Cardiac ruptures are life-threatening complications after acute myocardial infarction. Types of rupture include left ventricle free-wall rupture, ventricular septal rupture, and papillary muscle rupture. Double rupture is defined as the coexistence of two of the above-mentioned forms of rupture. It complicates approximately 0.3% of acute myocardial infarction with the most frequent combination being free-wall rupture and ventricular septal rupture. We present the case of a 74-year-old man whose recent acute myocardial infarction was complicated by a combination of free-wall rupture and ventricular septal rupture. The patient underwent successful surgical treatment of the double myocardial rupture along with bypass grafting.

Acute aortic dissection causes various complications, but rarely causes rhabdomyolysis before the operation. A 69-year-old woman was found to have fallen unconscious and was transported to our hospital. Chest contrast computed tomography revealed thrombosed type A acute aortic dissection. On admission, hypoxia with paradoxical breathing was recognized and she complained of chest and back pain, and severe leg pain. In blood examination, elevation of myogenic enzymes and acute renal dysfunction were recognized. However computed tomography showed no signs of the ischemia of the intraperitoneal organs and legs. Myogenic enzymes decreased gradually and acute renal dysfunction improved by conservative therapy. In spite of strict antihypertensive therapy, enlargement of the false lumen and re-dissection were occurred, for this reason we scheduled ascending aorta replacement. During the operation we did muscle biopsy, and myogenic changes, such as cytolysis and lymphocyte infiltration, were recognized in muscles pathologically. However all various autologous antibody examinations were negative. We concluded that rhabdomyolysis was due to transient shock and caused preoperative marked elevation of myogenic enzymes.

An 82-year-old man was referred to our hospital for heart failure due to severe mitral regurgitation and severe tricuspid regurgitation. We performed mitral annuloplasty and tricuspid annuloplasty (TAP). Three weeks after surgery, he developed hemolytic anemia (HA). Transesophageal echocardiography revealed a defect in the left ventricular outflow tract that communicated directly with right atrium, and the jet was striking with the TAP prosthetic ring. HA was not controlled, so we performed re-operation. The defect was found in the atrioventricular membranous septum. The defect was closed and TAP was performed using an autologous pericardial roll again. We report a rare case of acquired left ventricular to right atrium communication after TAP.

A 16-year-old boy had a motorcycle accident and was given a diagnosis of blunt aortic injury (BAI) by contrast computed tomography (CT), complicated by diffuse brain injury, lung contusions and blunt liver injury. Despite conservative treatment his anemia worsened and further CT images revealed mediastinal hematoma. It was difficult to perform cardiopulmonary bypass with systemic heparinization because of his multiple injuries and therefore decided to perform endovascular stentgrafting. Aortography revealed that the proximal stent-graft landing zone to be very small, and therefore it was necessary to the cover left common carotid artery. Before stentgrafting, we performed a right subclavian artery-left common carotid artery bypass to attain a sufficient proximal landing zone, and stentgrafting was successful. We concluded that endovascular stentgrafting is an effective initial treatment for BAI complicated with multiple injuries. However, endovascular stentgrafting for BAI has some limitations because of the morphologic and anatomical characteristics of the thoracic aorta in cases of BAI. It is therefore important to perform endovascular stentgrafting for BAI on a case-by-case basis.

A 71-year-old male was admitted to our institution because of right leg pain and paleness, accompanied by sudden chest-back pain. The right femoral artery was not palpable. The reticulated cyanosis appeared on the right leg. Contrast enhanced computed tomography (CT) revealed an acute type B aortic dissection (TBAD) extending from the descending thoracic aorta to the left common iliac artery and right external iliac artery. The intimal tear was located at thoraco-abdominal aorta. There was a severe stenosis of the true lumen at bilateral common iliac arteries because of the dynamic compression caused by the extended false lumen. Blood to the right leg was not supplied from the dissected iliac artery, the peripheral circulation was maintained by collateral flow. The patient was diagnosed acute TBAD complicated with lower limb ischemia. An emergent right axillary artery-bifemoral arteries bypass was carried out for malperfusion of lower extremities. The symptoms in the lower limbs disappeared immediately. The bilateral femoral arteries were well palpated. However, 4 days later, uncontrollable severe hypertension and anuria appeared suddenly. Contrast enhanced CT revealed the stenosis of true lumen at bilateral renal arteries and an exacerbation of stenosis of true lumen at abdominal aorta. Emergent thoracic endovascular aortic repair (TEVAR) for entry closure was performed to improve the renal function and prevent mesenteric ischemia. Postoperative contrast enhanced CT revealed the complete closure of the entry tear and dilatation of the true lumen at the descending and abdominal aorta. At the bilateral renal arteries, the blood flow improved. The renal function recovered and mesenteric ischemia did not occurred. In this report, we presented a case of acute TBAD complicated with lower limbs ischemia and late onset acute ischemic renal failure. We first performed the right axillary artery-bifemoral arteries bypass grafting, after that we had to perform TEVAR to close the entry tear. One-stage emergent TEVAR should be considered for acute TBAD with the dynamic compression at the level of abdominal aorta in future.

A 73-year-old man had been followed up in our hospital after surgery for mitral regurgitation. At the age of 67, he underwent mitral valve plasty through a right mini-thoracotomy approach for atrial functional mitral regurgitation at our hospital. The mean trans-mitral pressure gradient was 5 mmHg after surgery but no heart failure symptoms were observed. At the age of 72, he began to notice fatigue during exertion. Transthoracic echocardiography revealed that the mitral valve regurgitation was controlled to a trace level, but the mean trans-mitral pressure gradient increased to 10 mmHg. Transesophageal echocardiography and contrast-enhanced cardiac computed tomography revealed the restricted opening of the mitral valve and pannus formation around the prosthetic ring. We thus diagnosed mitral stenosis due to pannus overgrowth. He underwent pannus excision and removal of the artificial ring. Postoperative echocardiography revealed that the mean trans-mitral pressure gradient was reduced to 3 mmHg and no residual mitral regurgitation was observed. He was discharged on postoperative day 11 with no major symptoms. He was in New York Heart Association functional class I at 1 year after the surgery and continues to be an outpatient.

A 74-year-old woman was scheduled for total arch replacement because of an enlarging thoracic aortic aneurysm in the aortic arch. Her preoperative blood test showed an elevated cold agglutinin with a titre of 2,048. There was concern about hemagglutination during hypothermia and hemolysis when returning to natural temperature under hypothermic circulatory arrest. We usually use moderate hypothermia (a minimum rectal temperature of 27℃) with circulatory arrest during total arch replacement. A cooling test was performed with her blood, which found no coagulation reaction in vitro at 25℃. There was a possibility that the total arch replacement would be carried out under moderate hypothermia, but it was by no means certain. After discussing the case with the hematologist, anesthetist, and clinical engineer, we decided on a minimum temperature of 30℃ during circulatory arrest because hemagglutination or hemolysis can become an issue in cardiopulmonary bypass. Coronary perfusion was maintained by infusing blood cardioplegia at 30℃ every 30 min. The intra-aortic occlusion balloon was inflated in the descending aorta, and perfusion of the spinal cord and lower body was initiated via the left femoral artery during circulatory arrest. Total selective cerebral perfusion flow was maintained at 1.5 times normal (20 ml/kg/min). There was no hemagglutination or hemolysis during the operation and no neurological complications in the postoperative period. For patients with cold agglutinin, individual cardiopulmonary bypass planning is necessary, depending on the severity of the condition and operative method.