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Ann Thorac Surg 1996;61:1528-1530
© 1996 The Society of Thoracic Surgeons
Department of Thoracic and Cardiovascular Surgery, Tohoku University School of Medicine, Sendai, Japan
Accepted for publication October 30, 1995.
| Abstract |
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| Introduction |
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Low output syndrome developed in the immediate postoperative period. Although a systolic murmur was noticed at apex on the first postoperative day, paraprosthetic leakage could not be detected by repeated transthoracic echocardiogram. As the patient's condition worsened progressively, cardiac catheterization was performed on the 15th postoperative day. The pulmonary wedge pressure was markedly elevated. On left ventriculography, the contrast medium regurgitated first into a small space close to the mitral prosthesis, then into the left atrial cavity, and the whole left atrium became densely opacified. Although pathogenetic details of the complication could not be diagnosed, findings obtained so far suggested the presence of paraprosthetic leakage.
Reoperation was performed on the following day under cardiopulmonary bypass. The left atrium was enlarged, and a thrill was palpable on its surface. When the left atrium was entered through the right interatrial groove, an oval intimal tear with irregular margin was found about 3 cm from the mitral annulus (Fig 1
). The size of the tear was 12 x 16 mm in diameter. When the intimal tear was widened, it became clear that a large cavity, 42 x 30 mm in diameter, existed beneath the intimal floor, which communicated with the left ventricle through paraprosthetic channel. It seemed that the entry began at the suture site beneath the annulus and dissected into the left atrial wall, forming a cavity, then ruptured into the left atrial cavity (Fig 2A
). There was no disruption of sutures or malfunction of the prosthesis. The dissected cavity and the intimal tear were closed by six mattress sutures with Teflon pledgets from inside the left atrium. The paraannular orifice was closed by four mattress sutures with pledgets, and the prosthetic valve again was fixed (Fig 2B
). We took care not to injure the coronary vessels in the atrioventricular groove. The patient's subsequent clinical course was uneventful.
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| Comment |
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Maeda and colleagues [3] have described much the same lesion as reported here. Unlike our case, their patient did not decompensate until the fourth month postoperatively. They thought that the lesion was due to an injury to the posterior annulus that occurred when the mitral prosthesis was excised. Goda and colleagues [4] have reported a case of dissection of the interatrial septum, probably due to excessive debridement of the annular tissue.
Although in our case the posterior leaflet and its subvalvular complex were left intact, a complication ensued. Judging from the reoperative findings, excessive traction on sutures in the posterior annulus at the first operation could have resulted in tearing through the tissues and disruption [2]. Inadvertent injury to the endocardium of the left atrium during the time of left atrial thrombectomy also could have added to the complication.
The diagnosis in this case was delayed for a long time. Because transthoracic echocardiograms could not demonstrate the lesion, we had to resort to catheterization. To our regret, in Japan, transesophageal echocardiography was not in common use in the 1980s. If transesophageal echocardiography had been performed, the patient probably would have been diagnosed and reoperated on earlier. Today, transesophageal echocardiography should be the first choice for diagnosis in this particular case.
Although this complication is a paraprosthetic leakage from a hemodynamic point of view, it may represent another variation of atrioventricular discontinuity after mitral valve replacement in a patient with severe degenerative annular disease with calcification [6], or another form of type I left ventricular rupture.
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