Coronary artery obstruction, pulmonary stenosis, aortic valve regurgitation, and enlargement of the neo-aortic root are major complications of arterial switch operation (ASO) for transposition of the great arteries (TGA). Supravalvular aortic stenosis following ASO is rarely reported, and technical factors should be considered as causes in such cases. We report a case of supravalvular aortic stenosis following ASO, in which we speculated that the cause of the stenosis was tissue overgrowth caused by the surgical suture. The patient was a 4-month-old girl with TGA (II) who had undergone ASO on the 12th day after birth. Neo-aortic anastomosis was performed with 7-0 polydioxanone absorbable suture (PDS^®, Ethicon, Somerville, NJ, USA). Transthoracic echocardiography performed 1 month after the surgery showed severe stenosis at the aortic anastomosis which worsened progressively. Therefore, the patient was reoperated 4 months after the previous surgery. The concentrically stenosed aortic wall at the anastomotic site was resected and aortic reanastomosis was performed using an interrupted suture pattern with 7-0 polypropylene (Prolene^®, Ethicon). The histological findings showed proliferation of collagenous fibers around the PDS^® suture. Because of the worsening stenosis over time and the histological findings, we speculated that the tissue overgrowth in reaction to the PDS^® suture was the main cause of the stenosis. Absorbable sutures are useful because they do not leave a foreign substance in the body ; however, the possibility of tissue overgrowth leading to anastomotic stenosis cannot be denied. When using absorbable suture, careful observation is mandatory until the material is completely absorbed.

A 67-year-old man was admitted with heart failure. He had a past history of closed chest trauma due to a traffic accident at the age of 24. He had been complaining of a gradual increase of fatigue since a few years after the accident and received medical treatment. At approximately 40 years of age, he underwent cardiac catheterization and was given a diagnosis of Ebstein malformation. However surgery was not recommended. An echocardiogram showed a laceration at the tricuspid valve, enlargement of the tricuspid valve annulus and severe tricuspid regurgitation. The displacement of tricuspid valve was not present. His case was complicated with severe liver dysfunction of Child-Pugh class B and Model for End-Stage Liver Disease score 15. We performed tricuspid valve replacement with a Mosaic 31 mm tissue valve. The patient required pleurodesis for refractory severe pleural effusion at 2-months and was discharged 6 months after the operation.