Three-dimensional computed tomography angiography for the preoperative evaluation of coronary artery disease in lung cancer patients.

BACKGROUND: The number of elderly patients undergoing surgery for lung cancer is increasing. In this study, we assessed the usefulness of three-dimensional computed tomographicangiography (3D-CTA) for the detection of coronary disease in the elderly before surgical intervention for lung cancer. METHODS: One hundred twenty patients admitted to our institution for lung cancer resection were enrolled in the study. 3D-CTA was performed in all 120 patients. RESULTS: Seventy-one patients had normal findings, and forty-nine patients showed coronary stenosis on 3D-CTA examination. Among the latter 49 patients, 24 with slight stenosis underwent lung tumor resection, 23 had coronary angiography for severe stenosis before lung surgery and 2 were not eligible for lung resection because of very severe coronary stenosis. The diagnostic value of 3D-CTA was better than conventional CT. CONCLUSIONS: This study suggests the usefulness of 3D-CTA for the preoperative diagnosis of coronary ischemic disease in elderly lung cancer patients.

Immunohistochemical diagnosis of methylthioadenosine phosphorylase (MTAP) deficiency in non-small cell lung carcinoma.

Methylthioadenosine phosphorylase (MTAP) is involved in the metabolism of purines and converts methylthioadenosine (MTA) to adenine. It is abundant in all normal tissues but is deficient in various tumors. Here, we investigated MTAP deficiency in clinical samples of lung cancer using immunohistochemistry (IHC), and compared these results with those obtained by real-time PCR. Seventy-five samples were obtained from patients who underwent operations for non-small cell lung cancer (NSCLC). MTAP genetic analysis, using real-time PCR, and IHC were carried out on the samples. Methylation-specific primers were used to analyze methylation of the MTAP promoter, using DNA treated with sodium bisulfite. Sixty-nine of 75 samples were compared using both IHC and real-time PCR. The IHC results were consistent with those of real-time PCR in 56 samples. Of 62 positive samples tested by real-time PCR, only 49 (79%) were MTAP-positive by IHC. Seven samples were MTAP-negative by real-time PCR and IHC. In 13 samples of PCR (+) and IHC (-), six samples showed that the promoter region of MTAP was methylated. IHC is an accurate and useful diagnostic method for detecting MTAP deficiency in NSCLC, and the frequency of MTAP deficiency was found to be relatively high. The metabolic alterations diagnosed by IHC could be exploited for selective chemotherapy.

Correction to: Thoracic and cardiovascular surgery in Japan during 2001 : Annual report by the Japanese Association for Thoracic Surgery.

The original publication of the articles cited above included incorrect values.

Changes in false lumen after transluminal stent-graft placement in aortic dissections: six years' experience.

BACKGROUND: Transluminal stent-graft placements (TSGPs) are a new, less invasive procedure now recognized as the choice for aortic disease repair. Treatment of aortic dissections with TSGPs has resulted in good early results, but the long-term results and changes in the false lumen have not been elucidated in detail. METHODS AND RESULTS: TSGPs were performed in 49 patients with primary tears in their descending aortas, and the follow-up period ranged from 4 months to 6 years. The patients were divided into 32 acute-onset and 17 chronic dissections; of the acute-onset cases, there were 15 Stanford type A retrograde dissections. Periodic enhanced spiral CT was conducted after TSGP. The false lumen in the ascending aorta in 14 (93%) of the Stanford type A cases was obliterated completely within 3 months. The CT study was continued for >2 years for 17 acute-onset dissection and 11 chronic dissection patients. The average false lumen diameters of the proximal, middle, and distal descending aorta before treatment were 15.9, 16.2, and 15.6 mm in the acute-onset dissection group and 28.1, 25.2, and 21.0 mm in the chronic dissection group, respectively. The false lumen diameters 2 years after treatment were 3.0, 3.7, and 3.1 mm in the acute-onset dissection group and 10.6, 10.5, and 11.9 mm in the chronic dissection group, respectively. Two years after TSGPs, the false lumen of the thoracic aorta totally disappeared in 76% of the acute-onset dissection group and 36% of the chronic dissection group. No cases showed rupture after TSGP. CONCLUSIONS: Complete obliteration of the false lumen is more likely in acute-onset cases than in chronic cases.

Method of cell transplantation promoting the organization of intraarterial thrombus.

BACKGROUND: Endovascular aortic repairs have been developed as less invasive treatments for aortic aneurysms. Some aneurismal cavities, however, remain without organization, causing a re-expansion of the aneurysms. We studied cell transplantation into the aneurismal sac to promote the organization of thrombus for the complete healing of aneurysms. METHODS AND RESULTS: Skin fibroblasts and skeletal myoblasts were isolated from rats for cell transplantation. An intraarterial thrombus model was made by ligation of the carotid artery. Culture medium (medium group, n=11), collagen gel (gel group, n=11), fibroblasts with collagen gel (F group, n=15), myoblasts with collagen gel (M group, n=12), or mixture of fibroblasts and myoblasts with collagen gel (F+M group, n=14) were injected into the thrombus. After 28 days, histologically, the arterial lumens of the F and M groups were partly filled with fibrous tissues, whereas in the F+M group organization was almost completed and luminal sizes diminished. Immunohistochemical staining demonstrated that alpha-smooth muscle actin-positive cells were more abundantly contained in the organized area of the F+M group than in the other groups. We also analyzed cellular function in vitro with immunofluorescence; coculture of fibroblasts and myoblasts showed that the fraction of alpha-smooth muscle actin-positive fibroblasts increased. This phenomenon accounts for the rapid organization of thrombus in the F+M group in vivo. CONCLUSIONS: Cell transplantation accelerated thrombus organization. Especially, myoblasts enhanced differentiation of fibroblasts into myofibroblasts, contributing to rapid thrombus organization. Cell transplantation into unorganized spaces seems applicable to endovascular treatment of aneurysms.

Tenascin-C is an essential factor for neointimal hyperplasia after aortotomy in mice.

OBJECTIVE: Neointimal hyperplasia at the arterial anastomotic site is a critical problem during cardiovascular surgery. It has been suggested that tenascin-C (TN-C), an extracellular matrix (ECM) glycoprotein, might play an important role in neointimal hyperplasia. In this study, the direct contribution of tenascin-C to neointimal hyperplasia after aortotomy was examined using tenascin-C-deficient (TNKO) mice. METHODS AND RESULTS: A simple aortotomy model was constructed in mice. In wild-type (WT) mice, neointimal hyperplasia was observed at the suture sites at days 14 and 28. Immunohistochemical staining showed strong expression of tenascin-C in both neointima and media around the suture line at day 14. At day 28, tenascin-C staining was detected in neointima, but not in media. In tenascin-C-deficient mice, much less neointimal hyperplasia was seen compared to that in wild-type mice, and the mean neointima/media area ratio decreased to 52.8% and 34.3% at days 14 and 28, respectively. The proliferating cell nuclear antigen indices in wild-type mice were twice those in tenascin-C-deficient mice at day 14. There were fewer Alcian blue-positive proteoglycans deposited in the neointima of tenascin-C-deficient mice than in wild-type mice. These results suggest that tenascin-C promotes neointimal cell migration and proliferation, and the deposition of proteoglycans. CONCLUSIONS: We have presented direct evidence that tenascin-C is a crucial molecule in neointimal hyperplasia at anastomotic sites.

Role of dihydropyrimidine dehydrogenase inhibitory fluoropyrimidine against non-small cell lung cancer--in correlation with the tumoral expression of thymidylate synthase and dihydropyrimidine dehydrogenase.

5-Fluorouracil (5-FU) and its derivatives have been used worldwide for the treatment of several malignancies in solid organs. The effectiveness of these drugs is well proven in gastrointestinal malignancy, and has been reported upon the inverse correlation with the tumoral expression of dihydropyrimidine dehydrogenase (DPD). However, the significance of DPD expression in 5-FU based chemotherapy has not been well investigated in non-small cell lung cancer (NSCLC). We examined enzymatic activities and immunohistochemical expression of thymidylate synthase (TS) and DPD in 84 cases of NSCLC. In vitro sensitivity for 5-FU was tested in 53 cases of them to evaluate these predictive values for effectiveness of 5-FU. Efficacy of 5-chloro-2,4-dihydroxypyridine (CDHP), potent DPD inhibitor, was also examined in 27 cases of them. There was a reversal correlation between protein expression of DPD and sensitivity to 5-FU (r = -0.65; p < 0.001). Six (33.3%) of 18 cases with strong expression of DPD showed 10% or more increment of the anti-tumor effect by adding CDHP to 5-FU. DPD inhibitory fluoropyrimidine and examination of the tumoral expression of DPD might be a promising chemotherapeutic strategy in NSCLC.

Degradation of tenascin-C and activity of matrix metalloproteinase-2 are associated with tumor recurrence in early stage non-small cell lung cancer.

PURPOSE: To find out an effective prognostic factor for early stage non-small cell lung cancer (NSCLC), we examined the relationship of the degree of tenascin-C (TN-C) degradation in relapsed NSCLC tumors with the prognosis of the patients. The molecular mechanism of TN-C degradation was also evaluated. EXPERIMENTAL DESIGN: In 63 stage-1 NSCLC patients, TN-C protein was analyzed by Western blotting, and the activity of matrix metalloproteinase (MMP)-2 was examined by gelatin zymography in 23 stage-1 NSCLC patients. RESULTS: Degradation of TN-C was detected in 12 of 63 patients. TN-C degradation was detected in 9 of 17 patients (52.9%) that showed local and distant cancer recurrences. In short, in 9 of 12 patients (75%) showing TN-C degradation, lung cancer recurrence was recognized. The actual frequency of free-from-recurrence at 4 years was 28.1% in patients with tumors showing TN-C degradation, and actual frequency of free-from-recurrence at 4 years and 10 years was 82.1% and 76.6% in patients without TN-C degradation (P < 0.001). In 23 stage-1 NSCLC patients, in tumors with or without degraded TN-C, the mean ratio of tumor:normal-tissue of activated MMP-2 was 3.5 +/- 0.4 or 1.54 +/- 0.4, respectively. Significantly increased activity of MMP-2 was recognized in tumors showing TN-C degradation (P < 0.001). CONCLUSIONS: These results suggest that TN-C degradation is a reliable marker for recurrence potential of stage-1 NSCLC and that MMP-2 may be a protease breaking down TN-C in lung cancer.

Successful surgical treatment for an adult case of double aortic arch.

We present the case of a 39-year-old male who had complaints of dysphagia and throat pain. Computed tomography (CT), 3 dimensional CT and aortography revealed a double aortic arch (Edwards type IA). The patient underwent exploration through a left-sided thoracotomy and the left arch was divided at the distal site of the left subclavian artery, which completely relieved the esophageal compression.

Midterm results of stent-graft repair of acute and chronic aortic dissection with descending tear: the complication-specific approach.

BACKGROUND: Endovascular stent-graft placement for the treatment of patients with aortic dissection is emerging as an attractive alternative to conventional cardiac operations. However, there has been no report of longer-term follow-up. The purpose of this study is to describe our midterm results with endovascular stent-graft repair for the treatment of patients with aortic dissections. METHODS: Thirty-eight patients with aortic dissections with descending tears were treated with endovascular stent-grafting. Ten patients had acute type A, 14 patients had acute type B, and 14 patients had chronic type B dissection. Stent grafts fabricated from expanded polytetrafluoroethylene-covered Z stents were placed to close entry tears in all patients through the delivery systems introduced from the femoral or the iliac arteries. RESULTS: Two patients with complicated acute type B dissection, who would have required surgical intervention, died within 30 days of the procedure, although no other patients died within the same period. There were no late deaths during the mean follow-up period of 27 months. Early and late complication rates were 33% and 36%, respectively, in patients with acute dissection, whereas rates were 4% and 0% (P <.05 vs patients with acute dissection) in patients with chronic dissection. CONCLUSIONS: Entry closure with endovascular stent-graft placement may be a safe and effective method for the treatment of patients with aortic dissection. It could be an alternative to conventional surgical intervention in selected patients with chronic dissection. However, strict patient selection and close follow-up seem mandatory in patients with acute dissection receiving Z stent-based stent-grafts. Stent-graft repair should be delayed for acute type B dissection without complications.

Pharmacologic platelet anesthesia by glycoprotein IIb/IIIa complex antagonist and argatroban during in vitro extracorporeal circulation.

OBJECTIVE: Contact between blood and the synthetic surfaces of a cardiopulmonary bypass circuit leads to platelet activation, and resultant platelet dysfunction contributes to postoperative bleeding. We compared the effects of various platelet inhibitors on preservation of platelet function during simulated cardiopulmonary bypass circulation. METHODS: Fresh human blood was recirculated in an in vitro cardiopulmonary bypass model circuit. We measured various platelet activation markers including expressions of PAC-1 and P-selectin, annexin V binding, and microparticle formations by means of whole-blood flow cytometry. RESULTS: Two types of glycoprotein IIb/IIIa complex antagonists, peptide-mimetic FK633 and abciximab and prostaglandin E(1), significantly prevented platelet loss and the increase in binding of PAC-1, an antibody specific for fibrinogen receptor on activated platelets, during extracorporeal circulation of heparinized blood. These antagonists significantly suppressed but did not abolish P-selectin expression, annexin V binding, and microparticle formation. Anti-von Willebrand factor monoclonal antibody and aurin tricarboxylic acid (an inhibitor of glycoprotein Ib) had no effect on platelet activation during simulated cardiopulmonary bypass circulation. These data suggest that inhibition of fibrinogen binding glycoprotein IIb/IIIa complex is partly effective in attenuating platelet activation in a heparinized cardiopulmonary bypass model circuit. The direct thrombin inhibitor argatroban prevented platelet loss and expression of P-selectin significantly more than did heparin. A combination of FK633 with argatroban as a substitute for heparin further prevented platelet loss and platelet secretion during simulated cardiopulmonary bypass circulation, although the inhibition of microparticle formation was less. CONCLUSION: The inhibition of both platelet adhesion and thrombin may be effective to preserve platelet number and function during cardiopulmonary bypass circulation.

Locally applied cilostazol suppresses neointimal hyperplasia by inhibiting tenascin-C synthesis and smooth muscle cell proliferation in free artery grafts.

OBJECTIVE: Accumulation of smooth muscle cells and extracellular matrix in the intima of artery bypass grafts induces neointimal hyperplasia, resulting in graft failure. We investigated the inhibitory effect of locally applied cilostazol, an inhibitor of cyclic adenosine monophosphate phosphodiesterase III, on neointimal hyperplasia and the role of tenascin-C synthesis and smooth muscle cell proliferation in free artery grafts. Methods and results We established a distal anastomotic stricture model of free artery graft stenosis using rat abdominal aorta. In this model, neointimal hyperplasia was observed not only in the distal anastomotic site but also in the graft body at postoperative day 14 and was markedly progressed at day 28. Strong expression of tenascin-C was found in the media and neointima of the graft body. When cilostazol was locally administered around the graft using Pluronic gel, neointimal hyperplasia of the graft was significantly suppressed in comparison with gel-treated control graft. The mean neointima/media area ratio was reduced by 86.6% for the graft body and by 75.8% for the distal anastomotic site versus the control. Cilostazol treatment decreased cell proliferation and tenascin-C expression in the neointima. In an in vitro experiment using cultured smooth muscle cells isolated from rat aorta, cilostazol completely suppressed the tenascin-C mRNA expression induced by platelet-derived growth factor-BB. CONCLUSION: A single topical administration of cilostazol may suppress neointimal hyperplasia by inhibiting cell proliferation and tenascin-C synthesis in free artery grafts, presenting the potential for clinical use in vascular surgery.

Specific inhibition of p38 mitogen-activated protein kinase with FR167653 attenuates vascular proliferation in monocrotaline-induced pulmonary hypertension in rats.

OBJECTIVES: p38 mitogen-activated protein kinase is associated with many clinical entities characterized by inflammation. We postulated that inhibition of p38 mitogen-activated protein kinase with FR167653 attenuates inflammation and the development of pulmonary hypertension in monocrotaline-treated rats. METHODS: Rats were divided into 4 groups: (1) the control group (daily 0.9% saline), (2) the FR group (daily FR167653, 2 mg . kg(-1) . d(-1)), (3) the MCT group (daily 0.9% saline the day after a single monocrotaline dose, 60 mg/kg), and (4) the MCT+FR group (daily FR167653, 2 mg . kg(-1) . d(-1), the day after a single MCT dose). Body weight, pulmonary artery pressure, and morphometric changes of the pulmonary artery with the histopathologic method were observed weekly for 4 weeks. Also, p38 mitogen-activated protein kinase activity and inflammatory cytokine expression in the lung were measured. RESULTS: Four weeks after monocrotaline administration, mean pulmonary artery pressure in the MCT+FR group was lower than in the MCT group (MCT+FR vs MCT: 24.7 +/- 1.9 vs 36.5 +/- 2.1 mm Hg; P < .05). In morphometric analysis the percentage of medial wall thickness and the percentage of muscularization in the MCT+FR group were reduced compared with those in the MCT group after 4 weeks (P < .05); however, the number of macrophages was not significantly different. p38 mitogen-activated protein kinase activity was significantly attenuated in the MCT+FR group compared with in the MCT group (7.2 +/- 0.52 vs 2.1 +/- 0.23 fold-increase, P < .05, at 1 week). Although mRNA levels of tumor necrosis factor alpha and interleukin 1beta were reduced in the MCT+FR group compared with in the MCT group (tumor necrosis factor alpha: 1.18 +/- 0.36 vs 3.05 +/- 1.12 fold-increase, P < .05, at 2 weeks; interleukin 1beta: 2.2 +/- 0.34 vs 4.4 +/- 1.09 fold-increase, P < .05, at 1 week), FR167653 did not suppress increased monocyte chemotactic protein 1 mRNA expression induced by monocrotaline (3.2 +/- 0.62 vs 3.1 +/- 0.42 fold-increase, at 1 week). CONCLUSION: FR167653 significantly attenuates the expression of inflammatory cytokines, ultimately preventing the progression of pulmonary hypertension. These results suggest that p38 mitogen-activated protein kinase might play a central role in the molecular events that underlie the development and progression of pulmonary hypertension.

FR167653 diminishes infarct size in a murine model of myocardial ischemia-reperfusion injury.

OBJECTIVE: During myocardial ischemia-reperfusion injury, p38 mitogen-activated protein kinase is activated. We examined the effect of a highly specific inhibitor of p38 mitogen-activated protein kinase, FR167653, in an experimental model of regional myocardial ischemia-reperfusion. METHODS: CD-1 mice received FR167653 intraperitoneally 24 hours before 30 minutes of transient occlusion of the left anterior descending artery, followed by 120 minutes of reperfusion. The p38 mitogen-activated protein kinase activation and kinase activity were determined by Western blotting with monoclonal antibodies for the phosphorylated from of p38 mitogen-activated protein kinase or its substrate, activating transcription factor 2. Nuclear factor kappaB activity was measured by detecting translocation of nuclear factor kappaB to the nucleus. The expression of inflammatory cytokines was measured by ribonuclease protection assay. RESULTS: Pretreatment of mice with FR167653 before myocardial ischemia-reperfusion resulted in a reduction in p38 mitogen-activated protein kinase phosphorylation (P =.018), an inhibition of p38 mitogen-activated protein kinase activity (P =.047), a smaller amount of nuclear factor kappaB (P =.001), and a decrease in the expression of inflammatory cytokines (tumor necrosis factor alpha: P =.023, interleukin 1beta: P =.038, monocyte chemotactic protein 1: P =.0001) in the heart and the development of a significantly smaller infarct (P =.0069) relative to hearts from mice treated with vehicle alone. Activation of c-Jun N-terminal kinase and extracellular signal-regulated kinase were observed after myocardial ischemia-reperfusion without inhibition by FR167653. CONCLUSION: We conclude that FR167653 selectively inhibits p38 mitogen-activated protein kinase activation and activity during regional myocardial ischemia-reperfusion injury and efficaciously reduces infarct size (by 73.6%). Thus p38 mitogen-activated protein kinase inhibition may have a role in the treatment of myocardial ischemia-reperfusion.

Successful repair of an aortoesophageal fistula with aneurysm from esophageal diverticulum.

Aortoesophageal fistula is a rare, frequently fatal, cause of upper gastrointestinal bleeding, and there are few reported survivors of it. We report a successful surgical case of aortoesophageal fistula associated with an infective thoracic aortic aneurysm. The patient had been diagnosed as having an esophageal diverticulum 8 months before admission. The aortoesophageal fistula was completely resected, followed by esophagojejunum anastomosis and patch closure for the entry of the aneurysm and omental coverage to the wall of the descending aorta in one stage. In this case, esophageal diverticulum was diagnosed before the development of an aortoesophageal fistula associated with an aneurysm.

Effective cardiac resynchronization after Dor procedure and mitral annuloplasty.

Endoventricular circular patch plasty (Dor ventriculoplasty) is an effective strategy for severely impaired left ventricular function due to ischemic cardiomyopathy. Cardiac resynchronization therapy improves cardiac function in patients with severe congestive heart failure and an intraventricular conduction delay. The present case demonstrates the efficacy of adding cardiac resynchronization to Dor ventriculoplasty and mitral annuloplasty in a patient with severely impaired left ventricular function and an intraventricular conduction delay.

New Method of Evaluating Sublethal Damage to Erythrocytes by Blood Pumps.

We recently proposed a new concept, the total destruction time of erythrocytes, to indicate sublethal damage to erythrocytes by blood pumps. In this article, results of additional experiments concerning this new concept are reported. Five paired in vitro hemolysis tests with bovine blood were conducted using a cone-type centrifugal pump (Group A) and an impeller-type pump (Group B). A total pressure head of 100 mm Hg was applied. The factors evaluated were the normalized index of hemolysis and the total destruction time, or the pumping duration, required to raise the level of the plasma-free hemoglobin to 50% of the total hemoglobin. The morphologic change of the erythrocytes also was analyzed. The percentage of crenated cells was calculated from blood smear specimens 1 min after starting the pumps and 2 h before the total destruction time of Group A in each experiment. Although there was no statistical difference in the normalized index of hemolysis between the two groups, the total destruction time of Group A erythrocytes was significantly shorter than that of Group B (18.9 ± 4.5 h and 33.7 ± 9.9 h in Group A and group B, respectively; p < 2). The rate of crenated erythrocytes was higher in Group A than in Group B at a point 2 h before the total destruction time of Group A. The total destruction time values seem to define a good method for establishing sublethal traumatic damage to erythrocytes in blood pumps.

Clinical Experience with the Nikkiso Centrifugal Pump.

The Nikkiso HPM-15 is a minimally sized centrifugal pump. Preliminary results regarding clinical use of this pump for cardiopulmonary bypass (CPB) procedures have been reported previously. Recently, we have managed some additional cases using a newly developed controller. This article reports our clinical experiences with the use of this pump. We have managed 23 cases with a Nikkiso centrifugal pump. Twenty-two patients underwent CPB and 1 patient with fulminant viral myocarditis underwent percutaneous cardiopulmonary support (PCPS). With this pump, the circuit was extremely easy to prepare and deaeration was achieved readily. Hemodynamics during CPB and PCPS were stable in all cases. The increase in serum-free hemoglobin levels during CPB with this pump was as low as that seen in preliminary tests. A decrease in the platelet count was observed after the initiation of CPB with this pump; however, platelet counts returned to preoperative values 7 days after surgery. Moreover, urine output during CPB with this pump was as high as that seen in preliminary tests. No abnormalities in renal or liver function occurred during CPB. It appears that this new centrifugal pump is safe and easy to operate, and we conclude that it is useful for CPB and PCPS.

Successful treatment of persistent bronchorrhea by gefitinib in a case with Recurrent Bronchioloalveolar Carcinoma: a case report.

BACKGROUND: Bronchorrhea is one of late complaints in patients with bronchioloalveolar carcinoma (BAC) and hampers their quality of life. Although an effective treatment for bronchorrhea in these patients has not been established, recently we have treated effectively one case of persistent bronchorrhea associated with clinical recurrent BAC with gefitinib (ZD1839, 'Iressa trade mark '; AstraZeneca Japan; Osaka, Japan). CASE PRESENTATION: A 63-year-old Japanese female had undergone left pneumonectomy with radical lymph node dissection (ND2a) for diffuse type bronchioloalveolar carcinoma originated in left lower lobe. Multiple pulmonary metastases in right lung were found one year after operation. Pulmonary metastatic lesion has grown and she complained of progressive symptoms of massive watery sputum and dyspnea, four years after operation. Although her symptom was getting worse in spite of routine treatment, it completely disappeared within 2 weeks of starting oral gefitinib. Thereafter, she has been symptom-free and shows good partial response on repeat scan after 9 months of oral gefitinib. CONCLUSIONS: The dramatic remission of persistent bronchorrhea by gefitinib in the presented case suggests that gefitinib might be a promising option for bronchioloalveolar carcinoma, particularly in cases with severe bronchorrhea. Although it is not possible to comment on whether the improvement came from tumor cell death itself or suppressive effect of mucin synthesis by the epidermal growth factor receptor-tyrosine kinase inhibitory action.

Use of a new venous cannula for minimally invasive cardiac surgery.

Interest in minimally invasive cardiac surgery (MICS) for cardiac disease continues to increase, because it causes less surgical trauma and produces a better cosmetic appearance. We introduced the transxiphoid approach without sternotomy for correction of congenital heart defects. To improve exposure of the cardiac lesion during MICS, we developed a new venous cannula that is made of wire reinforced silicone, with an inflatable balloon attached at the tip. The advantages of this cannula are its extreme flexibility and that a tape does not need to be placed around the vena cava. During a period of 12 months, eight children underwent closure of atrial septal defects. The approach consisted of a 4 to 5 cm low midline incision with division of the xiphoid only. The new venous cannula was used as the superior vena cava cannula, all the patients survived the operation. This new venous cannula provided better exposure during cardiac surgery through a limited incision and is beneficial for minimally invasive cardiac surgery.