My name is Ani Anyanwu and I am a cardiac surgeon at Mount Sinai Medical Center, New York, and this presentation is on mitral valve re-repair. I have no disclosures.
Essentially, in understanding mitral valve re-repair, it is necessary to understand why mitral valve repairs actual fail. Essentially, there are two principle categories of failed mitral valve repair. You have residual mitral regurgitation which is due to an inadequate repair where the valve leaks immediately or you have recurrent mitral regurgitation which happens weeks, months, or years after mitral valve repair. Recurrent mitral regurgitation can either be due to technical failure such as dehiscence of a ring or suture, it could be due to a new disease for example endocarditis, or it could be due to a progression of native disease. It is important to know the reason for failure of repair as that would determine whether it is possible to repair the valve again and the technique that will be used to repair the valve again. So if we go to immediate failures; the mechanisms of immediate failure are usually due to unrecognized pathology such as a cleft that was not recognized, an uncorrected defect – for example you can have prolapse or restriction which was not corrected, or you could have residual dehiscence or perforations from sutures or instruments which were not recognized at the time of repair. Ideally, all these should be diagnosed in the operating room on the postoperative transesophageal echocardiography and rectified immediately; but sometimes they go undetected and the patient presents with significant regurgitation early after surgery, and really an imperfect immediate result of any sort seen on transesophageal echocardiography should almost always lead to the surgeon to reopen the atrium and fix the cause of regurgitation. This is very important because the freedom from immediate mitral regurgitation is a long-term predictor of the outcome of mitral valve repair. So valves that leak early on are more likely to leak significantly in the longer term and also impact the patient’s survival. This applies to both ischemic and degenerative disease.
These are some examples of intraoperative failure of repair:
This is a patient with a commissural prolapse which was repaired with a simple Magic suture and the cleft between P2 and P3 as illustrated was closed. The saline tested at the time showed a competent valve. However, on discontinuation of bypass, the echocardiography showed a leak coming from the P2-P3 region. So the thing to do in such a case is to go back on bypass and identify the cause of the leak. Looking at the echo, it looks like a type 1 defect; so you would expect that either there is a cleft or a perforation in this region. Indeed, going back on bypass you can see that there was an opening in the base of the leaflet, which we sutured with a simple figure-of-eight suture and the final echo shows no regurgitation.
Systolic anterior motion is a problem if there is excessive posterior and anterior leaflet height. This is a case of a giant Barlow valve. This was repaired by a triangular resection with Gore-Tex chords used to tie the valve down into the outflow tract. We can see on the echocardiography post bypass, there is significant systolic anterior motion; so the thing to do is to go back on bypass, which we have done. We are using the ink test and we can see that there is at least 1 cm of anterior leaflet behind the coaptation line.
There are various ways of dealing with this, but in this case we have done a limited triangular resection of the anterior leaflet and used Gore-Tex chords to further displace the posterior leaflet into the ventricle. You can see the final result; the coaptation line is lower and there is no outflow tract obstruction.
So these are things that should be detected and fixed in the operating room, otherwise they will be the cause of persistent regurgitation in the early postoperative period.
Flameng and colleagues were the first to study systematically mitral valve regurgitation recurrence after mitral valve repair. They showed a linearized recurrence rate of about 4% per year. The mechanism for these recurrences after degenerative repair are usually due to either new pathology, so you could for example have infection, scarring, or fibrosis; they are due to progression of native disease, or new chordal rupture or chordal elongation; or they could be due to some technical failure of surgery. I will go through a few examples:
This is a patient who had previously undergone a mitral valve repair for posterior leaflet prolapse and presented with recurrent regurgitation. You can see on examining the valve, there is prolapse again of the posterior leaflet. All the chordae are intact and what you see is new chordal elongation. This case can be easily treated by a limited resection of the prolapsing segment. Alternatively, it could also be treated by Gore-Tex chordoplasty. We are also transposing a secondary chord to support the prolapsing segment. In this case, there is no need to remove the annuloplasty ring, as there is no change in the surface of coaptation of the leaflets. With correction of the prolapse, we would still get a good surface of coaptation and the echo result is satisfactory.
Chordal rupture is also another way in which the native disease can cause recurrence regurgitation. You can see clearly there is a ruptured chord to the P1-P2 junction of the posterior leaflet. In this case, as in most cases, the first step should be to remove the annuloplasty ring, as often the leaflets have fibrosed and shrunken, and usually one would require a ring of a smaller size than was present previously. The easiest way to treat prolapse when there is limited tissue, as seen here, would be with an artificial chord. We are using a 5-0 Gore-Tex suture to re-suspend that. We have placed a Physio annuloplasty ring and there is good result.
Chordal elongation can occur in the context of leaflet scarring the further you are from the initial operation. This is an example of such a case. You can see there is prolapse mainly of the P2-P3 region and you can appreciate the elongated chord as shown. What we have done is to re suspend the leaflet, assuming the only problem is prolapse; this should fix it. You can see there is still a central leak even though the prolapse has been fixed and a simple way to test whether the leaflet has shrunken is to lift the annuloplasty ring with your forceps to narrow the septal-lateral dimension and then as we saw, that fixed the regurgitation. That means the solution is to place a smaller ring. We are excising the existing ring, and then we resized the valve based on the surface of the anterior leaflet, and often would find that you need one or two sizes smaller compared to the initial ring. We often use a classic ring for re-repairs because you can modulate the shape and size required. You can see from the ink test, there is a good result and good surface of coaptation.
Leaflet disruption is another mechanism of failure. This is usually a technical failure due to excessive tension on the repair and the failure is usually in the early postoperative period. You can see from the echocardiogram, there is a type 1 dysfunction with at least moderate regurgitation and on examination of the valve you can see there has been some form of resection in P2, which has completely dehisced. The ring has to be excised and the repair has to be essentially done from scratch. The posterior leaflet was detached from the annulus and a sliding plasty is being performed after annuloplication. Annuloplication is necessary in such a case to take the tension off the new repair. An annuloplasty ring is placed with good result.
This is another case of leaflet disruption, also resulting in a Type 1 Carpentier dysfunction and again the problem here is excessive tension. You can see that the triangular resection was performed with excessive tension on the suture line. Here there is limited tissue and there are two options open: one is to patch the defect with pericardium and the other would be to perform an aggressive annuloplication to take tension off the suture line. In this case, we have used a pericardial patch to reconstruct the defect, placed an annuloplasty ring, and there is a good result.
This case is slightly more complicated. You can see an eccentric jet coming in the posterior annulus that seems to be outside the annuloplasty ring. This is a patient that had a mitral valve repair 15 years previously. You can see that there is dehiscence of the ring with an eccentric leak. There is also extensive scaring and fibrosis around the ring. The ring is excised, restrictive secondary chordae also excised. A cleft is being closed between P1 and P2. You can see the anterior leaflet is quite pliable, which is the key in mitral valve re-repair. If the anterior leaflet is pliable with a good surface of area, you can almost always re-repair the valve. You again shape a classic Carpentier ring to fit your dimensions because often the anterior leaflet has shrunken and the relationship between the septal lateral and commissure to commissure dimension that you see in a primary case might not hold in a re-repaired case, again good echocardiographic result.
Endocarditis is a cause of re-repair, but often not necessarily a cause of recurrent regurgitation. As you can see in this case on the echocardiogram, there is a mass attached to the anterior annulus but there is minimal regurgitation. This patient had a mitral repair which we performed about 12 months previously. Surgical inspection showed this mass mainly at the anterior annulus and also a smaller one in the posterior annulus. We first removed these masses and then, exploring the ring, we found that there was not much adherence between the ring and the cardiac tissue. You can appreciate that there is a lot of inflammatory tissue around the ring. The ring was excised. Initially we had thought that this was an abnormal tissue reaction to the ring, but later cultures of the excised mass have ensured that this was indeed endocarditis with a slow growing bacterium. We did not replace a ring in a case such as this. The valve remained competent and remained so four months after surgery.
This is a case in which there has been disruption of the repair. You can see on inspection there is a dehiscence of the ring and there is also a disruption in the leaflets. It is unclear in a case like this whether this is a residual regurgitation or a recurrent regurgitation; you would need immediate echocardiograms to assess that. One would excise the ring, size again. You can see that there is still a lot of posterior leaflet tissue. In this case, we would perform a sliding plasty to reduce the posterior leaflet tissue to an appropriate height. These are the cases very favorable to re repair when there is excess tissue because you have a lot of tissue to play with. The annulus has been plicated to take tension off the sliding plasty. We have done a posterior leaflet sliding plasty now, and the classic ring to complete it.
The essence is that most of these cases can be re-repaired if one sticks to the first principles, i.e., identify the dysfunction, identify the lesions, and then fix the lesions.
Thank you for your audience.