[Sudden Chest Pain due to Early Bioprosthetic Valve Dysfunction:Report of a Case].

We report a case of bioprosthetic valve dysfunction and acute aortic valve regurgitation. The case was a 75-year-old female who had sudden onset chest pain. ST-segment depression in several leads on electrocardiogram( ECG) suggested acute coronary syndrome. Coronary angiography showed no significant stenosis in coronary arteries. Transesophageal echocardiography revealed severe aortic regurgitation, suggesting that angina was caused by myocardial ischemia associated with acute aortic regurgitation. She was diagnosed as having bioprosthetic valve dysfunction, and underwent redo aortic valve replacement. One leaflet of the bioprosthetic valve was torn along the stent post and caused bioprosthetic valve dysfunction. Failed bioprosthetic valve was removed and replaced by a mechanical valve.

[Traumatic Ascending Aortic Injury with Delayed Cardiac Tamponade due to Sternal Fracture].

The case was a 63-year-old male. He had a history of surgery for funnel chest at the age of 23. He overdrank and hit the anterior chest about two weeks before. He complained of persistent chest pain and palpitation, and was admitted because of atrial fibrillation and moderate pericardial fluid. Computed tomography (CT) showed a new sternal fracture, but dislocation and instability was mild. A few days later, sinus rhythm was restored and his heart failure improved. Unfortunately, on the 7th day, he suddenly suffered cardiopulmonary arrest. Ultrasonography revealed cardiac tamponade, and pericardiocentesis yielded 400 ml of bloody pericardial fluid collection. CT demonstrated clot mainly in the anterior pericardium, and emergent operation was performed. Bleeding from the anterior wall of the ascending aorta was repaired by placing one stitch. Postoperatively the patient remained unconscious, and CT of the brain showed hypoxic encephalopathy. After prolonged ventilator management, he was transferred to a rehabilitation hospital. In retrospect, the ascending aorta was close to the sternum in this patient, and sternal fracture might have caused injury of the ascending aorta.

Spinal cord injury following aortic arch replacement.

PURPOSE: Postoperative spinal cord injury is a devastating complication after aortic arch replacement. The purpose of this study was to determine the predictors of this complication. METHODS: A group of 254 consecutive patients undergoing aortic arch replacement via median sternotomy, with (n = 78) or without (n = 176) extended replacement of the upper descending aorta, were included in a risk analysis. The frozen elephant trunk technique was used in 46 patients. The patients' atherothrombotic lesions (extensive intimal thickening of > 4 mm) were identified from computed tomography images. RESULTS: Complete paraplegia (n = 7) and incomplete paraparesis (n = 4) occurred immediately after the operation (permanent spinal cord injury rate, 1.97%; transient spinal cord injury rate, 2.36%). A multivariable logistic regression analysis identified the use of the frozen elephant trunk technique (odds ratio 36.3), previous repair of thoracoabdominal aorta or descending aorta (odds ratio 29.4), proximal atherothrombotic aorta (odds ratio 9.6), chronic obstructive lung disease (odds ratio 7.1) and old age (odds ratio 1.1) as predictors of spinal cord injury (p < 0.0001, area under curve 0.93). CONCLUSIONS: Spinal cord injury occurs with a non-negligible incidence following aortic arch replacement. The full objective assessment of the morphology of the whole aorta and the recognition of the risk factors are mandatory.

[Severe Coronary Artery Spasm after Coronary Artery Bypass Grafting;Report of a Case].

Coronary artery spasm after coronary artery bypass grafting(CABG) is rare and often fatal. There is no established treatment for perioperative coronary spasm because of the rare and not fully understood complications. We report a 67-year-old male, who experienced perioperative spasm of native coronary arteries and the left thoracic artery graft following CABG. Several transcatheter intracoronary injections of isosorbide sulfate failed to relieve the spasm completely. After 5 days' circulatory support with intra-aortic balloon pumping, the cardiac function improved and the patient recovered. Echocardiography performed before discharge showed decreased left ventricular systolic function with apical akinesis. Postoperative coronary angiography revealed 4 of the 5 grafts were patent.

[Fifteen-year Follow-up of a Patient with Aortitis, Treated by Sino-tubular Junction Plication Using a Prosthetic Tube Graft for Aortic Regurgitation;Report of a Case].

A 43-year-old woman was diagnosed with aortitis associated with mild aortic regurgitation (AR) at the age of 25, which advanced to a severe grade requiring surgical treatment at age 28. Dilation of the sinotubular junction (STJ) was treated with ascending aortic replacement (Hemashield Gold 24 mm), which reduced AR from severe to mild. The patient conceived 9 years later and delivered a baby by cesarean section at 38 weeks of gestation. By appropriate control of inflammation with steroid, neither deterioration of the aortic valve nor cardiac function has been noted during the 15 years of follow-up after surgery.

Administration of anti-inflammatory M2 macrophages suppresses progression of angiotensin II-induced aortic aneurysm in mice.

Aortic aneurysm (AA) is a vascular disorder characterized pathologically by inflammatory cell invasion and extracellular matrix (ECM) degradation. It is known that regulation of the balance between pro-inflammatory M1 macrophages (M1Ms) and anti-inflammatory M2 macrophages (M2Ms) plays a pivotal role in AA stabilization. We investigated the effects of M2M administration in an apolipoprotein E-deficient (apoE-/-) mouse model in which AA was induced by angiotensin II (ATII) infusion. Mice received intraperitoneal administration of 1 million M2Ms 4 weeks after ATII infusion. Compared with a control group that was administered saline, the M2M group exhibited reduced AA expansion; decreased expression levels of interleukin (IL)-1ß, IL-6, tumor necrosis factor-α (TNF-α), and monocyte chemoattractant protein-1 (MCP-1); and a lower M1M/M2M ratio. Moreover, the M2M group exhibited upregulation of anti-inflammatory factors, including IL-4 and IL-10. PKH26-labeled M2Ms accounted for 6.5% of cells in the aneurysmal site and co-expressed CD206. Taken together, intraperitoneal administration of M2Ms inhibited AA expansion by reducing the inflammatory reaction via regulating the M1M/M2M ratio. This study shows that M2M administration might be useful for the treatment of AA.

[Severe coronary artery spasm immediately after aortic valve replacement].

We report a case of 72-year-old man with severe manifestations of coronary artery spasm immediately after aortic valve replacement (AVR), which was associated with hemodynamic and arrhythmic instability. The AVR was performed under mild hypothermic cardiopulmonary bypass (34 degrees C), and retrograde blood cardioplegia was intermittently delivered at the same temperature. Immediately after the operation, the patient suddenly developed severe bradycardia and hypotension, and repeated ventricular fibrillation. Percutaneous cardiopulmonary support system (PCPS) and intra-aortic balloon pumping (IABP) were required for this circulatory collapse. Echocardiography revealed left ventricular segmental dysfunction, and coronary artery bypass grafting (CABG) to the right coronary artery and the left ascending artery was performed [during CABG, coronary spasm was strongly suspected by repetitive ST elevation and depression on electrocardiogram (ECG) monitor]. Eventually, the spasm subsided with the intravenous infusion of nitrates, nicorandil, and diltiazem. The remaining postoperative course was uneventful and the patient was discharged on the 24th postoperative day in good clinical condition.

Clinical outcomes of medical treatment of acute type A intramural hematoma.

A retrospective study was performed in 30 patients who were treated for type A intramural hematoma from 1999 to 2008, of whom 24 were initially treated without surgical intervention. These 24 patients were followed up for 3.3 +/- 3.5 years (range, 0 days to 10.0 years). Four hospital deaths occurred (hospital mortality, 16.7%), there were 2 late deaths, and 2 other patients needed an operation during the follow-up period. The event-free survival rate (freedom from death or surgery) at 5 years was significantly lower in patients with maximal aortic diameter > or =48 mm than in those with diameters <48 mm (28.6% +/- 17.1% vs. 88.2% +/- 7.8%). Maximal aortic diameter > or =48 mm and computed tomography findings of a small intimal defect were significant predictors of rupture or progression of ascending aortic dissection. The outcome of medical treatment for type A intramural hematoma was acceptable during both the early and late periods, but patients with a relatively large aortic diameter or an intimal defect in the ascending aorta have a high probability of adverse outcome, and must be considered for surgery.