Ann Thorac Surg 1997;63:1774-1775
© 1997 The Society of Thoracic Surgeons
Case Report
Recanalization of the Left Atrial Appendage Demonstrated by Transesophageal Echocardiography
Mary Lynch, MD,
Jack S. Shanewise, MD,
George L. Chang, MD,
Randolph P. Martin, MD,
Stephen D. Clements, MD
Division of Cardiology, Department of Medicine, and Department of Anesthesiology, Emory University Hospital, Atlanta, Georgia
Accepted for publication January 21, 1997.
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Abstract
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Closure of the fibrillating left atrial appendage has been recommended during mitral valve operations to help prevent thrombus formation and systemic embolization postoperatively. We report recanalization of the appendage orifice in 6 patients after surgical closure by pursestring suturing at the time of mitral valve replacement. Transesophageal echocardiography demonstrated disruption of the closure line and partial recanalization of the sutured orifice with relatively high velocity flow between the left atrial body and the appendage.
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Introduction
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Left atrial thrombi are considered to be the major source of systemic embolization in patients with atrial fibrillation or rheumatic mitral valve disease [1, 2]. The majority of thrombi occur in the left atrial appendage [3]. Closure of the fibrillating appendage has been recommended during mitral valve operations to help prevent subsequent systemic embolization. In the past, amputation and pursestring suturing of the stump has been done; more recently, simple pursestring suturing or stapling from within the atrium without amputation has been favored [4]. The appendage can be clearly visualized only by transesophageal echocardiography or magnetic resonance imaging [5]. Before the advent of these imaging modalities, it would not have been possible to determine the success or failure of these techniques.
We report a series of 6 patients who were found to have partial recanalization of the left atrial appendage on a transesophageal echocardiographic study carried out either immediately after cardiopulmonary bypass or at a later date to evaluate valve function. All patients had undergone ligation of the left atrial appendage at the time of mitral valve replacement by pursestring suturing of the appendage from within the atrium without amputation.
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Case Reports
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A 57-year-old woman had both her aortic and mitral valves replaced in 1982 for rheumatic heart disease. She remained well until 1992, when she presented with increasing shortness of breath and was found to have severe mitral regurgitation through her bioprosthetic valve. She underwent replacement of both valves with St. Jude prostheses. At the time of operation her left atrial appendage was ligated. Three years later she presented with atrial fibrillation and hemolytic anemia. Transesophageal echocardiography revealed a moderate perivalvular jet of mitral regurgitation at the medial aspect of the mitral sewing ring that extended posteriorly along the interatrial septum. A small communication between the main left atrial body and the appendage was noted in the superior border of the ligated appendage (Fig 1
). Color-flow and pulsed-wave Doppler investigation indicated a relatively high velocity jet in and out of the appendage (Fig 2
). This jet was noted to be separate from the mitral paravalvular jet, which was confined to a different location of the left atrium. She subsequently underwent replacement of her prosthetic mitral valve and religation of the left atrial appendage, with resolution of her anemia.

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Fig 1. . (A) Transesophageal horizontal plane image of the left atrium (LA) demonstrates a small, slit-like orifice (arrow) in the surgically ligated left atrial appendage (LAA). (B) Blood flow into the appendage from the body of the LA is shown. (RA = right atrium).
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Fig 2. . Pulsed-wave Doppler tracing demonstrates flow in and out of the left atrial appendage. Peak velocity is 1 m/s.
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A 50-year-old man underwent replacement of a mitral valve with a Carbomedics prosthetic valve for severe mitral regurgitation, and the appendage was ligated. Three years later, he had a transient ischemic attack and underwent a transesophageal echocardiographic study to evaluate his prosthetic valve. His valve was functioning normally and no evidence of thrombus was present. A small communication was seen between the left atrium and its appendage at the superior-lateral border. A high-velocity jet was noted to enter the appendage during ventricular systole and empty during ventricular diastole. The patient was in atrial fibrillation, and no significant mitral regurgitation was found. There was no evidence of thrombus within the left atrial body or appendage.
A further 4 patients who had the left atrial appendage ligated at the time of mitral valve replacement were noted to have similar small, high-velocity jets by transesophageal echocardiographic assessment immediately after cardiopulmonary bypass. The communications were all located at the same site, through a small orifice at the superior-lateral aspect of the appendage. All patients were in atrial fibrillation.
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Comment
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All patients demonstrated a small communication between the body and appendage of the left atrium at the same anatomic location, the superior-lateral border of the appendage. As the recanalizations were all noted to be at the same location, this may indicate a possible weakness of the surgical closure at this point. The high-velocity flow demonstrated a to-and-fro pattern, entering the restricted appendage during ventricular systole and exiting during ventricular diastole, even in the presence of atrial fibrillation. Because all patients were in atrial fibrillation, it can be inferred that the regurgitation of blood into the left atrial body is due to increased filling pressure in the appendage and not due to atrial contraction.
In those 2 patients found to have recanalization of the appendage orifice several years after ligation of the appendage, it would seem unlikely that this communication would close off with time. Both of these patients were receiving long-term anticoagulation, which might have predisposed to incomplete sealing of the sutured orifice. The four communications found immediately after cardiopulmonary bypass may subsequently close. However, the relatively high velocity of these jets into the enclosed appendage space may prevent this.
The high-velocity jets seen could be confused with a mitral regurgitant jet. This confusion can be avoided by carefully evaluating the ligated appendage and following the anatomic course of any jet found. One of our patients had hemolytic anemia, which resolved after replacement of her malfunctioning mitral valve. The hemolysis was almost certainly due to her perivalvular regurgitation, although it is possible that turbulent flow through the narrow left atrial appendage orifice could have been a contributory factor. Thrombotic events are a potential complication of an incompletely ligated appendage, but they are unlikely to occur, as the velocities of the jets are high, preventing any stasis. The turbulence of the jets may predispose to further breakdown of the pursestring suture, leading to an enlargement of the communicating orifice. Should this occur, the velocity of the jets would fall due to equalization of pressures between the left atrial body and appendage. In this scenario, it is possible thrombi could form.
Flow into an incompletely ligated left atrial appendage is of clinical significance in that it can be confused with mitral regurgitation, it potentially could be a source of hemolysis, and it could lead to additional tension on suture lines, leading to further breakdown of the sutured orifice and resulting in complete reopening of the orifice of the sutured appendage. We recommend that a technique other than pursestring suturing should be considered for closure of the left atrial appendage.
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Footnotes
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Address reprint requests to Dr Lynch, Echo Lab D-433, Emory University Hospital, 1364 Clifton Rd, NE, Atlanta, GA 30322.
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References
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- Wolf PA, Abbott RD, Kannel WB. Atrial fibrillation: a major contributor to stroke in the elderly. The Framingham study. Arch Intern Med 1987;147:15614.[Abstract/Free Full Text]
- Coulshed N, Epstein EJ, McKendrick CS, Galloway RW, Walker E. Systemic embolism in mitral valve disease. Br Heart J 1970;32:2632.[Free Full Text]
- Shrestha NK, Moreno FL, Narciso FV, Torres L, Calleja HB. Two-dimensional echocardiographic diagnosis of left atrial thrombus in rheumatic heart disease: a clinico-pathological study. Circulation 1983;67:3417.[Abstract/Free Full Text]
- Landymore R, Kinley CE. Staple closure of the left atrial appendage. Can J Surg 1984;27:1445.[Medline]
- Aschenberg W, Schluter M, Kremer P, Schroder E, Siglow V, Bleifeld W. Transesophageal two-dimensional echocardiography for the detection of left atrial appendage thrombus. J Am Coll Cardiol 1986;7:1636.[Abstract]
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