Degenerative Disease

A 70 year-old male with a known history of mitral regurgitation presented with new onset dyspnea on
exertion and fatigue. He was diagnosed with mitral regurgitation 5 years ago and followed very closely
by his cardiologist.
Transthoracic echocardiography showed type II dysfunction with anterior leaflet prolapse causing severe
mitral valve regurgitation. Left ventricular size was increased with an end-diastolic diameter of 5.7
cm. The left ventricular function was preserved with an ejection fraction of 70 %. Echocardiography
showed only minimal tricuspid regurgitation.The patient was referred for reconstructive mitral valve
surgery. Preoperative cardiac catheterization showed normal coronaries. Pulmonary artery pressure was
30/10 mmHg.

Intraoperative Transesophageal Echocardiography:

Intraoperative transesophageal echocardiography confirmed the diagnosis of anterior leaflet prolapse
involving the A3 segment of the anterior leaflet. Doppler echocardiography showed a posteriorly
directed jet and mitral regurgitation was graded severe.

Mitral Valve Analysis:

Following the exposure of the mitral valve, we first performed valvular analysis using Carpentier's
reference point technique. The goal of mitral valve analysis is to confirm , complete or modify
echocardiographic findings. As shown in the video, the free edge of the P1 segment , which is rarely
affected by abnormal leaflet motion, served as the reference point. We confirmed the normal leaflet
motion of P1 by pulling its free edge upward with a nerve hook. The P1 segment was neither prolapsing
as its free edge was not overriding the plane of the mitral annulus nor restricted. Using a second
hook, other valvular segments were examined in a systematic manner and compared to P1 to verify if they
were prolapsing. In this particular case, valvular analysis confirmed the prolapse of the anterior
leaflet (A3 segment ) due to chordae rupture. We also noticed excess leaflet tissue of the prolapsing
segment. The length of the free margin of the A3 segment was slightly less than 20 mm. There was

secondary mitral annular dilatation.

Following this complete valvular analysis, we can summarize the pathophysiological triad as follows:
Etiology : Fibroelastic deficiency
Lesions: chordae rupture
Dysfunction: Type II anterior leaflet

Reconstructive Procedure:

Anterior leaflet prolapse due to chordae rupture can be corrected by a variety of techniques including :
Limited triangular resection
Anterior leaflet secondary chordae transposition
Posterior leaflet chordae transposition
Artificial chordae

In this case, we were able to identify two strong secondary chordae which were attached to the
ventricular aspect of the A3 segment and suitable to be transferred to its free edge(fig A)

Considering Carpentier's rule that "no portion of the free edge greater than 4 mm should be left
unsupported", two secondary chordae were insufficient to correct the entire A3 prolapse as the length
of its free margin was about 20 mm. We then performed a composite technique applying two very limited
triangular resections to shorten the length of A3 free margin combined with two secondary chordae
transposition(fig B)

It is important to emphasize that these very limited resections were performed in this particular
setting where significant excess tissue of the A3 segment was present. An alternative reconstructive
technique would have been the additional use of artificial chordae. Finally a 34 mm remodeling
prosthetic ring was inserted (fig C)

A saline test was performed and showed a symetrical line of closure parallel and proximal to the
posterior leaflet attachment . Postbypass transesophageal echocardiography showed a competent mitral
valve with no residual regurgitation. Mean transvalvular gradient was 1 mmHg.