between the centripetal mitral leaflet tension and centrifugal left ventricle myocardial force at annulus in systole. AT is defined as a leaflet tension force at the annulus per unit length of the annulus perimeter. The MV leaflets and left ventricular myocardium are in force equilibrium at the annulus during MV closure in the normal heart without initiation of annulus dilatation. This equilibrium implies that AT is equal to and thus interpreted as myocardial force in the normal MV-left ventricle system. Alteration in either one due to pathologies will break the equilibrium, which ultimately results in annulus geometry changes such as annulus dilatation. We found that AT decreases in MV bileaflet prolapse due to papillary muscle elongation and is thus lower than the normal left ventricular myocardial force (He and Bhattacharya, 2008). This imbalanced annular mechanics due to MV bi-leaflet prolapse causes annular dilatation even in the normal left ventricle according to the mechanism of annular dilatation. This mechanism has successfully explained some MV physiologies and pathologies on the MV annulus, especially in the normal left ventricle size (Bhattacharya and He, 2009; He and Bhattacharya, 2008; He and Bhattacharya,
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2010). In addition, clinical study reports annular dilatation without any pathology in a normal left ventricle, also called as ‘‘pure annular dilatation’’ (Glower et al., 2009). This pure annular dilatation could also be caused by imbalanced annular mechanics. Now we have a question about MV prolapse: can it be corrected by ETER without further annulus dilatation? Therefore, the objective of this research was to understand AT of a prolapsed MV corrected by ETER.
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cylinder through a PVC hose in the downstream of the MV. When the MV closed under a trans-mitral pressure, the MV annulus tended to shrink towards the center of the MV orifice. Strings connected to MV annulus, prevented the MV
Left ventricle side
Commissure Posterior
Anterior 2. Methods
5 mm
2.1. MV closure test rig and annulus tension measurement We followed the same method for AT measurement as described in our earlier papers (Bhattacharya and He, 2009; He and Bhattacharya, 2010). A total of ten fresh porcine hearts were obtained from a local slaughterhouse and transported to the lab. The MVs of annulus size M36 measured in an Edwards ring sizer (Edwards LifeSciences LLC, Irvine, CA) were selected and dissected from porcine hearts. Each MV was mounted in a MV closure test rig, which was designed to measure the AT at a static trans-mitral pressure shown in Fig. 1. Each MV was mounted on the plastic ring glued on the annulus mounting board, with the MV annulus coinciding with the plastic ring. The ring had a saddle shape and a 5 mm saddle height as shown in Fig. 2, because the ratio of the saddle height to intercommissural diameter is usually 15% in a prolapsed MV (Grewal et al., 2010). The annulus ring was made according to M36 on an Edwards ring sizer, and the ring area and perimeter were 7.63 cm2 and 122 mm, respectively. The commissural axis length was 35 mm, and the septal-lateral axis length was 30 mm. The annulus mounting board separated the atrium in the bottom chamber and left ventricle in the top chamber. The atrial chamber had an opening below the MV, which was connected through a plastic pipe to a lower reservoir. The left ventricle chamber was open to the air and contained saline in which the MV was immersed. The papillary muscles were sutured to two papillary muscle holders made of steel rods, the positions of which could be adjusted three-dimensionally. A static trans-mitral pressure was built up by the difference in the saline levels of the two reservoirs when the MV closed. Any leakage across the MV was measured in a measuring
L5
L6 L77 L8 L9
Anterior
35 mm Ciommissure
30 mm Posterior
Fig. 2. A picture of normal annulus support ring with 5 mm saddle height made according to the M36 Edwards ring sizer.
Edge-to-edge repair L10
L4
L11 L12 L13
L3 L2 L1 Anterior leaflet
Annulus plane
#
#
#
L14 Posterior leaflet
#
# #
#
#
#
#
String Papillary muscle holder
Fourteen force transducers are labeled as L1-L14. Others are posts without force transducers labeled as # “#” Saline level
Papillary muscle Chordae
String force transducer
H
Annulus mounting board Atrium reservoir
Saline
Left ventricle reservoir
Drain Plastic ring PVC Hose Adjustable Shut-off support valve l
Measuring cyylinder Fig. 1. (a) Schematic of the MV closure test rig for AT measurement system, (b) and (c) Photograph of the actual test rig for AT measurement system.
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annulus from shrinking towards the MV orifice center. Fourteen strings were connected to the anterolateral section of the annulus, as shown in Fig. 1. Each of them was attached to a force transducer (Load Cell Central, Monroeton, PA) installed in each post. String tension was measured and divided by the distance between stitches in the annulus to obtain AT in units of N/m.
2.2. Normal and prolapsed MV The normal papillary muscle position was set up in the normal state controlled by papillary muscle holders as used in previous studies (He and Bhattacharya,
2008; He et al., 2003; Krishnamurthy et al., 2009; He et al., 2003). In order to simulate leaflet prolapse, the papillary muscles were dissected apically and split into anterior and posterior parts to separate chords that insert into the anterior and posterior leaflets, as shown in Fig. 3. The posterior leaflet prolapse was simulated by moving both the posterior papillary muscle parts from two papillary muscles 5 mm towards the annulus with respect to the normal anterior papillary muscle parts. The average static leakage under trans-mitral pressure 16.0 kPa (120 mmHg) in the posterior leaflet prolapse was 1.089 L/min. Then, the posterior leaflet prolapse was followed by the anterior leaflet prolapse, which was simulated by moving both the anterior papillary muscle parts from two papillary muscles 5 mm towards the annulus with respect to the normal posterior papillary
Papillary muscle shifting Papillary muscle
5 mm Leaflet prolapse
String tension
String tension
Annulus ring
Leakage
Prolapsed anterior Leaflet
Posterior leaflet
Fig. 3. (a) Papillary muscles were dissected apically and split into anterior and posterior parts to separate chords that insert into the anterior and posterior leaflets. The posterior leaflet prolapse was simulated by moving both the posterior papillary muscle parts from two papillary muscles 5 mm towards the annulus with respect to the normal anterior papillary muscle parts, (b) a schematic of shifting split papillary muscles towards the annulus plane to simulate mono-leaflet prolapse due to chordal elongation, (c) a atrial view of the anterior leaflet prolapse by the papillary muscle shifting method.
Anterior leaflet
Posterior leaflet
Suture
Chord
Papillary muscle Fig. 4. (a) A apical view of a porcine mitral valve corrected by edge-to-edge-repair technique with suture length 20 mm, (b) a schematic of the central suture in edge-toedge repair with 5 mm deep bites placed through the rough zone of the leaflets to prevent tearing of the leaflets.
S. Bhattacharya, Z. He / Journal of Biomechanics 45 (2012) 562–568 muscle parts. The average static leakage under 16.0 kPa in the anterior leaflet prolapse was 1.527 L/min. It is estimated to be mild to moderate mitral regurgitation based on the regurgitant volume (Verma and Mesana, 2009; He et al., 1997). 2.3. Edge-to-edge repair
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ETER was applied to repair the posterior leaflet prolapse. Then, the anterior leaflet prolapse was simulated on the same MV, and leakage was measured after removal of the suture. Last, the AT and leakage were measured for anterior leaflet prolapse after ETER was applied again. A total of 10 MVs were tested.
2.5. Data analysis
The MV prolapse was corrected by suturing two leaflets together using the ETER technique. The details of the suture were shown in Fig. 4. The suture was started from the middle position of both leaflets from the atrial side. The suture had a depth of 5 mm distributed symmetrically over both leaflets and a length of 20 mm along the free edge. All ten MVs exhibited reduced static leakage under trans-mitral pressure 16.0 kPa after ETER.
Statistical analysis was based on the assumption that the observations of the ATs were normally distributed. For the comparison between control and other conditions, a paired t-test for means was used. The p-value was based on two-tail distribution, with p o 0.05 used as the accepted value for significance. The control was the same MVs with the normal valve configuration. In order to assess the functional model of the prolapsed MV and ETER, the leakage of the prolapsed MV was compared with the leakage after ETER was applied on the same MV.
2.4. Experiment conditions The AT was measured in the trans-mitral pressure of 16.0 KPa (120 mmHg) at the anterolateral segment of the annulus. All the experiments were carried out at room temperature and data were collected within a 2 h period. All the MVs coapated normally in the normal MV. The string position in the annulus was represented by a length of the annulus from mid-anterior position, and normalized by a total length of the semi-annulus perimeter. The anterior and the posterior centers of the annulus were 0% and 100% positions, respectively. First, the AT was measured for the normal MVs. Then posterior leaflet prolapse was simulated and leakage was measured. AT and leakage were recorded again after
Leakage of Mono-leaflet Prolapse 2.5 2 1.5 1 0.5 0 Posterior leaflet prolapse
Anterior leaflet prolapse
Before ETER
After ETER
Fig. 5. Leakages before and after ETER was applied to the anterior and posterior leaflet prolapse. The error bars are in the format of 7 1 standard deviation.
3. Results All the normal MVs coaptated well without leakage, but failed to coaptate when MV prolapse was simulated. Leakage of the prolapsed MVs was significantly reduced (p-valueso0.01) after ETER was used to correct the prolapsed MVs. Fig. 5 shows leakage of the prolapsed MVs before and after ETER. Average ATs at 14 string positions along the normalized perimeter of the anterolateral segment of the annulus are shown in Fig. 6 with error bars of 7standard deviation centered on the average values. Three curves in the figure represent AT of the normal MVs, MVs with the anterior and posterior leaflet prolapse corrected by ETER. AT distribution along the annulus exhibited a concave curve for both the normal and repaired MVs, with the lowest AT in the commissural segment of the annulus. Fig. 7 shows AT superimposed on the MV annulus. For the posterior leaflet prolapse corrected by ETER, ATs did not change much in the posterior segment of the annulus from the L8 to L14 positions. There was no significant difference in AT between the normal and repaired MVs (all p-values40.24) except L13 position (p-valueo0.002). In the anterior segment from L1 to L7 positions, the AT was significantly lower in the repaired MVs (all p-valueso0.03) than that in the normal MVs. AT in the anterior leaflet prolapse corrected by ETER was significantly less (all p-valueso0.01) than that of the normal MVs in the whole annulus. The AT in the anterior leaflet prolapse
AT of the normal MV, posterior and anterior leaflet prolapse corrected by ETER Normal MV Posterior leaflet prolapse correcetd by ETER Anterior leaflet prolapse correcetd by ETER 45 L2 40 L4 L14
AT (N/m)
35 L6
30 25
L12 L10
L8
20 15 10 0 Anterior annulus center
20
40
60
80
100 Posterior annulus center
Normalized perimeter (%) Fig. 6. AT distribution in the annulus of normal MV, anterior and posterior leaflet prolapse corrected by ETER. The error bars are in the format of 71 standard deviation centered on the averaged values.
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AT distribution superimposed on the normal MV annulus L1
L2
L3 L4
AT in the normal MV AT in posterior leaflet prolapse corrected by ETER
Averaged AT (N/m) overlapping on the annulus
L5 0% L6 6
Anterior annulus 61 mm
AT in anterior leaflet prolapse corrected by ETER
L7
Anterolateral annulus Posterior annulus
L8 L9 L10
100%
L11 L12 L13 L14 Fig. 7. AT superimposed on the annulus in the normal MV, anterior and posterior leaflet prolapse corrected by ETER.
corrected by ETER is significantly less than that in the posterior leaflet prolapse corrected by ETER (all p-valueso0.02).
4. Discussion We propose a novel mechanism of annular dilatation as a consequence of imbalanced annulus mechanics between centripetal AT and centrifugal myocardial force at annulus during systole. This implies that AT is balanced with the myocardial force due to absent initiation of annular dilatation in the normal MV-left ventricle system and thus can be interpreted as the normal myocardial force, which is not measurable. AT and myocardial forces are normally in the annulus plane and determine annulus size, while forces acting on the annulus and perpendicular to the annulus plane (in apical direction) determine annulus shape. These apical forces are usually generated from basal chords that directly insert into commissural and posterior annulus segments, and from AT component in the apical direction, in MV prolapse or dilative left ventricle diseases. The new mechanism of annulus dilatation can be used to explain two cases of annulus dilatation from dilative left ventricle diseases with left ventricle remodeling, and from MV prolapse without left ventricle remodeling (He and Bhattacharya, 2010). Hence this mechanism unifies annulus dilatation due to etiologies of left ventricle remodeling and non-left ventricle remodeling, and is more general in application. It is noted that difference or imbalance between AT and myocardial force is a driving force for MV annulus to dilatate in order to regain a new balanced annulus mechanics usually in the well-developed pathologies. Therefore, this mechanism leads to a theory to predict annulus size: annulus
is dilatated to compensate AT in order to rebalance myocardial force until a new balanced annulus mechanics in pathologies is reached or approached. MV prolapse lowers leaflet coaptation (contact) height from the annulus plane and causes the lower AT component in the annulus plane than the AT, or, myocardial force in the normal MV (He and Bhattacharya, 2008). This imbalanced annulus mechanics initiates annular dilatation, which requires leaflet stretching (decrease in curvature) and covering the dilatated annulus. This coaptation adaptation to the dilatated annulus usually increases the coaptation height, and thus AT component in the annulus plane until the AT is balanced with the normal myocardial force, which remains unchanged during the MV adaptation process. Therefore, annular dilatation is MV compensation for AT to regain balanced annular mechanics. However, this MV adaptation mechanism fails in chord rupture, which has no MV coaptation, or leaflet enlargement, which causes MV coaptation position below annulus plane. The more the difference between AT and myocardial force is, the greater is the annulus dilatation. In the onset MV prolapse without left ventricle remodeling, we predict potential of annular dilatation by comparing two stable states in development of annulus dilatation from normal heart: (1) normal heart: normal MV AT¼normal myocardial force, (2) well-developed prolapsed MV: pathological MV AT¼myocardial force. We assume that the myocardial force in a prolapsed MV remains normal myocardial force because of no left ventricle remodeling. The difference in AT between two states is actually the driving force between pathological AT in the MV prolapse state and the myocardial force in the normal left ventricle right at onset of the MV prolapse. MV prolapse can be either acute (chord rupture) or progressive (chord elongation) case. Therefore, we compared the AT in pathologies with the AT in
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the normal MV-left ventricle system, which is interpreted as the normal myocardial force. The difference in AT is used to evaluate potential of annulus dilatation. We already found that actual AT in MV bileaflet prolapse is lower than normal myocardial force and has a potential of annular dilatation even without left ventricle remodeling (He and Bhattacharya, 2008). That is why the MV annulus is dilatated in MV prolapse while the left ventricle size remains normal and supported by the clinical study (Mihalatos et al., 2007; David et al., 2003). ETER reduced or eliminated leakage, but not annular dilatation as AT decreased more or less in mono-leaflet prolapse. ETER does not restore the MV AT to a normal MV AT to balance the normal myocardial force, which suggests ETER cannot potentially prevent annular dilatation in the MV mono-leaflet prolapse. The annular dilatation may ultimately compromise MV function in a long-term view. Suboptimal mid-term results of ETER without annuloplasty support our theory (Timek et al., 2003). Therefore, annuloplasty is recommended to maintain long-term ETER efficacy. Further, the potential of annular dilatation for the anterior and posterior leaflet prolapse differs. The greater drop in AT was observed in the anterior leaflet prolapse than in the posterior leaflet prolapse. As a driving force for the annulus to dilatate, difference between the actual AT and normal myocardial force may be compensated by greater annular dilatation in the anterior leaflet prolapse than the posterior leaflet prolapse. That may be why it is found that anterior leaflet or bileaflet prolapse is harder to repair than posterior leaflet prolapse (David et al., 2005). High rate of recurrent mitral regurgitation may be due to progressive annulus dilatation. As for the model of MV prolapse, no in-vitro or in-vivo model is generally available except chord rupture. We created an extensive (multi-segment) MV prolpase to simulate elongation of multiple chords that insert into either MV leaflet, or multiple chord rupture. Our prolapse model simulates a multi-segment MV prolapse and differs in prolapsed area from a model due to rupture or elongation of local chords or elongation of whole papillary muscles. Although the MV leaflets in our model were not enlarged and thickened, or slack like in fibroelastic deficiency or myxomatous diseases, leakage of the prolapsed MV was used as a measure and seemed reasonable to control MV prolapse. Lack of leaflet thickening makes our model close to MV prolapsed due to fibroelastic deficiency. However, the leaflet size and chord structure are two factors, which are hard to simulate in-vitro and in-vivo. It should be mentioned that large leaflets and concurrently large annulus in MV prolapse may not necessarily lead to mitral regurgitation, which depends on complicated MV coaptation. Large annulus may be good for MV function with large leaflets (Adams et al., 2006). Therefore, MV annular dilatation could occur regardless of MV regurgitation or left ventricle remodeling and is often asymptomatic (David et al., 2003). ETER alters MV geometry and thus AT according to suture pattern, which affects leaflet stress (Gao et al., 2009; He et al., 2009) and suture tension (He et al., 1997; Mihalatos et al., 2007; David et al., 2003). If the tension in the suture is high, it may pull the leaflets towards the center. This suture tension may transfer to the annulus during MV closure. This suture tension usually does not affect AT for enlarged and redundant leaflets in MV prolapse during MV closure. On the other hand, the way the suture is done (Maisano et al., 2000) affects the coaptation depth (contact part) as well as the leaflet profile and curvature, and thus an AT in the leaflets. AT is a vector and acts approximately along the annulus plane in a normal MV. MV prolapse deflects AT from annulus plane and reduces the AT force component in the annulus plane, which further facilitates annular dilatation. The AT direction should be characterized to enable quantification of AT component in the annulus plane in order to evaluate accurate AT effect on the annulus.
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Tension of basal chords that directly insert onto commissural and posterior segments of the annulus may have effect on annulus mechanics if these chords are tight in pathologies. These chords are basically perpendicular to annulus plane, and thus tension from these chords predominantly affect annulus shape, not the annular size. However, basal chord force component that is aligned in the annulus plane may be significant in effect on annulus size if the basal chords are too tight or not perpendicular to annulus plane. Chord shortening could correct regurgitation clinically and should restore AT to preclude annulus dilatation.
5. Study limitations The model of the MV prolapse was an extensive (multisegment) prolapse without enlarged leaflets and did not represent all the MV prolapse conditions, especially, local prolapse caused by rupture of an individual chord or prolapse due to enlarged leaflets. The results may have been different if human MV is used. The AT was obtained in a static configuration, which may differ in dynamic annulus and MV closure conditions. AT direction was not characterized for understanding delicate annulus mechanics. Difference between the ETER for the posterior prolapse and redone ETER for the anterior prolapse might affect AT. In clinical practice, difference in ETER surgical procedure might affect AT and thus surgical outcome.
6. Conclusions ETER alone does not restore the normal AT and thus leads to potential of annular dilatation. The anterior leaflet prolapse has a greater potential of annular dilatation than the posterior leaflet prolapse after ETER. Annuloplasty is recommended to maintain long-term ETER efficacy.
Conflict of interest statement None
Acknowledgments The pig hearts were donated by the Klemke Sausage Haus in Slaton, Texas, USA. References Alfieri, O., Maisano, F., De Bonis, M., Stefano, P.L., Torracca, L., Oppizzi, M., La Canna, G., 2001. The double-orifice technique in mitral valve repair—a simple solution for complex problems. Journal of Thoracic and Cardiovascular Surgery 122, 674–681. Adams, D.H., Anyanwu, A.C., Rahmanian, P.B., Abascal, V., Salzberg, S.P., Filsoufi, F., 2006. Large annuloplasty rings facilitate mitral valve repair in Barlow’s disease. The Annals of Thoracic Surgery 82, 2096–2100 discussion 2101. Bhattacharya, S., He, Z., 2009. Role of annulus tension in annular dilatation. Journal of Heart Valve Disease 18, 481–487. David, T.E., Ivanov, J., Armstrong, S., Rakowski, H., 2003. Late outcomes of mitral valve repair for floppy valves: Implications for asymptomatic patients. Journal of Thoracic Cardiovascular Surgery 125, 1143–1152. David, T.E., Ivanov, J., Armstrong, S., Christie, D., Rakowski, H., 2005. A comparison of outcomes of mitral valve repair for degenerative disease with posterior, anterior, and bileaflet prolapse. Journal of Thoracic Cardiovascular Surgery 130, 1242–1249. Fucci, C., Sandrelli, L., Pardini, A., Torracca, L., Ferrari, M., Alfieri, O., 1995. Improved results with mitral valve repair using new surgical techniques. European Journal of Cardiothoracic Surgery 9, 621–626 discuss 626–627. Glower, D.D., Bashore, T.M., Harrison, J.K., Wang, A., Gehrig, T., Rankin, J.S., 2009. Pure annular dilation as a cause of mitral regurgitation—a clinically distinct entity of female heart disease. Journal of Heart Valve Disease 18, 284–288.
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Grewal, J., Suri, R., Mankad, S., Tanaka, A., Mahoney, D.W., Schaff, H.V., Miller, F.A., Enriquez-Sarano, M., 2010. Mitral annular dynamics in myxomatous valve disease: new insights with real-time 3-dimensional echocardiography. Circulation 121, 1423–1431. Gao, B., Sun, W., Mathew, S., He, Z., 2009. Effects of papillary muscle position on anterior leaflet stretches under mitral valve edge-to-edge repair. Journal of Heart Valve Disease 18, 135–141. He, Z., Bhattacharya, S., 2008. Papillary muscle and annulus size effect on anterior and posterior annulus tension of the mitral valve: an insight into annulus dilatation. Journal of Biomechanics 41, 2524–2532. He, Z., Bhattacharya, S., 2010. Mitral valve annulus tension and the mechanism of annular dilation: an in-vitro study. Journal of Heart Valve Disease 19, 701–707. He, S., Jimenez, J., He, Z., Yoganathan, A.P., 2003. Mitral leaflet geometry perturbations with papillary muscle displacement and annular dilatation: an in-vitro study of ischemic mitral regurgitation. Journal of Heart Valve Disease 12, 300–307. He, Z., Sacks, M.S., Baijens, L., Wanant, S., Shah, P., Yoganathan, A.P., 2003. Effects of papillary muscle position on in-vitro dynamic strain on the porcine mitral valve. Journal of Heart Valve Disease 12, 488–494. He, S., Fontaine, A.A., Schwammenthal, E., Yoganathan, A.P., Levine, R.A., 1997. Integrated mechanism for functional mitral regurgitation—leaflet restriction versus coapting force: in vitro studies. Circulation 96, 1826–1834.
He, Z., Gao, B., Bhattacharya, S., Harrist, T., Mathew, S., Sun, W., 2009. In vitro stretches of the mitral valve anterior leaflet under edge-to-edge repair condition. Journal of Biomechanical Engineering 131, 111012. Krishnamurthy, G., Itoh, A., Swanson, J.C., Bothe, W., Karlsson, M., Kuhl, E., Craig Miller, D., Ingels Jr., N.B., 2009. Regional stiffening of the mitral valve anterior leaflet in the beating ovine heart. Journal of Biomechanics 42, 2697–2701. Maisano, F., Caldarola, A., Blasio, A., De Bonis, M., La Canna, G., Alfieri, O., 2003. Midterm results of edge-to-edge mitral valve repair without annuloplasty. Journal of Thoracic Cardiovascular Surgery 126, 1987–1997. Mihalatos, D.G., Joseph, S., Gopal, A., Bercow, N., Toole, R., Passick, M., Grimson, R., Norales, A., Reichek, N., 2007. Mitral annular remodeling with varying degrees and mechanisms of chronic mitral regurgitation. Journal of the American Society of Echocardiography 20, 397–404. Maisano, F., Schreuder, J.J., Oppizzi, M., Fiorani, B., Fino, C., Alfieri, O., 2000. The double-orifice technique as a standardized approach to treat mitral regurgitation due to severe myxomatous disease: surgical technique. European Journal of Cardio-Thoracic Surgery 17, 201–205. Timek, T.A., Nielsen, S.L., Lai, D.T., Tibayan, F.A., Liang, D., Rodriguez, F., Daughters, G.T., Ingels Jr., N.B., Miller, D.C., 2003. Edge-to-edge mitral valve repair without ring annuloplasty for acute ischemic mitral regurgitation. Circulation 108 (Suppl 1), II122–127. Verma, S., Mesana, T.G., 2009. Mitral-valve repair for mitral-valve prolapse. The New England Journal of Medicine 361, 2261–2269.
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Annulus tension of the prolapsed mitral valve corrected by edge-to-edge repair Shamik Bhattacharya, Zhaoming He n Department of Mechanical Engineering, Texas Tech University, Lubbock, TX 79409, 7th and Boston, PO Box 41021, Lubbock, TX 79409-1021
a r t i c l e i n f o
a b s t r a c t
Article history: Accepted 9 November 2011
Background: Mitral valve (MV) performance after edge-to-edge repair (ETER) without ring annuloplasty is suboptimal. ETER efficacy needs to be evaluated from annulus tension (AT) of a prolapsed MV corrected by ETER to understand annular dilatation. Methods: Ten porcine MVs were harvested and mounted on a MV closure test rig. The MV annulus tissue rested on top of a saddle-shaped plastic ring on which the annulus could slide freely. The annulus was held by strings in the periphery during MV closure under a hydrostatic trans-mitral pressure. String tensions were measured and further divided by string spacing to obtain AT. The MVs were then prolapsed by shifting split papillary muscles to simulate mono-leaflet prolapse due to elongation of chords, which insert into a single leaflet. Last, MV prolapse was corrected by ETER applied in the central leaflet region and AT was measured. Results: AT in both anterior and posterior leaflet prolapse corrected by ETER was less than that of normal MVs. AT in the anterior leaflet prolapse corrected by ETER was less than that in the posterior leaflet prolapse corrected by ETER. Conclusion: ETER does not restore the normal AT and therefore leads potential of annular dilatation. The anterior leaflet prolapse has a greater potential of annular dilatation than the posterior leaflet prolapse after ETER. Annuloplasty is recommended to maintain long-term ETER efficacy. & 2011 Elsevier Ltd. All rights reserved.
Keywords: Mitral valve In vitro study Valve repair Surgical instruments
1. Introduction Mitral valve (MV) prolapse is a typical disease of the MV caused by papillary muscle elongation, chordal elongation or rupture, or enlarged leaflets, and is responsible for mitral regurgitation. A repair technique known as edge-to-edge repair (ETER) has been used extensively to correct MV prolapse (Alfieri et al., 2001; Fucci et al., 1995). ETER is most commonly performed on the center of the main scallop of leaflets with ring annuloplasty, which is required to reshape the annulus and reduce the annular orifice (Alfieri et al., 2001). ETER performed without ring annuloplasty yields suboptimal midterm results when compared to ETER, performed with annuloplasty (Maisano et al., 2003; Timek et al., 2003). Annular dilatation may persist after ETER without annuloplasty. Therefore, the success of ETER largely depends on the use of ring annuloplasty and ETER is thus considered as a secondary procedure. It elicits a question: why does ETER not prevent the MV from annular dilatation in the long run? Therefore we investigated annulus tension (AT) in ETER using a novel system that is able to reveal the mechanism of annular dilatation
n
Corresponding author. Tel.: þ806 742 3563x225; fax: þ 806 742 3540. E-mail address: [email protected] (Z. He).
0021-9290/$ - see front matter & 2011 Elsevier Ltd. All rights reserved. doi:10.1016/j.jbiomech.2011.11.005
(Bhattacharya and He, 2009; He and Bhattacharya, 2008; He and Bhattacharya, 2010). We proposed a mechanism of annulus dilatation that mitral annulus dilatation is a consequence of imbalanced annulus mechanics between the centripetal mitral leaflet tension and centrifugal left ventricle myocardial force at annulus in systole. AT is defined as a leaflet tension force at the annulus per unit length of the annulus perimeter. The MV leaflets and left ventricular myocardium are in force equilibrium at the annulus during MV closure in the normal heart without initiation of annulus dilatation. This equilibrium implies that AT is equal to and thus interpreted as myocardial force in the normal MV-left ventricle system. Alteration in either one due to pathologies will break the equilibrium, which ultimately results in annulus geometry changes such as annulus dilatation. We found that AT decreases in MV bileaflet prolapse due to papillary muscle elongation and is thus lower than the normal left ventricular myocardial force (He and Bhattacharya, 2008). This imbalanced annular mechanics due to MV bi-leaflet prolapse causes annular dilatation even in the normal left ventricle according to the mechanism of annular dilatation. This mechanism has successfully explained some MV physiologies and pathologies on the MV annulus, especially in the normal left ventricle size (Bhattacharya and He, 2009; He and Bhattacharya, 2008; He and Bhattacharya,
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2010). In addition, clinical study reports annular dilatation without any pathology in a normal left ventricle, also called as ‘‘pure annular dilatation’’ (Glower et al., 2009). This pure annular dilatation could also be caused by imbalanced annular mechanics. Now we have a question about MV prolapse: can it be corrected by ETER without further annulus dilatation? Therefore, the objective of this research was to understand AT of a prolapsed MV corrected by ETER.
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cylinder through a PVC hose in the downstream of the MV. When the MV closed under a trans-mitral pressure, the MV annulus tended to shrink towards the center of the MV orifice. Strings connected to MV annulus, prevented the MV
Left ventricle side
Commissure Posterior
Anterior 2. Methods
5 mm
2.1. MV closure test rig and annulus tension measurement We followed the same method for AT measurement as described in our earlier papers (Bhattacharya and He, 2009; He and Bhattacharya, 2010). A total of ten fresh porcine hearts were obtained from a local slaughterhouse and transported to the lab. The MVs of annulus size M36 measured in an Edwards ring sizer (Edwards LifeSciences LLC, Irvine, CA) were selected and dissected from porcine hearts. Each MV was mounted in a MV closure test rig, which was designed to measure the AT at a static trans-mitral pressure shown in Fig. 1. Each MV was mounted on the plastic ring glued on the annulus mounting board, with the MV annulus coinciding with the plastic ring. The ring had a saddle shape and a 5 mm saddle height as shown in Fig. 2, because the ratio of the saddle height to intercommissural diameter is usually 15% in a prolapsed MV (Grewal et al., 2010). The annulus ring was made according to M36 on an Edwards ring sizer, and the ring area and perimeter were 7.63 cm2 and 122 mm, respectively. The commissural axis length was 35 mm, and the septal-lateral axis length was 30 mm. The annulus mounting board separated the atrium in the bottom chamber and left ventricle in the top chamber. The atrial chamber had an opening below the MV, which was connected through a plastic pipe to a lower reservoir. The left ventricle chamber was open to the air and contained saline in which the MV was immersed. The papillary muscles were sutured to two papillary muscle holders made of steel rods, the positions of which could be adjusted three-dimensionally. A static trans-mitral pressure was built up by the difference in the saline levels of the two reservoirs when the MV closed. Any leakage across the MV was measured in a measuring
L5
L6 L77 L8 L9
Anterior
35 mm Ciommissure
30 mm Posterior
Fig. 2. A picture of normal annulus support ring with 5 mm saddle height made according to the M36 Edwards ring sizer.
Edge-to-edge repair L10
L4
L11 L12 L13
L3 L2 L1 Anterior leaflet
Annulus plane
#
#
#
L14 Posterior leaflet
#
# #
#
#
#
#
String Papillary muscle holder
Fourteen force transducers are labeled as L1-L14. Others are posts without force transducers labeled as # “#” Saline level
Papillary muscle Chordae
String force transducer
H
Annulus mounting board Atrium reservoir
Saline
Left ventricle reservoir
Drain Plastic ring PVC Hose Adjustable Shut-off support valve l
Measuring cyylinder Fig. 1. (a) Schematic of the MV closure test rig for AT measurement system, (b) and (c) Photograph of the actual test rig for AT measurement system.
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annulus from shrinking towards the MV orifice center. Fourteen strings were connected to the anterolateral section of the annulus, as shown in Fig. 1. Each of them was attached to a force transducer (Load Cell Central, Monroeton, PA) installed in each post. String tension was measured and divided by the distance between stitches in the annulus to obtain AT in units of N/m.
2.2. Normal and prolapsed MV The normal papillary muscle position was set up in the normal state controlled by papillary muscle holders as used in previous studies (He and Bhattacharya,
2008; He et al., 2003; Krishnamurthy et al., 2009; He et al., 2003). In order to simulate leaflet prolapse, the papillary muscles were dissected apically and split into anterior and posterior parts to separate chords that insert into the anterior and posterior leaflets, as shown in Fig. 3. The posterior leaflet prolapse was simulated by moving both the posterior papillary muscle parts from two papillary muscles 5 mm towards the annulus with respect to the normal anterior papillary muscle parts. The average static leakage under trans-mitral pressure 16.0 kPa (120 mmHg) in the posterior leaflet prolapse was 1.089 L/min. Then, the posterior leaflet prolapse was followed by the anterior leaflet prolapse, which was simulated by moving both the anterior papillary muscle parts from two papillary muscles 5 mm towards the annulus with respect to the normal posterior papillary
Papillary muscle shifting Papillary muscle
5 mm Leaflet prolapse
String tension
String tension
Annulus ring
Leakage
Prolapsed anterior Leaflet
Posterior leaflet
Fig. 3. (a) Papillary muscles were dissected apically and split into anterior and posterior parts to separate chords that insert into the anterior and posterior leaflets. The posterior leaflet prolapse was simulated by moving both the posterior papillary muscle parts from two papillary muscles 5 mm towards the annulus with respect to the normal anterior papillary muscle parts, (b) a schematic of shifting split papillary muscles towards the annulus plane to simulate mono-leaflet prolapse due to chordal elongation, (c) a atrial view of the anterior leaflet prolapse by the papillary muscle shifting method.
Anterior leaflet
Posterior leaflet
Suture
Chord
Papillary muscle Fig. 4. (a) A apical view of a porcine mitral valve corrected by edge-to-edge-repair technique with suture length 20 mm, (b) a schematic of the central suture in edge-toedge repair with 5 mm deep bites placed through the rough zone of the leaflets to prevent tearing of the leaflets.
S. Bhattacharya, Z. He / Journal of Biomechanics 45 (2012) 562–568 muscle parts. The average static leakage under 16.0 kPa in the anterior leaflet prolapse was 1.527 L/min. It is estimated to be mild to moderate mitral regurgitation based on the regurgitant volume (Verma and Mesana, 2009; He et al., 1997). 2.3. Edge-to-edge repair
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ETER was applied to repair the posterior leaflet prolapse. Then, the anterior leaflet prolapse was simulated on the same MV, and leakage was measured after removal of the suture. Last, the AT and leakage were measured for anterior leaflet prolapse after ETER was applied again. A total of 10 MVs were tested.
2.5. Data analysis
The MV prolapse was corrected by suturing two leaflets together using the ETER technique. The details of the suture were shown in Fig. 4. The suture was started from the middle position of both leaflets from the atrial side. The suture had a depth of 5 mm distributed symmetrically over both leaflets and a length of 20 mm along the free edge. All ten MVs exhibited reduced static leakage under trans-mitral pressure 16.0 kPa after ETER.
Statistical analysis was based on the assumption that the observations of the ATs were normally distributed. For the comparison between control and other conditions, a paired t-test for means was used. The p-value was based on two-tail distribution, with p o 0.05 used as the accepted value for significance. The control was the same MVs with the normal valve configuration. In order to assess the functional model of the prolapsed MV and ETER, the leakage of the prolapsed MV was compared with the leakage after ETER was applied on the same MV.
2.4. Experiment conditions The AT was measured in the trans-mitral pressure of 16.0 KPa (120 mmHg) at the anterolateral segment of the annulus. All the experiments were carried out at room temperature and data were collected within a 2 h period. All the MVs coapated normally in the normal MV. The string position in the annulus was represented by a length of the annulus from mid-anterior position, and normalized by a total length of the semi-annulus perimeter. The anterior and the posterior centers of the annulus were 0% and 100% positions, respectively. First, the AT was measured for the normal MVs. Then posterior leaflet prolapse was simulated and leakage was measured. AT and leakage were recorded again after
Leakage of Mono-leaflet Prolapse 2.5 2 1.5 1 0.5 0 Posterior leaflet prolapse
Anterior leaflet prolapse
Before ETER
After ETER
Fig. 5. Leakages before and after ETER was applied to the anterior and posterior leaflet prolapse. The error bars are in the format of 7 1 standard deviation.
3. Results All the normal MVs coaptated well without leakage, but failed to coaptate when MV prolapse was simulated. Leakage of the prolapsed MVs was significantly reduced (p-valueso0.01) after ETER was used to correct the prolapsed MVs. Fig. 5 shows leakage of the prolapsed MVs before and after ETER. Average ATs at 14 string positions along the normalized perimeter of the anterolateral segment of the annulus are shown in Fig. 6 with error bars of 7standard deviation centered on the average values. Three curves in the figure represent AT of the normal MVs, MVs with the anterior and posterior leaflet prolapse corrected by ETER. AT distribution along the annulus exhibited a concave curve for both the normal and repaired MVs, with the lowest AT in the commissural segment of the annulus. Fig. 7 shows AT superimposed on the MV annulus. For the posterior leaflet prolapse corrected by ETER, ATs did not change much in the posterior segment of the annulus from the L8 to L14 positions. There was no significant difference in AT between the normal and repaired MVs (all p-values40.24) except L13 position (p-valueo0.002). In the anterior segment from L1 to L7 positions, the AT was significantly lower in the repaired MVs (all p-valueso0.03) than that in the normal MVs. AT in the anterior leaflet prolapse corrected by ETER was significantly less (all p-valueso0.01) than that of the normal MVs in the whole annulus. The AT in the anterior leaflet prolapse
AT of the normal MV, posterior and anterior leaflet prolapse corrected by ETER Normal MV Posterior leaflet prolapse correcetd by ETER Anterior leaflet prolapse correcetd by ETER 45 L2 40 L4 L14
AT (N/m)
35 L6
30 25
L12 L10
L8
20 15 10 0 Anterior annulus center
20
40
60
80
100 Posterior annulus center
Normalized perimeter (%) Fig. 6. AT distribution in the annulus of normal MV, anterior and posterior leaflet prolapse corrected by ETER. The error bars are in the format of 71 standard deviation centered on the averaged values.
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AT distribution superimposed on the normal MV annulus L1
L2
L3 L4
AT in the normal MV AT in posterior leaflet prolapse corrected by ETER
Averaged AT (N/m) overlapping on the annulus
L5 0% L6 6
Anterior annulus 61 mm
AT in anterior leaflet prolapse corrected by ETER
L7
Anterolateral annulus Posterior annulus
L8 L9 L10
100%
L11 L12 L13 L14 Fig. 7. AT superimposed on the annulus in the normal MV, anterior and posterior leaflet prolapse corrected by ETER.
corrected by ETER is significantly less than that in the posterior leaflet prolapse corrected by ETER (all p-valueso0.02).
4. Discussion We propose a novel mechanism of annular dilatation as a consequence of imbalanced annulus mechanics between centripetal AT and centrifugal myocardial force at annulus during systole. This implies that AT is balanced with the myocardial force due to absent initiation of annular dilatation in the normal MV-left ventricle system and thus can be interpreted as the normal myocardial force, which is not measurable. AT and myocardial forces are normally in the annulus plane and determine annulus size, while forces acting on the annulus and perpendicular to the annulus plane (in apical direction) determine annulus shape. These apical forces are usually generated from basal chords that directly insert into commissural and posterior annulus segments, and from AT component in the apical direction, in MV prolapse or dilative left ventricle diseases. The new mechanism of annulus dilatation can be used to explain two cases of annulus dilatation from dilative left ventricle diseases with left ventricle remodeling, and from MV prolapse without left ventricle remodeling (He and Bhattacharya, 2010). Hence this mechanism unifies annulus dilatation due to etiologies of left ventricle remodeling and non-left ventricle remodeling, and is more general in application. It is noted that difference or imbalance between AT and myocardial force is a driving force for MV annulus to dilatate in order to regain a new balanced annulus mechanics usually in the well-developed pathologies. Therefore, this mechanism leads to a theory to predict annulus size: annulus
is dilatated to compensate AT in order to rebalance myocardial force until a new balanced annulus mechanics in pathologies is reached or approached. MV prolapse lowers leaflet coaptation (contact) height from the annulus plane and causes the lower AT component in the annulus plane than the AT, or, myocardial force in the normal MV (He and Bhattacharya, 2008). This imbalanced annulus mechanics initiates annular dilatation, which requires leaflet stretching (decrease in curvature) and covering the dilatated annulus. This coaptation adaptation to the dilatated annulus usually increases the coaptation height, and thus AT component in the annulus plane until the AT is balanced with the normal myocardial force, which remains unchanged during the MV adaptation process. Therefore, annular dilatation is MV compensation for AT to regain balanced annular mechanics. However, this MV adaptation mechanism fails in chord rupture, which has no MV coaptation, or leaflet enlargement, which causes MV coaptation position below annulus plane. The more the difference between AT and myocardial force is, the greater is the annulus dilatation. In the onset MV prolapse without left ventricle remodeling, we predict potential of annular dilatation by comparing two stable states in development of annulus dilatation from normal heart: (1) normal heart: normal MV AT¼normal myocardial force, (2) well-developed prolapsed MV: pathological MV AT¼myocardial force. We assume that the myocardial force in a prolapsed MV remains normal myocardial force because of no left ventricle remodeling. The difference in AT between two states is actually the driving force between pathological AT in the MV prolapse state and the myocardial force in the normal left ventricle right at onset of the MV prolapse. MV prolapse can be either acute (chord rupture) or progressive (chord elongation) case. Therefore, we compared the AT in pathologies with the AT in
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the normal MV-left ventricle system, which is interpreted as the normal myocardial force. The difference in AT is used to evaluate potential of annulus dilatation. We already found that actual AT in MV bileaflet prolapse is lower than normal myocardial force and has a potential of annular dilatation even without left ventricle remodeling (He and Bhattacharya, 2008). That is why the MV annulus is dilatated in MV prolapse while the left ventricle size remains normal and supported by the clinical study (Mihalatos et al., 2007; David et al., 2003). ETER reduced or eliminated leakage, but not annular dilatation as AT decreased more or less in mono-leaflet prolapse. ETER does not restore the MV AT to a normal MV AT to balance the normal myocardial force, which suggests ETER cannot potentially prevent annular dilatation in the MV mono-leaflet prolapse. The annular dilatation may ultimately compromise MV function in a long-term view. Suboptimal mid-term results of ETER without annuloplasty support our theory (Timek et al., 2003). Therefore, annuloplasty is recommended to maintain long-term ETER efficacy. Further, the potential of annular dilatation for the anterior and posterior leaflet prolapse differs. The greater drop in AT was observed in the anterior leaflet prolapse than in the posterior leaflet prolapse. As a driving force for the annulus to dilatate, difference between the actual AT and normal myocardial force may be compensated by greater annular dilatation in the anterior leaflet prolapse than the posterior leaflet prolapse. That may be why it is found that anterior leaflet or bileaflet prolapse is harder to repair than posterior leaflet prolapse (David et al., 2005). High rate of recurrent mitral regurgitation may be due to progressive annulus dilatation. As for the model of MV prolapse, no in-vitro or in-vivo model is generally available except chord rupture. We created an extensive (multi-segment) MV prolpase to simulate elongation of multiple chords that insert into either MV leaflet, or multiple chord rupture. Our prolapse model simulates a multi-segment MV prolapse and differs in prolapsed area from a model due to rupture or elongation of local chords or elongation of whole papillary muscles. Although the MV leaflets in our model were not enlarged and thickened, or slack like in fibroelastic deficiency or myxomatous diseases, leakage of the prolapsed MV was used as a measure and seemed reasonable to control MV prolapse. Lack of leaflet thickening makes our model close to MV prolapsed due to fibroelastic deficiency. However, the leaflet size and chord structure are two factors, which are hard to simulate in-vitro and in-vivo. It should be mentioned that large leaflets and concurrently large annulus in MV prolapse may not necessarily lead to mitral regurgitation, which depends on complicated MV coaptation. Large annulus may be good for MV function with large leaflets (Adams et al., 2006). Therefore, MV annular dilatation could occur regardless of MV regurgitation or left ventricle remodeling and is often asymptomatic (David et al., 2003). ETER alters MV geometry and thus AT according to suture pattern, which affects leaflet stress (Gao et al., 2009; He et al., 2009) and suture tension (He et al., 1997; Mihalatos et al., 2007; David et al., 2003). If the tension in the suture is high, it may pull the leaflets towards the center. This suture tension may transfer to the annulus during MV closure. This suture tension usually does not affect AT for enlarged and redundant leaflets in MV prolapse during MV closure. On the other hand, the way the suture is done (Maisano et al., 2000) affects the coaptation depth (contact part) as well as the leaflet profile and curvature, and thus an AT in the leaflets. AT is a vector and acts approximately along the annulus plane in a normal MV. MV prolapse deflects AT from annulus plane and reduces the AT force component in the annulus plane, which further facilitates annular dilatation. The AT direction should be characterized to enable quantification of AT component in the annulus plane in order to evaluate accurate AT effect on the annulus.
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Tension of basal chords that directly insert onto commissural and posterior segments of the annulus may have effect on annulus mechanics if these chords are tight in pathologies. These chords are basically perpendicular to annulus plane, and thus tension from these chords predominantly affect annulus shape, not the annular size. However, basal chord force component that is aligned in the annulus plane may be significant in effect on annulus size if the basal chords are too tight or not perpendicular to annulus plane. Chord shortening could correct regurgitation clinically and should restore AT to preclude annulus dilatation.
5. Study limitations The model of the MV prolapse was an extensive (multisegment) prolapse without enlarged leaflets and did not represent all the MV prolapse conditions, especially, local prolapse caused by rupture of an individual chord or prolapse due to enlarged leaflets. The results may have been different if human MV is used. The AT was obtained in a static configuration, which may differ in dynamic annulus and MV closure conditions. AT direction was not characterized for understanding delicate annulus mechanics. Difference between the ETER for the posterior prolapse and redone ETER for the anterior prolapse might affect AT. In clinical practice, difference in ETER surgical procedure might affect AT and thus surgical outcome.
6. Conclusions ETER alone does not restore the normal AT and thus leads to potential of annular dilatation. The anterior leaflet prolapse has a greater potential of annular dilatation than the posterior leaflet prolapse after ETER. Annuloplasty is recommended to maintain long-term ETER efficacy.
Conflict of interest statement None
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