Augmentation of estrogen receptor-mediated transcription by steroid and xenobiotic receptor.

The estrogen receptor (ER) is a key regulator of proliferation and differentiation in breast cancer cells. In the present study, the effect of steroid and xenobiotic receptor (SXR) on 17/beta-estradiol (E2)-induced transcription through ERalpha was studied. SXR augmented ER-mediated transcription in the presence of E2 in MCF-7 breast cancer-derived cells and CV-1 fibroblast-derived cells. On the other hand, SXR alone did not affect the estrogen response element (ERE)-containing promoter activity in CV-1 cells. SXR did not directly bind to ERalpha or ERE in vitro, indicating that SXR may affect ER-mediated transcription by altering cofactor binding to ER. Although SXR did not alter the binding between ERalpha and p300/CBP interacting protein (p/CIP), it decreased the binding of a specific corepressor, silencing mediator of retinoid and thyroid hormone receptors (SMRT) to liganded ERalpha as assessed by mammalian two-hybrid, glutathione S-transferase pull-down, immunoprecipitation and newly developed Liquid Chemiluminescent DNA Pull-Down Assays. These results indicate that SXR augmented ER-mediated transcription by dissociating SMRT from ERalpha. Thus, the expression of SXR in breast cancer cells may alter the ER signaling, which may play crucial role for growth and differentiation of breast cancer cells.

Endotoxin removal with a polymyxin B-immobilized hemoperfusion cartridge improves cardiopulmonary function after cardiopulmonary bypass.

BACKGROUND: Cardiac surgery using cardiopulmonary bypass (CPB) is performed widely, given the progress in cardioprotective methods. However, endotoxemia caused by CPB leads to systemic inflammatory response syndrome and deterioration of organ function. We evaluated the effectiveness of endotoxin removal with a polymyxin B-immobilized hemoperfusion cartridge (PMX) in CPB. MATERIALS AND METHODS: Pigs weighing about 25 kg were divided into control (n = 5) and PMX (n = 5) groups. Normothermic CPB was performed in the control group, while endotoxin was removed with PMX under normothermic CPB in the PMX group. Endotoxin removal was performed from the start to end of CPB. The end-systolic pressure-volume ratio (E(max)), left ventricular pressure (LVP), maximum and minimum rates of increase in LVP (+/-LVdp/dt), and cardiac output (CO) were measured 2 h after CPB, and the recovery rates of the parameters were compared between the two groups. A histopathological study was also conducted. RESULTS: The recovery rates of E(max), CO, and LVP were significantly better (P < 0.05) in the PMX group than in the control group. The PaO(2) 2 h after CPB was significantly higher (P < 0.05) in the PMX group than in the control group. The interleukin (IL)-8 level 2 h after CPB was significantly lower (P < 0.05) in the PMX group. Histopathologically, the heart and pulmonary tissues were better preserved in the PMX group. CONCLUSION: The PMX treatment reduced the inflammatory reaction caused by CPB, and cardiac and pulmonary functions after normothermic CPB were well preserved.

Effects of the COX-2 inhibitor FK3311 on ischemia - reperfusion injury in the rat lung.

Ischemia-reperfusion injury is induced by activation of the arachidonic acid cascade following the induction of cyclooxygenase-2. This study evaluated the effects of a selective cyclooxygenase-2 inhibitor, FK3311, on warm ischemia-reperfusion injury in the lung. Male Wistar rats were divided into two groups. In the FK3311 group (n = 27), FK3311 (4 mg/kg) was administered intravenously 5 min before ischemia, while in the control group (n = 27) only vehicle was injected. Warm ischemia was induced for 1 h by clamping the left hilus. The arterial oxygen pressure (PaO(2)) and saturation (SaO(2)) were measured 30 and 120 min after reperfusion. Serum thromboxane B(2) and 6-keto-prostaglandin F(1alpha) were also measured 30 min after reperfusion. Lung specimens were harvested 120 min after reperfusion for histologic examination and polymorphonuclear counts, and immunostained with cyclooxygenase-2. The 1-week survival rate in the two groups was compared. PaO(2) and SaO(2) 30 and 120 min after reperfusion were significantly (p < .05) better in the FK3311 group. Serum thromboxane B(2) levels were significantly (p < .05) lower in the FK3311 group. However, there was no significant difference in 6-keto-prostaglandin F(1alpha). Histologically, tissue damage was mild and polymorphonuclear infiltration was reduced in the FK3311 group compared to the control group. The expression of cyclooxygenase-2 in the alveolar epithelium based on immunostaining was suppressed in the FK3311 group. The 1-week survival rate was significantly (p < .05) higher in the FK3311 group. We conclude that FK3311 has protective effects on pulmonary ischemia-reperfusion injury, and results in improvement in the 1-week survival rate.

The effects of a cyclooxygenase-2 inhibitor, FK3311, on total hepatic ischemia-reperfusion injury of the rat.

BACKGROUND/AIMS: This study was designed to investigate the effects of a selective cyclooxygenase-2 inhibitor, FK3311, on warm ischemia-reperfusion injury of the rat liver. METHODOLOGY: Male Sprague-Dawley rats were used in this experimental study. Total hepatic ischemia was induced with a clamping portal triad. The animals were divided into two groups: the control group and the FK group, in which FK3311 (FK, 1.0 mg/kg) was administered via the penile vein. The serum levels of aspartate aminotransferase (AST), alanine aminotransferase (ALT), and lactate dehydrogenase (LDH) were measured 2 h after reperfusion, while those of thromboxane (Tx) B2 and 6-ketoprostaglandin (PG) F1alpha (stable metabolites of TxA2 and PGI2) were measured 30 min after reperfusion. The liver tissue blood flow was measured at preischemia, end-ischemia, and 30, 60, 90, and 120 min after reperfusion. The liver tissues obtained from animals at 2h after reperfusion were excised for histopathology. RESULTS: The serum levels of AST, ALT, and LDH were significantly lower in the FK group than in the control group. Similarly, in the FK group, the serum levels of TxB2 were significantly lower than in the control group. By contrast, the 6-keto-PG F1a levels were not significantly reduced. The liver tissue blood flow at 120 min after reperfusion was significantly higher in the FK group than in the control group. The histopathological study showed that hepatic tissue damage was milder in the FK group than in the control group. CONCLUSIONS: FK has protective effects on hepatic ischemia-reperfusion injury stemming from the marked inhibition of TxA2.

Mass screening of multiple abdominal solid organs using mobile helical computed tomography scanner--a preliminary report.

OBJECTIVE: The possibility of a new screening procedure for multiple abdominal solid organs using a mobile helical computed tomography (CT) scanner was evaluated. METHODS: A total of 4,543 residents, who were 40 years of age or older, received CT scanning without contrast medium. The mean age of participants was 64 years including 2,022 males and 2,521 females. RESULTS: A total of 2,105 abnormal findings were uniquely detected in 1,594 participants. Liver and kidney diseases including ureter occupied around 30% of total abnormal findings, respectively. Besides frequent cystic or calcified lesions, solid tumours were suspected in 56 lesions, which received further examination by specialized physicians. Five (9%) of them were confirmed as being malignant tumours including pancreatic cancer in two patients, and liver, lung and ovary cancers in one patient each, respectively. All five patients with each malignant lesion received curative operations. Small-sized abdominal aortic aneurysms and heart valve diseases were uniquely found in 22 and two patients, respectively. CONCLUSION: Qualitative diagnoses of solid tumours were difficult using CT findings without contrast medium. CT screening procedures require further investigation in aspect of the selection of examinees, CT scanning procedure, sensitivity and specificity, and cost-effectiveness.

Convenient and improved method to distinguish the intersegmental plane in pulmonary segmentectomy using a butterfly needle.

In the traditional method of segmentectomy, the plane between segments where removal is to occur is demarcated by inflating the normal lung, while keeping the segment to be removed airless. Our method, the opposite of convention, involves inflating only the involved segment by instilling oxygen through a butterfly needle into the bronchus subtending the segment. This saves time and therefore benefits the patient.

The comparison of mitogen-activated protein kinases that become activated within the left ventricular and right atrial tissues following heart transplantation in canine model.

The activation of p38 mitogen-activated protein kinase (MAPK) plays an important role in ischemia/reperfusion injury. Some reports have documented MAPKs activation of the myocardium in human models, using right atrial (RA) tissue for samples. This study compared the activation of MAPKs in left ventricle (LV) and RA tissues in canine heart transplantation. Four dogs were used as baseline data at two points, before and 20 min after warm ischemia (baseline model), and eight dogs (four pairs of donor and recipient) were used at other points: 4 h after cold ischemia, and at 10, 60, and 180 min after reperfusion (transplantation model). In the transplantation model, donor hearts were left in situ for 20 min after cardiac arrest, and were immersed in Celsior solution for 4 h after coronary flushing. Orthotopic heart transplantation was then performed. Two groups were created: the LV and RA groups (n = 4 in each group). Heart tissue was harvested from the left ventricular wall in the LV group and from the right atrial appendage in the RA group. The activation of MAPKs, including p38 MAPK, c-Jun N-terminal protein kinase (JNK), and extracellular signal-regulated protein kinase (ERK), was evaluated at each point. The activation patterns of p38 MAPK and ERK were similar in the RA and LV groups, but JNK activation was different in the two groups, after ischemia and reperfusion. Thus, RA tissue may be deliberately used as a substitute for LV tissue when investigating the activation of MAPKs in a human model.

Factors for weaning from a percutaneous cardiopulmonary support system (PCPS) in patients with severe cardiac failure: a comparative study in weaned and nonweaned patients.

The percutaneous cardiopulmonary support system (PCPS) has been widely accepted for the treatment of patients with severe cardiac failure. This system, which uses Seldinger's method through a percutaneous approach, enables rapid application in emergency situations. However, the indication for deployment and discontinuation of PCPS has not yet been established. We evaluated the results of PCPS use for the treatment of patients with severe cardiac failure and investigated factors that would predict successful weaning from PCPS. A total of 32 patients (23 men and 9 women) who had PCPS for the treatment of severe cardiac failure between January 1997 and October 2004 were retrospectively reviewed. The mean age of the patients was 57 +/- 17 years (range, 14 to 78 years). PCPS was necessary for severe cardiac failure after cardiac surgery in 15 patients, pulmonary infarction in 4, acute myocardial infarction in 3, acute myocarditis in 3, and other causes in 7. The mean duration of PCPS support in all 32 patients was 134 +/- 117 hours (range, 8 to 532). Twelve patients (38%) could be weaned from PCPS (group A), while the remaining 20 patients (62%) could not (group B). The incidence of cardiac arrest prior to PCPS use (n = 10, 31%) was significantly (P < 0.05) lower in group A (1/12, 8%) than in group B (9/20, 45%). There were significant differences in the APACHE II scores, urine output, serum lactate levels, and epinephrine and dopamine dose received from PCPS induction to 72 hours after PCPS use between the 2 groups (P < 0.05). Multivariate logistic regression analysis showed that an episode of cardiac arrest prior to PCPS induction was the only significant predictor for the unsuitability for discontinuation of PCPS. This retrospective study showed the limitation of PCPS therapy for patients with an episode of cardiac arrest who did not show improvement in their APACHE II score, urine output, serum lactate levels, and catecholamine dose received within 72 hours after PCPS induction. These results may help formulate criteria for indication and discontinuation of PCPS for patients with severe cardiac failure.

Human leukocyte antigen as a predictive factor of developing bilateral breast cancer in Japanese women.

To investigate the relationship between human leukocyte antigen (HLA) type and bilateral breast cancer, a total of 213 female breast cancer patients were entered into this study. The lymphocyte cytotoxicity test was used for HLA typing. HLA frequency and haplotype antigen frequency were calculated with a microcomputer. A chi-squared test was used for comparing HLA frequency. At the start point of follow-up, 187 patients (87.8%) had unilateral and 26 patients (12.2%) had bilateral breast cancer. After a 10-year follow-up, 183 patients (85.9%) were unilateral and 30 patients (14.1%) were bilateral. Haplotype frequency of A24-Cw7 was significantly higher in bilateral breast cancer patients compared with unilateral breast cancer patients (p < 0.001). After the 10-year follow-up, 4 of 187 patients (2.1%) with unilateral breast cancer developed bilateral breast cancer. Two of 19 patients (10.5%) with haplotype A24-Cw7 developed bilateral breast cancer, whereas only 2 of 168 patients (1.2%) without haplotype A24-Cw7 developed bilateral breast cancer (p < 0.01). The true frequency of developing contralateral breast cancer in patients with haplotype A24-Cw7 was 93 per 100,000 per year. The risk of bilateral breast cancer in patients with haplotype A24 and Cw7 is 12 times higher compared with those without the haplotype. HLA typing is useful for selecting patients who are at high risk of contralateral breast cancer.

Effect of the free radical scavenger MCI-186 on pulmonary ischemia-reperfusion injury in dogs.

BACKGROUND: Free radical scavengers and superoxide dismutase have been found to protect against cerebral ischemic damage, and it was suggested that oxygen free radicals contribute to ischemia-reperfusion injury induced by cerebral ischemic damage. MCI-186 (3-methyl-1-phenyl-2-pyrazolin-5-one) is a potent scavenger and inhibitor of hydroxyl radicals and protective agent of peroxidative injury. The purpose of this study was to evaluate the effects of MCI-186 on pulmonary ischemia-reperfusion injury in a simulated transplanted lung model. METHODS: Fourteen dogs were divided into two groups (n = 7 each). In the MCI group, MCI-186 was continuously administered at 3 mg/kg/hour intravenously (IV) from 30 minutes before reperfusion until 30 minutes after reperfusion (total administration time 1 hour). Vehicle was administered in the control group. Warm ischemia was induced for 3 hours by clamping the left pulmonary artery and veins. Simultaneously, the left stem bronchus was bisected and then anastomosed before reperfusion. The right pulmonary artery was ligated 15 minutes after reperfusion, and the right stem bronchus was then bisected. RESULTS: The respiratory gas exchange, hemodynamic changes, wet-to-dry weight ratio (WDR) and malondialdehyde (MDA) concentration in the tissue were significantly improved (p < 0.05) in the MCI group. The histologic damage was more severe in the control group and polymorphonuclear neutrophil (PMN) infiltration was reduced in the MCI group. CONCLUSION: MCI-186 has a protective effect on pulmonary ischemia-reperfusion injury through the inhibition of lipid peroxidation.

Pharmacokinetics of paclitaxel in a hemodialysis patient with advanced gastric cancer: A case report.

We report for the first time the possibility of weekly paclitaxel chemotherapy for a patient with advanced, nonresectable gastric cancer undergoing hemodialysis. A 50-year-old man with chronic renal failure due to bilateral polycystic kidneys, who had undergone hemodialysis three times a week for 5 years, presented with hematemesis in December 2004. Based on the diagnosis of gastric cancer with lymph node metastases, surgery was performed. On the 15th postoperative day, the patient was treated with chemotherapy using paclitaxel. Paclitaxel was administered at a dose of 60 mg/m2 as a 1 h iv infusion in 250 mL of saline. Hemodialysis was started 1 h after the completion of the paclitaxel infusion and was performed for 3 h. Paclitaxel was administered weekly on d 1, 8, and 15 on a 28-d cycle. The maximum plasma concentration of paclitaxel was 1390 microg/L. The area under the curve of paclitaxel was 4398.6 microg x h/L. Grade 2 leukopenia was encountered during the first cycle. The plasma concentrations of paclitaxel from 6 to over 24 h after the infusion were 0.01 to 0.1 micromol/L in our patient, and these concentrations have been shown to be effective on inhibiting the growth of gastric cancer cells without producing adverse side effects in the patient. The plasma concentration of paclitaxel was not influenced by hemodialysis. We conclude that the pharmacokinetics of paclitaxel is not altered in a patient with renal failure, and that weekly paclitaxel is a suitable treatment regimen for hemodialysis patients with advanced gastric cancer.

Xanthogranulomatous cholangitis causing obstructive jaundice: a case report.

This article reports the case of a 34-year-old woman with xanthogranulomatous cholangitis who developed obstructive jaundice. Microscopically, the bile duct was surrounded and narrowed by a xanthogranulomatous lesion, but no xanthogranulomatous cholecystitis was seen. Although percutaneous cholangiograms done via the transhepatic biliary drainage showed smooth narrowing of the upper to middle bile duct, the cytology of bile was diagnosed as class V adenocarcinoma. Therefore, right extended hepatectomy and extrahepatic bile duct resection were performed. The differentiation of benign and malignant strictures at the hepatic hilum is often difficult. Xanthogranulomatous cholangitis is one possible diagnosis of a bile duct stricture. Precise review of all the preoperative information is required to make a correct diagnosis.

Significance of local recurrence as a prognostic factor in the treatment of breast cancer.

The aim of this study was to evaluate both the risk factors of local recurrence and the prognostic significance of local recurrence in relation to surgical treatment and/or radiation therapy of breast cancer. A total of 1574 primary breast cancer patients, undergoing surgical treatment and/or radiation therapy between 1980 and 2001, were included in this study. Radical mastectomy was performed in 1144 patients, subcutaneous mastectomy in 141 and breast-conserving therapy in 289. The clinical stage was significantly earlier in the subcutaneous mastectomy and breast-conserving therapy groups than in the radical mastectomy group. A positive surgical margin was observed in 9 (6.4%) out of 141 patients in the subcutaneous mastectomy group and 51 (176%) out of 289 in the breast-conserving therapy group. Local recurrence occurred more frequently in the subcutaneous mastectomy and breast-conserving therapy groups than in the radical mastectomy group. Independent prognostic factors in local recurrence were lymph node metastasis in the radical mastectomy group, and surgical margin in the subcutaneous mastectomy group and the breast-conserving therapy group. Independent prognostic factors in overall survival were local recurrence, lymph node metastasis and estrogen receptor status in the radical mastectomy group, and lymph node metastasis and estrogen receptor status in the breast-conserving therapy group. In conclusion, the surgical margin status is an important factor in the risk of local recurrence in patients who have undergone a subcutaneous mastectomy or breast-conserving therapy. The significance of local recurrence for overall survival may be different among these three treatments.

Successful video-assisted mediastinoscopic drainage of descending necrotizing mediastinitis.

Descending necrotizing mediastinitis is an uncommon form of mediastinitis that can rapidly progress to septacemia. To date, the optimal surgical approach has remained controversial. We report a case of descending necrotizing mediastinitis that was treated successfully through a transcervical approach with video-assisted mediastinoscopy. In our case, because the abscess was separated into small compartments, especially in the paratracheal space, the abscess was drained using video-assisted mediastinoscopy. This less-invasive approach may be an option in the treatment of descending necrotizing mediastinitis, especially when the abscess in the paratracheal space is separated into small compartments.

Inhibition of cyclooxygenase-2 improves cardiac function following long-term preservation.

BACKGROUND: Cyclooxygenase (COX) is an intracellular enzyme that converts arachidonic acid to prostaglandin endoperoxide (PGG(2)). There are two isoforms of COX, namely constitutive COX-1 and inducible COX-2. It has been reported that COX-2 plays an important role in ischemia-reperfusion injury and that COX-2 mRNA and protein expression were up-regulated during cardiac allograft rejection. FK3311 is a suppressor of COX-2 activation. The purpose of this study was to evaluate the effectiveness of inhibiting COX-2 with FK3311 for the minimization of ischemia-reperfusion injury and for the improvement of donor heart function following transplantation in a canine model. MATERIALS AND METHODS: Adult mongrel dogs were used. After the measurement of hemodynamic parameters [cardiac output (CO), left ventricular pressure (LVP), and the maximum rates of increase and decrease in LVP (+/-LVdp/dt)], coronary vascular beds were washed out with a hypothermic (4 degrees C) University of Wisconsin (UW) solution following cardiac arrest in response to cold (4 degrees C) glucose-insulin-potassium solution. The heart was then excised and preserved in hypothermic (4 degrees C) UW solution for 12 h. FK3311 (3 mg/kg) was administered intravenously to five dogs prior to reperfusion, while vehicle was administered intravenously to a control group (n = 5). After 3 h of orthotopic transplantation using cardiopulmonary bypass, the hemodynamic parameters were compared with preoperative values of the donor animals under the condition of 10 mm Hg right atrial pressure and 5 mug/kg/min dopamine support. RESULTS: The recovery rates of CO and +/-LVdP/dt were significantly (P < 0.05) higher in the FK-treated dogs than in the controls (CO: 93 +/- 6 versus 66% +/- 4%; +LVdp/dt: 125 +/- 8 versus 77 +/- 10%; and -LVdp/dt: 81 +/- 7 versus 52 +/- 6%; for FK-treated versus control dogs, respectively). The recovery rate of LVP was higher in the FK-treated dogs than in the controls (90 +/- 5 versus 72 +/- 5%), but this difference was not statistically significant. Immunohistochemical staining revealed that COX-2 expression was reduced significantly in the myocardium of FK-treated dogs compared with controls. CONCLUSION: Hemodynamic parameters following transplantation were improved significantly in dogs treated with FK3311. Therefore, the inhibition of COX-2 improves transplanted cardiac function following long-term preservation.

The regulatory effect of tamoxifen on fibronectin expression in estrogen-dependent MCF-7 breast carcinoma cells.

We investigated the regulatory effect of tamoxifen (TAM) on fibronectin (FN) expression in estrogen-dependent MCF-7 breast carcinoma cells both in vitro and in vivo. in vitro, MCF-7 cells were cultured with 17beta-estradiol (E2) and/or TAM. In the animal experiment in vivo, MCF-7 tumors were grown in ovariectomized athymic mice by implanting a sustained release E2 pellet. The E2 pellets were removed after 3 weeks of E2 treatment. Animals were then divided into four groups: 1) an E2 (0.72 mg/pellet) pellet [E2(+)]; 2) an E2 and a TAM (5 mg/pellet) pellet [E2(+)TAM]; 3) no treatment [E2(-)] and 4) a TAM pellet [E2(-)TAM]. Following each treatment for 4 weeks, all animals were sacrificed and tumors were removed. Specimens, cells (in vitro) or tumors (in vivo), were homogenized and assayed for FN by Western blots. In the in vitro experiment, FN expression in MCF-7 cells decreased by incubating with 10(-9) M E2 and increased with 10(-6) M TAM. The effect of TAM increasing FN expression was inhibited by incubation accompanied with 10(-9) M E2 or 1 microg/ml transforming growth factor-beta (TGF-beta) neutralizing antibody. In the in vivo animal experiment FN expression in the tumors of E2(+) mice was lower than that of E2(-) mice. However, TAM increased FN expression in the tumors regardless of E2 pellet. These results suggest that TAM increases FN expression of MCF-7 breast carcinoma cells and that these regulatory effects of TAM on FN expression are partly mediated by TAM-induced TGF-beta.

The role of mitogen-activated protein kinases and the participation of intestinal congestion in total hepatic ischemia-reperfusion injury.

BACKGROUND/AIMS: The mitogen-activated protein kinase (MAPK) pathways are comprised of key regulatory proteins that control the cellular responses to both proliferation and stress signals. This study was performed to examine the degree of liver damage and MAPK activation induced by ischemia of varying durations, and the association between intestinal congestion and liver dysfunction after hepatic ischemia-reperfusion injury. METHODOLOGY: Male Sprague-Dawley rats were divided into five groups: sham-operated controls (no hepatic ischemia); 15, 30, or 45 min of total hepatic ischemia; or 45 min of total hepatic ischemia with a portosystemic shunt. Serum levels of aspartate aminotransferase, alanine aminotransferase, lactate dehydrogenase, interleukin-1beta and tumor necrosis factor-alpha, as well as liver tissue blood flow were measured. Liver was also sampled for MAPK analysis and histopathological examination. RESULTS: Total hepatic ischemia for over 30 min, with intestinal congestion, caused severe liver damage and an inflammatory cytokine response. A portosystemic shunt attenuated ischemia-reperfusion injury and inhibited inflammatory cytokine expression. Extracellular signal-regulated kinase was markedly phosphorylated in all groups other than the sham-operated group. p38 MAPK and c-Jun N-terminal kinase were highly phosphorylated in all groups receiving 30 min or more of ischemia. CONCLUSIONS: Prolonged warm total hepatic ischemia-reperfusion injury is associated with small intestinal congestion; a portosystemic shunt reduces liver damage by inhibiting inflammatory cytokine expression. MAPKs are markedly phosphorylated after reperfusion.

Superior vena cava rupture caused during balloon dilation for treatment of SVC syndrome due to repetitive catheter ablation--a case report.

A 29-year-old woman with an implanted AAI mode permanent pacemaker, who had undergone catheter ablation for inappropriate sinus tachycardia 4 times, experienced complications of superior vena cava (SVC) syndrome. Severe stenosis of the SVC wall was observed in computed tomograms. During balloon dilation for the treatment of SVC syndrome, the SVC was ruptured, resulting in cardiac tamponade. An emergency operation was performed using percutaneous cardiopulmonary support (PCPS). A longitudinal tear 1 cm in length was identified at the junction of the right atrium and the SVC, requiring a patch plasty using an autologous pericardium 2.5 cm x 3 cm in size. SVC rupture is a complication to be completely avoided when we perform balloon dilation for the treatment of SVC syndrome. Therefore, the indication of balloon dilation for the treatment of SVC syndrome requires critical examination and attention.