[Spontaneous Renal Rupture of Acquired Cystic Kidney Disease after Coronary Artery Bypass Grafting:Report of a Case].

We described a hemodialysis patient with spontaneous renal rupture of acquired cystic kidney disease (ACKD) after off-pump coronary artery bypass grafting(OPCAB). A 53-year-old man was transfer to our hospital with a diagnosis of unstable angina pectoris. He became ventilated due to congestive heart failure 3 days and underwent OPCAB on schedule 6 days after hospitalization. He suddenly complainted of colicky frank pain 31 days after surgery. Computed tomography (CT) demonstrated bulky hematoma with swollen kidney. Treatment included blood transfusions, withdrawal of anticoagulation, administration of vitamin K, and bed rest. The patient's symptom disappeared. A month later CT showed that the hematoma had been absorbed.

[Coronary Artery Bypass Grafting to the Left Anterior Descending Artery via Anterior Minithoracotomy after Surgery for Acute Papillary Muscle Rupture;Report of a Case].

We presented a case with chronic occlusion of the left anterior descending artery(LAD) after mitral valve replacement (MVR). An 80-year-old man was transferred to our hospital with a diagnosis of acute myocardial infarction. Before coronary angiography, the patient suddenly fell in a state of cardiogenic shock. Echocardiography revealed acute mitral regurgitation due to anterior papillary muscle rupture. Although emergency MVR was performed, introduction of percutaneous cardiopulmonary support (PCPS) and intraaortic balloon pumping ( IABP) was needed to come off cardiopulmonary bypass. Postoperative coronary angiography revealed chronic occlusion of LAD. The left internal thoracic artery was anastomosed to LAD via anterior minithracotomy to avoid median re-sternotomy. The postoperative course was uneventful and the cardiac function improved.

[Valve Replacement for Tricuspid Regurgitation with Congenitally Corrected Transposition of the Great Arteries].

Congenitally corrected transposition of the great arteries accounts for less than 1% of congenital heart diseases, and is defined as ventriculoarterial and atrioventricular discordance. We report a case of a 56-year-old woman complaining of persistent cough, who was diagnosed with congenitally corrected transposition of the great arteries and dextrocardia. Moderate regurgitation of the systemic tricuspid valve was revealed. The surgeon was positioned on the left side of the patient, and performed tricuspid valve replacement through the left atrium. Furthermore, mitral valve annuloplasty, atrial septal defect closure, and myocardial electrode implantation were performed. The postoperative course was uneventful.

[Successful treatment using thoracic endovascular aortic repair (TEVAR) to mycotic aortic aneurysm; report of a case].

We describe a case with mycotic aneurysm in a descending thoracic aorta. We applied thoracic endovascular aortic repair (TEVAR) technique to that aortic aneurysm after administering the high dose antibiotics and controlling the infection. Postoperative course was uneventful and he was in a good condition.

Multiple papillary fibroelastoma: report of a case and implications for management.

A 59-year-old woman with chest discomfort was transferred to our hospital. Echocardiography was suggestive of multiple papillary fibroelastoma (PFE). Tumors on both the left and right coronary cusps were confirmed macroscopically and pathologically and a small tumor was noted microscopically on the non-coronary cusp. Aortic valve replacement was successfully performed. The treatment and recurrence rate of PFE is controversial due to its rarity. Given that multiple tumors were seen in the present case and that possible recurrence has been reported elsewhere, valve replacement may be a better choice for surgical repair than valvoplasty in some cases, such as a single PFE in which plasty may be difficult or multiple PFEs regardless of impaired valve function.

Surgery for aortic regurgitation due to dehiscence of aortic valve commissure.

A 74-year-old man underwent aortic valve replacement due to aortic regurgitation after two months of medication for congestive heart failure. At surgery, the cause of the aortic regurgitation appeared to be dehiscence of an aortic valve commissure. Dehiscence was closed with mattress sutures from outside of the sinus. Dehiscence of an aortic valve commissure is rare and difficult to be diagnosed preoperatively, and we carefully repaired it, and the patient had a good recovery.

Repair of traumatic tricuspid regurgitation by bicuspidization.

Traumatic tricuspid regurgitation is a fairly rare complication following blunt chest trauma but not as uncommon as it was believed to be before the advent of transthoracic echocardiography. We report a case of severe tricuspid regurgitation with ruptured chordae tendineae 10 years after blunt chest trauma that was successfully repaired with a simple method. The operative technique consisted of plication of the anteroposterior commissure to create a bicuspid valve, along with ring annuloplasty.

Interleukin-1 induces the expression of vascular endothelial growth factor in human pericardial mesothelial cells.

Vascular endothelial growth factor (VEGF) is a mitogen for endothelial cells. We have studied the production of VEGF by human pericardial mesothelial cells. Mesothelial cells were separated by scraping the pericardial surface during cardiac surgery and cultured. When stimulated with interleukin (IL)-1alpha, pericardial mesothelial cells expressed VEGF mRNA and protein in concentration- and time-dependent manners. Hypoxia was also found to enhance mesothelial VEGF mRNA expression. The cells expressed mRNA for Flt-1 (VEGF receptor 1) and Flk-1 (VEGF receptor 2), and exogenous VEGF was found to have migration-promoting activity on cultured cells. We conclude that pericardial mesothelial cells express VEGF, which may serve as an autocrine growth-regulatory mechanism.

Interferon-gamma upregulates retinoic acid-inducible gene-I in human pericardial mesothelial cells.

OBJECTIVE: Retinoic acid-inducible gene-I (RIG-I) is a member of the DExH box family proteins and serves as an intracellular signalling molecule involved in the regulation of various genes. Mesothelial cells are active in generating a variety of bioactive factors, and RIG-I may serve as a potential intracellular molecule regulating part of these factors. We have addressed the expression of RIG-I in pericardial mesothelial cells. METHODS AND RESULTS: Cultures of human mesothelial cells separated during cardiac surgery were established. Interferon (IFN)-gamma was found to stimulate the expression, in cultured mesothelial cells, of RIG-I mRNA and protein in time- and concentration-dependent manners. We also performed immunohistochemical analysis of heart tissues to examine the expression of RIG-I in mesothelial cells. Intense immunoreactivity was detected in reactive pericardial mesothelial cells in non-specific pericarditis and in dilated cardiomyopathy. CONCLUSION: RIG-I may be involved in the inflammatory reaction in pericardial mesothelial cells.

Systolic anterior motion of the mitral valve despite the sliding leaflet technique for repair of the mitral valve.

We report a systolic anterior motion of the anterior mitral leaflet despite employing the sliding leaflet technique for repair of mitral valve regurgitation. A 65-year-old man with chronic, symptomatic mitral regurgitation due to ruptured chordae tendineae underwent mitral valve repair by quadrangular resection of the posterior leaflet and sliding leaflet technique with ring annuloplasty. After weaning from cardiopulmonary bypass, left ventricular outflow obstruction developed and transesophageal echocardiography demonstrated systolic anterior motion of the mitral valve and severe mitral regurgitation. Non-operative treatment resolved the outflow tract obstruction, systolic anterior motion and mitral regurgitation. We conclude that post-repair systolic anterior motion can still occur after the sliding plasty procedure and that medical treatment can successfully resolve systolic anterior motion and outflow tract obstruction in most patients.

Platelet-activating factor enhances the expression of nerve growth factor in normal human astrocytes under hypoxia.

Nerve growth factor (NGF) is required for the survival of neurons. We have addressed the effect of platelet-activating factor (PAF), one of the mediators of ischemic injury of the brain, on NGF expression in astrocytes. Normal human astrocytes in culture were stimulated with PAF, and levels of NGF mRNA and protein were analyzed by reverse transcription-polymerase chain reaction (RT-PCR), real-time quantitative PCR and enzyme-linked immunosorbent assay (ELISA). PAF increased the expressions of NGF mRNA and protein in astrocytes in time- and concentration-dependent manners. After 48-h stimulation, 10 nmol/L PAF increased the levels of NGF protein in astrocyte-conditioned medium by 1.4-fold. The PAF-induced stimulation of NGF expression was further enhanced (2.1-fold of the control) in the cells under hypoxic culture condition. BN52021 (Ginkgolide B), an antagonist for PAF binding sites, suppressed the effect of PAF. We conclude that PAF enhances NGF gene expression in human astrocytes, and the PAF-induced increase in the expression of NGF under hypoxia may benefit the protection of the nervous tissue by promoting neuronal survival.

Upregulation of retinoic acid-inducible gene-I in T24 urinary bladder carcinoma cells stimulated with interferon-gamma.

Urinary bladder epithelial cells play an important role in the host defense against urinary tract infections. Interferon-gamma (IFN-gamma) is a potent cytokine that regulates immune responses by inducing multiple genes in many types of cells including urinary bladder epithelial cells. Retinoic acid-inducible gene-I (RIG-I) is a member of the DExH-box family, which is involved in various reactions related to RNA metabolism, and is induced in leukemic cells by retinoic acid or in endothelial cells by lipopolysaccharide. We have studied the expression of RIG-I in T24 cells, a cell line derived from human urinary bladder epithelial carcinoma cells. IFN-gamma stimulated T24 cells to express RIG-I mRNA and protein in concentration- and time-dependent manners. Immunohistochemical analysis revealed the expression of RIG-I in the urinary bladder epithelium from a patient with chronic urinary tract infection and in a bladder epithelial carcinoma. We conclude that RIG-I may play some role in inflammatory reactions in the urinary tract epithelium.

Expression of retinoic acid-inducible gene-I in vascular smooth muscle cells stimulated with interferon-gamma.

Vascular smooth muscle cells (SMC) play an important role in atherogenesis and vasospasm. Interferon-gamma (IFN-gamma) is a potent cytokine that regulates immune and inflammatory responses by inducing multiple genes in many types of cells including SMC. Retinoic acid-inducible gene-I (RIG-I) is a putative RNA helicase, but its physiological function is not known. RIG-I is induced in leukemic cells by retinoic acid or in endothelial cells by lipopolysaccharide. We have studied the expression of RIG-I in cultured SMC from human umbilical artery. IFN-gamma stimulated SMC to express RIG-I mRNA and protein in concentration- and time-dependent manners. Immunohistochemical analysis revealed the expression of RIG-I in SMC in vivo. We conclude that RIG-I may play some pathophysiological role in immune and inflammatory reactions in SMC.

Heparin inhibits IFN-gamma-induced fractalkine/CX3CL1 expression in human endothelial cells.

Heparin is primarily used as an anticoagulant but has many biological functions as well. It binds with high affinity to a range of cytokines including interferon-gamma (IFN-gamma) and members of chemokine superfamily. IFN-gamma is a proinflammatory cytokine that plays a pivotal role in immune and inflammatory responses; and in endothelial cells, it regulates the expression of fractalkine/CX3CL1 that is a potent agonist for the chemotaxis and adhesion of monocytes and lymphocytes. We have investigated the effect of heparin on the fractalkine expression in human umbilical vein endothelial cells (HUVEC) in culture. HUVEC were treated with approximately 100 mg/mL heparin and the expression of the IFN-gamma-induced fractalkine mRNA and protein were measured by reverse transcription-PCR and western blotting. The IFN-gamma-induced expressions of fractalkine mRNA and protein were inhibited by heparin in a concentration-dependent manner. Heparin also inhibited adhesion of mononuclear cells (MNC) to HUVEC monolayers stimulated with IFN-gamma, but it did not inhibit the MNC adhesion to the monolayers stimulated with interleukin-1beta. Electrophoretic analysis demonstrated direct binding of heparin to IFN-gamma and heparin was found to partially block the binding of IFN-gamma to IFN-gamma receptor (IFN-gamma R). Heparin may play a regulatory role in inflammatory and immune responses by modulating the interaction between leukocytes and the vascular endothelium.

Effect of double-stranded RNA on the expression of epithelial neutrophil activating peptide-78/CXCL-5 in human endothelial cells.

Epithelial neutophil activating peptide-78 (ENA-78)/CXCL-5 is a member of CXC chemokines. ENA-78 was originally described as a factor produced by epithelial cells only. But other types of cells including vascular endothelial cells also produce it. ENA-78 production by endothelial cells may be important for the regulation of neutrophil activation in inflammatory reactions. Polyinosinic-polycytidylic acid (poly IC) is a synthetic double-stranded RNA, which mimics the viral infection when applied to cells and affects the expression of various genes related to inflammatory reactions. In the present study, we examined the effect of poly IC on the expression of ENA-78 in human umbilical vein endothelial cells (HUVEC). HUVEC in culture were treated with poly IC and the expression of ENA-78 mRNA and protein were analyzed by reverse-transcription polymerase chain reaction and enzyme-linked immunosorbent assay. Poly IC induced ENA-78 expression in time- and concentration-dependent manners. Th2-type cytokine IL-4 partially inhibited the induction of ENA-78 by poly IC. 2-Aminopurine, an inhibitor of dsRNA-dependent kinase, suppressed the induction of ENA-78 by poly IC. ENA-78 may be involved in the inflammatory reactions elicited by viral infection in endothelial cells.

Left thoracotomy approach in reoperative off-pump coronary revascularization: bypass grafting from the left axillary artery or descending thoracic aorta.

OBJECTIVE: Reoperative coronary bypass grafting is at high risk. Particularly in redo cases where the patent graft is running near the midline of the sternum, the graft may be exposed to injury by a median sternotomy and subsequent dissection. Whereas, off-pump bypass grafting from the left axillary artery or descending thoracic artery by a left thoracotomy approach is safe for preventing graft damage. METHODS: From March 1998 to February 2002, we performed off-pump coronary artery bypass grafting by a left thoracotomy approach in 9 patients. The left axillary artery was used as the inflow vessel in 4 cases, and the descending thoracic aorta in 5. RESULTS: The radial artery was anastomosed proximally to the axillary artery in 4 cases and the descending thoracic aorta in one case. The saphenous vein graft was anastomosed proximally to the descending thoracic aorta in 4 cases. Transdiaphragmatic minimally invasive bypass grafting for the right coronary artery was simultaneously performed in 3 cases. Postoperative cardiac events were ventricular arrhythmia in 6 cases and supraventricular arrhythmia in 3 cases. There was no damage to the patent grafts. Postoperative coronary angiography performed in 8 cases revealed all the grafts to be patent without stenosis. Cardiac symptoms were not found after the operation in any of the cases. CONCLUSIONS: These procedures can prevent the injury to patent grafts caused by a median sternotomy, and will be one of the useful strategies for reoperative off-pump coronary artery bypass grafting.