Methods: Posterior quadrangular resection and sliding leaflet techniques were simulated in 24 cases in bovine heart. In all cases, posterior mitral leaflet indentations were closed with 5-0 silk sutures. The indentational chords were left untouched in group 1 (n=12), and were resected in group 2 (n=12). The coaptation lines between anterior and posterior leaflets were assessed in both groups. Presence of tethering chords in posterior leaflet was investigated while the mitral valve competence was tested under the pressure of 170 cmH2O (125 mmHg).
Results: While coaptation lines were asymmetric in all cases in group 1, no asymmetric coaptation line was detected in group 2 (p<0.001). It was determined that the asymmetric coaptation lines in group 1 were caused by the primary chords supporting the intentionally closed indentations during the procedure.
Conclusion: It can be suggested that after closing the indentations, the primary chords supporting these indentations function as secondary chords which restrain leaflet mobilization in sliding posterior leaflet technique.
The posterior leaflet of the mitral valve in our model is inserted approximately two-thirds of the way up on the annulus, and the free edge is usually divided into three scallops by two indentations (sometimes improperly called clefts) that are supported by indentational chords (Figure 1).[8] However, in some cases, it is preferable to close the indentation in order to avoid separation, and this is especially in sliding leaflet plasty. Another reason for closing the indentation is to decrease the height of the posterior leaflet by creating a curtain effect. This approach, which allows for the coaptation line to be closer to the posterior annulus, is particularly helpful for treating systolic anterior motion. Sliding leaflet plasty is primarily indicated for cases involving systolic anterior motion and extensive leaflet prolapse. In this technique, it is necessary to resect all secondary chords close to the edge of the detached leaflet remnants to facilitate “sliding” after the quadrangular resection of the posterior leaflet.[9]
Figure 1: Indentations and their supporting chordae tendineae.
The rules that usually apply in sliding leaflet plasty procedure should be strictly obeyed in routine practice. This goal of this study was to analyze and identify the underlying mechanisms of the asymmetric coaptation line as well as the tethering over the posterior leaflet, both of which can be easily observed when performing this technique.
Ex vivo isolated heart model[7]
The ex vivo heart model consisted of a bovine
heart and a study table (Figure 2). The table included
three main parts: a pressure system to test the
valve competence under 170 cmH2O (=125 mmHg),
green dressing, which was designed to cover the
heart to avoid ventricular overdistention, and two
atrial retractors, each capable of moving in three
dimensions, which were designed for stabilization
and valve exposure.
Although bovine hearts are not identical to human hearts, they have the same anatomical structures, including anterior and posterior leaflets, two papillary muscles, primary and secondary tertiary chords, and a mitral annulus. The posterior leaflets are usually divided into three segments (the P1, P2, and P3 scallops) by two indentations. The most important factor is that both hearts work with the same mechanical and physiological principles, making it possible to simulate the state of the heart’s cardioplegic arrest period.
Study protocol
The aortic cusps were first resected, and the
pressure system was then connected to the aorta.
The heart was tested under static pressure to reveal
any structural injury that might have occurred at the
slaughterhouse, and the valve analysis was performed.
Next, the indentations were marked with stay sutures
(Figure 3a) and then closed with interrupted 5-0 silk sutures (Figure 3b). Both the P1 and P3 scallops were
then detached from the posterior annulus, and the
quadrangular resection width on the P2 scallop of the
posterior leaflet was 15 mm in all of the experiments
(Figure 3c). Afterwards, the primary chords supporting
the indentations were preserved in group 1 (Figure 4a,
white arrow) but resected in group 2. In addition, all
of the secondary chords of the detached P1 and P3
scallops were also resected to facilitate leaflet mobility
in both groups (Figure 3d and 4a, black arrows).
Three posterior annular plicating sutures were then
used in each case to decrease the posterior annular
circumference (Figure 4b), and the repair process
was completed using the sliding leaflet technique. At
the end of each instance of mitral valve competence,
the valve geometry and coaptation line between the anterior and posterior leaflet were evaluated under a
static pressure of 170 cmH2O (=125 mmHg).
In the evaluation process, the coaptation scores were given based on whether the valve was competent or not (0 points if it was not competent). If the valve was competent, then we determined whether the coaptation line was parallel to the posterior annulus. (1 point if not parallel and 2 points if parallel). After that, the posterior annular sutures were removed to analyze the subvalvular apparatus in both groups. After this, the indentational chords in group 1, which had been preserved in group 1, were resected, and the posterior leaflets were sutured to the posterior annulus. Subsequently, the mitral valves were reevaluated under static pressure.
Statistical analysis
Statistical analyses were performed using the
SPSS Statistics for Windows version 17.0 (SPSS Inc.,
Chicago, IL, USA) software program. The parameters
between independent groups were compared using with
the Mann-Whitney U test, and statistical significance
was set at a p value of <0.05.
Assessment of the asymmetric coaptation
line in group 1
After removing the posterior suture lines, the
subvalvular apparatus indicated that the cause of the
asymmetric coaptation line was the chordae tendineae,
which were supporting the indentations that had been
preserved prior to the surgery and pulling them to
the corresponding papillary muscle. Moreover, due
to the tethering, the mean height of the asymmetrical
coapting segments (Figure 4c) was smaller than the
symmetrical coapting segments (Figure 4c) in the
posterior leaflet (13.7±1.1 mm vs. 3.5±1.0 mm; p<0.05)
because the tethering chords supporting the closed
indentation were pulling the posterior leaflet down into
the left ventricle in the coapting segments that were
asymmetrical.
After the chords of the indentations were resected in group 1, the asymmetric coaptation lines and posterior leaflet height were normalized (Figure 4d); thus, symmetric coaptation lines were achieved. Moreover, the coaptation scores in group 1 and 2 were now similar (2±0 vs. 1.8±0.4; p=0.15), and the two cases with mitral insufficiencies in group 1 were also corrected. In addition, the discordant height between the symmetrical and asymmetrical coapting segments in the posterior leaflet was resolved (p=0.653).
Assessment of the symmetric closure
line in group 2
Resecting the indentational chordae tendineae
before suturing them initially resulted in increased
leaflet mobility with no tethering chords. However, removing the indentational chords led to the appearance
of a symmetric coaptation line.
Assessment of the mitral insufficiency in group 1
Although, tethering was observed in all cases
in group 1 under static pressure, only two of them
had regurgitation. The reason for this was not only
attributable to the tethering. The hypoplasia that was
identified in the P1 scallop in the first case and the
P3 scallop in the second case were also responsible.
These two cases had also double indentations at the
contralateral side. Therefore, when the hypoplasia was
present in the P1 or P3, the contralateral indentational
chords caused more tethering than usual by acting as
secondary chords after they were sutured. Therefore,
when the supporting indentational chords were resected
in the second evaluation, we then slid the leaflet over
slightly, which caused the mitral insufficiency to
disappear.
The indentations of the posterior leaflet are normal anatomical structures that allow the leaflet to fully open during diastole.[8] Perier[16] analyzed indentations between the P1 and P2 and the P2 and P3 and found that if they were deep, they could interfere with the goal of transforming the posterior leaflet into a smooth and regular vertical buttress. In a natural mitral valve, these indentations allow the posterior leaflet to expand and follow the diastolic dilation of the annulus without tension on the free edge. However, because the annulus is fixed to the systolic position by the implantation of an annuloplasty ring, these indentations can no longer serve their physiological purpose and may even cause residual leaks. Accordingly, when the indentations are deep, it may be desirable to suture them with a 5-0 monofilament running suture to ensure a perfect result.[16]
In order to perform the sliding leaflet technique without annular plication, it is accepted that the gap between the two leaflet remnants in the posterior leaflet should be equal to or greater than 20 mm.[9] However, in our study, this technique was implemented after only a 15 mm gap had been created because it could have otherwise been concluded that excessive leaflet resection caused the asymmetric coaptation line and tethering chords. Therefore, we limited the resection width to 15 mm. The chords supporting the closed indentations resulted in tethering when they were not resected, and the contralateral indentational chords caused more tethering because the contralateral leaflet segment required more sliding than usual, especially in the hypoplastic segments in the P1 or P3 scallop.[9] Hence, these chords stretched the median suture line and decreased the height of the posterior leaflet in the asymmetrical coapting segments. This not only led to the asymmetric coaptation line between the anterior and posterior leaflet, but it also increased the coaptation depth in the asymmetrical coapting segments of the posterior leaflet. In spite of the posterior translocation of the coaptation line, if the height of the anterior leaflets was sufficient, no regurgitation leaks were observed. However, when the height was insufficient, as in the two cases in group 1, a posteriorly directed regurgitant jet flow can be seen.
We realized that after closing the indentation of the posterior leaflet, mobilizing the leaflet remnant in and of itself was not enough to avoid separation between the scallops even if the secondary chords were resected because new secondary chords were created when the indentations were closed. In other words, after closing the indentation, the supporting chords acted as secondary chords that restricted leaflet mobility.
Another decision that must be made is whether or not to decrease the posterior annular circumference. If this is deemed necessary, then the next question concerns whether the transverse compression sutures or vertical plication sutures are the most appropriate.[9] In this study, we chose the first option. However, we determined that transverse compression sutures were not as effective for decreasing the posterior annular circumference.
Our experimental model also allowed for the observation of the most common lesions found in cases involving fibroelastic deficiency. The two main forms of degenerative mitral valve disease are fibroelastic deficiency and Barlow’s disease,[17] but these are both completely different from each other. The lesions associated with Barlow’s disease have excessively thick and billowing leaflet segments, chordal elongation and rupture, calcification of the papillary muscles and/or an annulus with chordae restriction, and severe annular dilatation with giant valves.[17] In contrast, patients with mitral regurgitation due to fibroelastic deficiency lack the connective tissue that triggers leaflet and chordal thinning, which can eventually lead to chordal rupture.[9,17] As opposed to patients with excessive tissue, extensive leaflet resection or complex leaflet remodeling procedures are rarely indicated for those with fibroelastic deficiency.[9,17] In general, a limited quadrangular or triangular resection or simple leaflet resuspension with a chordal transfer or artificial chord is all that is required to correct the leaflet prolapse. Unlike cases with Barlow’s disease, a normal bovine heart does not have any excess leaflet tissue, which is frequently seen in fibroelastic deficiency. Keeping this in mind, this study may provide a model for the lesions observed in patients with fibroelastic deficiency when posterior leaflet prolapse is present.
One of the limitations of our study was that we used bovine hearts because they can be easily procured and are similar in structure to human hearts.[7] However, none of the bovine hearts used in our model were diseased, and there was no annular dilatation. In addition, bovine hearts are normally larger than human hearts, but in our experimental model, the final state after repair compensates for this anomaly, which eliminates this potential limitation. Furthermore, while the non-beating flaccid bovine heart used in our model could not precisely mimic the functions of a mitral valve, it did adequately imitate the state of the arrested left ventricle after cardioplegia. Therefore, we believe that our model displays most of the features that surgeons experience during saline testing. Moreover, analyzing the mitral valve under a static pressure of 125 mmHg revealed the inadequacy of the surgical techniques that have been previously implemented. Now that the theoretical thought process has been validated by simulation studies such as ours, the next step is to use an in vivo model to try and replicate the results obtained from the ex vivo model.
Declaration of conflicting interests
The authors declared no conflicts of interest with
respect to the authorship and/or publication of this
article.
Funding
The authors received no financial support for the
research and/or authorship of this article.
1) Keçeligil HT, Demirağ MK, Ersoy G, Bahçıvan M, İriz E,
Kolbakır F ve ark. St. Jude medikal kapak protezi ile mitral
kapak replasmanı: 179 hastaya ilişkin 10 yıllık deneyim.
Turk Gogus Kalp Dama 1999;7:303-8.
2) Gürbüz A, Akel S, Işık Ö, İpek G, Dikmengil DM, Sezer H.
Mekanik protez kapaklar ile mitral kapak replasmanı: Orta
dönem klinik sonuçları. Turk Gogus Kalp Dama 1994;2:16-9.
3) Onan B, Erkanlı K, Onan İS, Ersoy B, Aktürk İF, Bakır
İ. Clinical outcomes of mitral valve repair: a singlecenter
experience in 100 patients. Turk Gogus Kalp Dama
2014;22:19-28.
4) Joyce DL, Dhillon TS, Caffarelli AD, Joyce DD, Tsirigotis
DN, Burdon TA, et al. Simulation and skills training
in mitral valve surgery. J Thorac Cardiovasc Surg
2011;141:107-12.
5) Yamauchi H, Vasilyev NV, Marx GR, Loyola H, Padala M,
Yoganathan AP, et al. Right ventricular papillary muscle
approximation as a novel technique of valve repair for
functional tricuspid regurgitation in an ex vivo porcine
model. J Thorac Cardiovasc Surg 2012;144:235-42.
6) Tavlasoglu M, Jahollari A, Amrahov A, Sahin MA. An instrument facilitates mitral valve repair training at home.
Eur J Cardiothorac Surg 2012;41:940-1.
7) Tavlasoglu M, Durukan AB, Arslan Z, Kurkluoglu M,
Amrahov A, Jahollari A. Evaluation of skill-acquisition
process in mitral valve repair techniques: a simulation-based
study. J Surg Educ 2013;70:318-25.
8) Carpentier A, Adams DH, Filsoufi F. Mitral Valve
Reconstruction, Chapter 5. Surgical Anatomy and Physiology.
In: Carpentier’s reconstructive valve surgery. Missouri:
Saunders; 2010. p. 33.
9) Carpentier A, Adams DH, Filsoufi F. Mitral valve
reconstruction. Chapter 11. Techniques in Type II posterior
leaflet prolapse. In: Carpentier’s reconstructive valve surgery.
Missouri: Saunders; 2010. p. 115-26.
10) Rabbah JP, Siefert AW, Spinner EM, Saikrishnan N,
Yoganathan AP. Peak mechanical loads induced in the in
vitro edge-to-edge repair of posterior leaflet flail. Ann
Thorac Surg 2012;94:1446-53.
11) Padala M, Gyoneva L, Yoganathan AP. Effect of anterior
strut chordal transection on the force distribution on the
marginal chordae of the mitral valve. J Thorac Cardiovasc
Surg 2012;144:624-633.e2.
12) Poglajen G, Harlander M, Gersak B. Ex vivo study of altered
mitral apparatus geometry in functional mitral regurgitation.
Heart Surg Forum 2010;13:E172-6.
13) Prieto D, Antunes P, Antunes MJ. Donor mitral valve repair
in cardiac transplantation. Transplant Proc 2009;41:932-4.
14) Massad MG, Smedira NG, Hobbs RE, Hoercher K,
Vandervoort P, McCarthy PM. Bench repair of donor
mitral valve before heart transplantation. Ann Thorac Surg
1996;61:1833-5.
15) Pawale A, Tang GH, Milla F, Pinney S, Adams DH,
Anyanwu AC. Bench mitral valve repair of donor hearts
before orthotopic heart transplantation. Circ Heart Fail
2012;5:e96-7.