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February 25, 2021
Case Study 2

Case Study 2

Brief Case Description

The patient is a 52 year-old male who presented with new onset dyspnea on exertion. He has a known history of systolic murmur of mitral regurgitation for several years.

Transthoracic Echocardiography

Transthoracic echocardiography showed type II dysfunction with posterior leaflet prolapse causing mitral valve regurgitation. Doppler echocardiography showed an anteriorly directed jet and mitral regurgitation was graded severe. Both mitral valve leaflets were thickened and the anterior leaflet motion was normal. The morphology of the valve was in favor of Barlows disease. Left ventricular size was increased with an end-diastolic diameter of 6.1 cm. The left ventricular function was preserved with an ejection fraction of 61 %. Echocardiography also showed significant pulmonary hypertension with a peak gradient of 71 mmHg. There was mild (2+) tricuspid regurgitation.

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The patient was referred for reconstructive mitral and tricuspid valve surgery. Preoperative cardiac catheterization showed normal coronaries. Pulmonary artery pressure was 50/25 mmHg. Right atrial pressure was 10 mmHg.

Operative Procedure

Intraoperative transesophageal echocardiography confirmed the diagnosis of posterior leaflet prolapse involving the P2 segment.

Mitral Valve Analysis

Following the exposure of the mitral valve, we first performed valve analysis using Carpentiers reference point technique. The goal of mitral valve analysis is to confirm, complete or modify echocardiographic findings. 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 case, valve analysis confirmed the prolapse of the P2 segment due to both chordae elongation and rupture. We also noticed excess leaflet tissue of the prolapsing segment. The anterior leaflet was large with moderate excess tissue.

Following this complete echocardiographic and operative valve analysis, we can summarize the pathophysiological triad as follows:

Etiology : Form fruste of Barlows disease ( the age of the patient, the long-lasting history of systolic murmur and morphology of the valve on echocardiography and during intraoperative valve analysis were all in favor of this etiology)

Lesions: chordae rupture and elongation

Dysfunction: Type II posterior leaflet

Reconstructive Procedure

This was a case of extensive prolapse of P2 segment as more than one third of the length of the free edge of P2 was involved. Therefore we performed a quadrangular resection of the P2 segment. This technique has the advantages of excising most pathological tissues, creating a more normal geometry of the leaflet, and decreasing the tension on the reconstructed leaflet.

As shown below, the height of remnants P1 and P3 was 18 mm and 17 mm respectively (Fig A). The gap between the two segments was 18 mm. As these measures were all inferior to 20 mm, we used annular plication technique to reduce the size of the posterior annulus and to approximate P1 and P3 segments (Fig B). Leaflet continuity was restored with interrupted 5-0 monofilament sutures. Finally, a remodeling annuloplasty was performed using a 38 mm Carpentier Edwards Physio ring (Fig C). The correct sizing of the ring is of critical importance in patients with Barlows disease to minimize the risk of post-repair systolic anterior motion (SAM).

The patient also underwent a tricuspid remodeling annuloplasty with a 34 mm Carpentier-Edwards Classic ring for type I dysfunction due to annular dilatation. The indications for tricuspid valve reconstruction were primarily the presence of mild (2+) tricuspid regurgitation and pulmonary hypertension.

Postbypass Transesophageal Echocardiography

Postbypass transesophageal echocardiography showed a competent mitral and tricuspid valve with no residual regurgitation.

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