Brief Case Description

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 also showed mild 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 valve 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 valve segments were examined in a systematic manner and compared to P1 to verify if they were prolapsing. In this particular case, valve 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 valve analysis, we can summarize the pathophysiological triad as follows:

     Etiology : Fibroelastic deficiency

     Lesions: Chordae rupture

     Dysfunction: Type II anterior leaflet (A3 segment)

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. Therefore we 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 symmetrical line of closure parallel and proximal to the posterior leaflet attachment (See video). The patient also underwent a tricuspid valve remodeling annuloplasty. Postbypass transesophageal echocardiography (2D and 3D) showed a competent mitral valve with no residual regurgitation. Mean transvalvular gradient was 1 mmHg.

For more information refer to Current Status >> Degenerative Disease Section