A 39-year-old woman, who had undergone aortic valve replacement with a Carpentier-Edwards pericardial bioprosthesis 16 years previously, was admitted to our hospital with a diagnosis of acute heart failure due to acute aortic regurgitation. An emergency operation was undertaken with the patient in a state of shock due to sudden cardiac arrest. The ascending aorta was cross clamped, and cardiac arrest was induced, and aortotomy was done. One of the leaflets of the CEP was entirely collapsed and dislocated to the LV side, which caused acute aortic regurgitation. Although there was no evidence of endocarditis, slight calcification and small perforation of the leaflet of the valve was observed. Aortic valve replacement was performed with a mechanical heart valve but it was impossible to wean from ECC, and therefore we additionally performed mitral valve annuloplasty with a prosthetic ring for moderate mitral regurgitation. After 4 h cardiopulmonary assistance, ECC was successfully withdrawn. She was discharged in a good condition an post operative day 29th.

Papillary muscle rupture is one of the common complications of acute myocardial infarction. We report a case of 77-years-old man with an acute posterior papillary muscle rupture without obvious coronary artery disease. The patient presented with cardiogenic shock and pulmonary edema. Emergency coronary angiogram showed no obstruction in coronary arteries. An echocardiogram and right heart catheterization data suggested acute mitral regurgitation caused by ruptured posterior papillary muscle. Percutaneous cardiopulmonary support was induced because of his unstable hemodynamics, and then emergency mitral valve replacement was performed. Intraoperative findings suggested some ischemic changes in the posterior papillary muscle. Pathologically, both old and new ischemic lesion presented in the same papillary muscle. Moreover, severe thickening of a small vessel wall was noted. This case presented one of the possible mechanisms of so-called idiopathic papillary muscle rupture.

The patient was a 50-year-old man who had undergone ascending aortic replacement and coronary artery bypass grafting at another hospital for acute type A aortic dissection 4 years before. He was diagnosed with hemolytic anemia 1 year after surgery for his progressive anemia and high serum lactate dehydrogenase level. He was referred to our hospital because frequent transfusion was required. A computed tomography showed severe kinking of the graft (110°), which we considered to be the cause of hemolysis. Peak pressure gradient was 60 mmHg. To remove the cause of hemolysis and to precipitate thrombosis of the residual false lumen, we performed re-ascending aortic replacement and total arch replacement with a frozen elephant trunk. The postoperative course was uneventful and hemolysis resolved soon after the operation. Surgeons should be aware that severe kinking of a Dacron graft can be a cause of hemolysis.