Percutaneous transcatheter closure of ostium secundum atrial septal defect (ASD) has become an alternative to conventional open surgical repair. Cardiac perforation is a rare complication after transcatheter closure of ASD by an Amplatzer Septal Occluder (ASO). We present a patient with hemodynamic collapse secondary to cardiac perforation occurring 5 months after placement of the ASO and discuss the complications of this device. A 14-year-old girl underwent transcatheter closure of ASD by the ASO in our institution. Transesophageal echocardiography showed ASD sized 17.4×15.0mm, with no aortic rim. The placement of the ASO was performed without complications, but 5 months after the procedure she started to complain of chest pain and subsequent syncope. She was brought to a local emergency department. Transthoracic echocardiography showed an important cardiac effusion with signs of cardiac tamponade. Emergency pericardial drainage was performed under echocardiographic control from the subxiphoidal region. Once she was hemodynamically stabilized, the patient was transferred to our institution immediately for the necessary emergency surgical procedure. The operation was performed through a median sternotomy and the bleeding source was identified. The left-side of the ASO disc had cut through the roof of the left atrium between the superior vena cava and the aortic root, creating a 5-mm perforation. There was another perforation at the aortic root in the region of the non-coronary sinus of Valsalva, approximately 5 mm. The metallic rim of the ASO could be easily seen protruding through the roof of the left atrium. Cardiopulmonary bypass was established and cardiac arrest induced. After opening the right atrium we found the ASO, which was positioned well. The ASO was removed and the perforations of the aortic root and the left atrium were closed with 5-0 polypropylene directly. Then the ASD was closed using an autopericardial patch. The patient was weaned off bypass without difficulty. The postoperative course of the patient was uneventful and free of neurologic events. Finally, we conclude that patients with an aortic rim defect may be at higher risk for device perforation. Such a patient should be carefully followed up by echocardiography.

An 81-year-old man underwent aortic valve replacement with a 21-mm Medtronic Mosaic porcine bioprosthesis for the treatment of bicuspid aortic valve stenosis. In addition to the appearance of chest discomfort on effort and a new diastolic murmur, echocardiography performed 2 years and 3 months after the surgery showed a high pressure gradient across the bioprosthetic valve and a reduction in the valve orifice area. Prosthetic valve dysfunction was diagnosed. During a repeat operation, 2 large tears on the left cusp and a subvalvular overgrown abundant pannus were observed, and the bioprosthetic valve was replaced with a 19-mm On-X mechanical heart valve. On analysis of the explant bioprosthesis, the right non-coronary stent post was bent outwards by approximately 9°, it compressed the left cusp by pulling the left right and left non-coronary stent posts closer together, thus altering the leaflet geometry and function. We speculated that pannus formation had resulted from turbulent blood flow caused by impaired or altered leaflet function. The 2 large tears appeared to be the result of contact with the bias cloth secondary to the stent distortion.

We evaluated bedside learning in the department of pediatric surgery by conducting a questionnaire survey of senior medical students at Chiba University School of Medicine. We obtained responses from 70 of 95 students (74%). Although 84% of students responded by making lists of patients' problems. Many students indicated insufficient knowledge about diseases and insufficient technical skills for medical treatment as the reasons they could not solve these problems. This finding indicates that students do not have sufficient basic knowledge and clinical skills for bedside learning. These skills must be acquired and evaluated before bedside learning can be started.

Liver fibrosis reflects tissue scarring in the liver due to the accumulation of excessive extracellular matrix in response to chronically persistent liver injury. Hepatocyte cell death can trigger capillarization of liver sinusoidal endothelial cells, stimulation of immune cells including macrophages and Kupffer cells, and activation of hepatic stellate cells (HSCs), resulting in progression of liver fibrosis. Liver cirrhosis is the terminal state of liver fibrosis and is associated with severe complications, such as liver failure, portal hypertension, and liver cancer. Nevertheless, effective therapy for cirrhosis has not yet been established, and liver transplantation is the only radical treatment for severe cases. Studies investigating HSC activation and regulation of collagen production in the liver have made breakthroughs in recent decades that have advanced the knowledge regarding liver fibrosis pathophysiology. In this review, we summarize molecular mechanisms of liver fibrosis and discuss the development of novel anti-fibrotic therapies.

Liver fibrosis reflects tissue scarring in the liver due to the accumulation of excessive extracellular matrix in response to chronically persistent liver injury. Hepatocyte cell death can trigger capillarization of liver sinusoidal endothelial cells, stimulation of immune cells including macrophages and Kupffer cells, and activation of hepatic stellate cells (HSCs), resulting in progression of liver fibrosis. Liver cirrhosis is the terminal state of liver fibrosis and is associated with severe complications, such as liver failure, portal hypertension, and liver cancer. Nevertheless, effective therapy for cirrhosis has not yet been established, and liver transplantation is the only radical treatment for severe cases. Studies investigating HSC activation and regulation of collagen production in the liver have made breakthroughs in recent decades that have advanced the knowledge regarding liver fibrosis pathophysiology. In this review, we summarize molecular mechanisms of liver fibrosis and discuss the development of novel anti-fibrotic therapies.