近藤 ゆか

PURPOSE: The aim of this study was to elucidate the association between pancreatic fistula (PF) and the sequential changes in the perioperative exocrine function after pancreatectomy. METHODS: The subjects were 96 patients who underwent a 13C-trioctanoin breath test before and 1 month after pancreatectomy, between 2006 and 2018. We retrospectively compared the pre- and postoperative fat absorption levels between patients with PF (PF group; n = 17) and without PF (non-PF group; n = 79) using the breath test. RESULTS: The preoperative level of 13C-trioctanoin absorption (%dose/h) was comparable between the non-PF and PF groups (36.5 vs. 36.9). In the non-PF group, 13C-trioctanoin absorption was significantly decreased after surgery in comparison to the preoperative setting (post-operative 28.5; pre-operative 36.5; p < 0.0001), whereas these values were comparable (post-operative 36.9; pre-operative 34.5; p = 0.129) in the PF group. Moreover, postoperative absorption in the PF group was significantly better than that in the non-PF group (34.5 vs. 28.5%, p = 0.0003). The maximum drain amylase level was significantly higher in patients with a 13C-trioctanoin absorption level (%dose/h) of ≥ 30 in comparison to patients with levels of < 30 (2502 vs. 398 U/L, p = 0.001). CONCLUSION: PF did not exacerbate the pancreatic exocrine function in the early postoperative period, and the acceleration or preservation of the exocrine function after surgery may be an important cause of PF.

BACKGROUND: We present a case of pancreatic and splenic metastases following alveolar soft part sarcoma (ASPS), which was successfully treated by surgery. CASE PRESENTATION: A 41-year-old male was referred to our hospital in 2012. Computed tomography (CT) showed the presence of a pancreatic tumor. In 2002, the patient had undergone surgical resection of an ASPS of the anal region. In 2009, during follow-up, CT revealed lung metastases, which prompted surgical resection of the lung, followed by resection of the head skin in 2011. Abdominal ultrasonography (US) revealed the presence of isodense masses sized 34 mm in the pancreatic head and 60 mm within the spleen. The contrast-enhanced US revealed a solitary lesion with enhancement. Contrast-enhanced CT revealed solitary lesions with enhancement within the pancreatic head, spleen, and liver. The patient underwent metastasectomies from the pancreas, spleen, and liver. The patient was discharged on postoperative day 22 without recurrence for 18 months after metastasectomy. Twelve years after primary resection and 2 years after metastasectomy, the patient died as a consequence of multiple metastases. CONCLUSIONS: We have presented a rare case of pancreatic and spleen metastases from ASPS. Resection by radical metastasectomy was successful without morbidity. Thus, for improved survival of patients with multiple metastases from ASPS, metastasectomy may be indicated. If multiple metastases are resectable, surgical approaches may be the preferred treatment.

Objective: Nogo-B mediates vascular protection and facilitates monocyte- and macrophage-dependent vascular remodeling. PirB is an alternate receptor for Nogo-B, but a role for the Nogo-PirB axis within the vascular system has not been previously reported. We examined whether Nogo-B or PirB play a role in regulating macrophage-mediated vascular remodeling and hypothesized that endothelial Nogo-B regulates vein graft macrophage infiltration via its alternate receptor PirB. Methods: Vein grafts were performed using Nogo and PirB wild type and knockout mice. Human vein grafts were similarly analyzed. The hindlimb ischemia model was performed in PirB wild type and knockout mice. Accompanying in vitro work included isolation of macrophages from PirB wild type and knockout mice. Results: Increased Nogo-B and PirB mRNA transcripts and protein expression were observed within mouse and human vein grafts. Both Nogo knockout and PirB knockout vein grafts showed increased wall thickness and increased numbers of F4/80- positive macrophages. Macrophages derived from PirB knockout mice had increased adhesion to fibronectin, increased EC-specific binding, and increased numbers of mRNA transcripts of M2 markers as well as MMP3 and MMP9. PirB knockout vein grafts had increased active MMP9 compared to wild type vein grafts. PirB knockout mice had increased recovery from hindlimb ischemia and increased macrophage infiltration compared to wild type mice. Conclusions: Vein graft adaptation shows increased expression of both Nogo-B and PirB. Loss of PirB, or its endothelial ligand Nogo-B, results in increased inflammatory cell infiltration and vein graft wall thickening. These findings suggest that PirB regulates macrophage activity in vein grafts and that Nogo-B in the vein graft limits macrophage infiltration and vein graft thickening. PirB may play a more general role in regulating macrophage responses to vascular injury. Macrophage inhibition via Nogo-PirB interactions may be an important mechanism regulating vein graft adaptation to the arterial circulation.

Primary dissecting aneurysms of the hepatic artery are extremely rare and only 15 cases, including the present case, have been reported in the literature. Surgery was performed in 5 cases, of which 3 cases were successfully treated. This report presents a case of a dissecting aneurysm of the proper hepatic artery that was successfully treated by aneurysmorraphy and vein patch angioplasty.

Jadlowiec CC, Feigel A, Yang C, Feinstein AJ, Kim ST, Collins MJ, Kondo Y, Muto A, Dardik A. Reduced adult endothelial cell EphB4 function promotes venous remodeling. Am J Physiol Cell Physiol 304: C627-C635, 2013. First published December 26, 2012; doi:10.1152/ajpcell.00333.2012.-Reduced EphB4 expression is observed during vein graft adaptation and is associated with increased venous wall thickening. These findings suggest that EphB4 may mediate normal adult venous endothelial cell (EC) function and vein graft adaptation. We therefore tested the functional significance of EphB4 using EC with genetically reduced EphB4 signaling. EC were isolated from EphB4(+/+) and EphB4(+/-) mice. In vitro function was assessed through EC proliferation, migration, nitric oxide (NO) synthesis, and chemokine production. A mouse vein graft model was used to correlate in vitro findings with in vivo vein grafts. Smooth muscle cells (SMC) were subjected to proliferation and migration assays using EphB4(+/+) and EphB4(+/-) EC-conditioned medium. EphB4(+/-) EC exhibited diminished proliferation (P &lt; 0.0001, n = 6), migration (P &lt; 0.0001, n = 3), and NO production (P = 0.0012, n = 3). EphB4(+/-) EC had increased VEGF-A mRNA (P = 0.0006, n = 6) and protein (P = 0.0106, n = 3) as well as increased secretion of VEGF-A (P = 0.0010, n = 5), PDGF-BB (P &lt; 0.0001, n = 6), and TGF-beta 1 (P &lt; 0.0001, n = 6). EphB4(+/-)-conditioned medium promoted SMC proliferation (P &lt; 0.0001, n = 7) and migration (P = 0.0358, n = 3). Vein grafts and EphB4(+/-) EC showed similarity with regard to VEGF-A and eNOS mRNA and protein expression. In conclusion, reduced venous EC EphB4 function is associated with a proangiogenic and mitogenic phenotype. EphB4(+/-) EC have increased secretion of SMC mitogens and reduced NO production that correlate with the thickened neointima formed during vein graft adaptation. These findings suggest that EphB4 remains active in adult venous EC and that loss of EphB4 plays a role in vein graft adaptation.

A 69-year-old man with a history of infectious abdominal aortic aneurysm, which had resulted in removal of the infrarenal abdominal aorta and bilateral axillofemoral bypass 9 years previously, underwent total arch replacement for an aortic arch aneurysm. The patient had the interrupted abdominal aorta and highly atherosclerotic proximal aorta, which precluded the possibility of endovascular stent grafting in combination with arch vessel debranching technique. Therefore, open arch repair was the only treatment option. The operation was successful with his axillofemoral bypass graft being exposed and used for arterial inflow during cardiopulmonary bypass, including integrated selective antegrade cerebral perfusion. (Ann Thorac Surg 2012;94:e145-7) (C) 2012 by The Society of Thoracic Surgeons

Carotid angioplasty is associated with adverse events in elderly patients; it is unclear whether this is related to an altered inflammatory axis. The carotid arteries of young (6 months) or aged (22-24 months) Fischer 344 rats were balloon injured. Aged rats had reduced lumen area (0.18 +/- 0.03 vs 0.24 +/- 0.01 mm(2), p = .02) and increased neointimal thickening (0.15 +/- 0.04 vs 0.08 +/- 0.03 mm(2), p = .006). Aged rats had increased circulating monocytes (96 +/- 21 vs. 54 +/- 7; p = .002) as well as increased numbers of monocytes at the post-angioplasty site. Aged rats had sustained monocyte chemotactic protein-1 expression after angioplasty but young rats did not. Aged arteries also exhibited defective vasorelaxation and abnormal eNOS localization. Aged (&gt;= 80 years) human patients with high-grade carotid stenosis had increased number of monocytes (9.1% +/- 0.4%) compared with younger (65-80 years) patients (8.1% +/- 0.3%, p = .013). Aged rats develop neointimal hyperplasia after carotid angioplasty with increased numbers of monocytes, and elderly humans with carotid stenosis have increased numbers of circulating monocytes. These preliminary results may suggest a role for monocytes in the response to carotid angioplasty.

Background. The link of aging to specific mechanisms of vascular biology is not well understood. We have previously shown that aging is associated with increased vein graft wall thickness and that this process involves the VEGF-Delta/Notch-ephrin/Eph cascade. Therefore, we examined whether Dll-4 or Notch-4 are differentially expressed, according to age, during vein graft adaptation. Materials and Methods. Vein grafts were performed in 6-mo and 24-mo Fischer 344 rats. Gene expression was analyzed by quantitative real-time PCR, and the distribution of DII-4 and Notch-4 was observed by immunofluorescence. Results. The expression of DII-4 and Notch-4 was reduced in vein grafts performed in aged rats compared with the expression in young adult rats. Both DII-4 and Notch-4 were distributed in vein graft endothelium as well as the outer adventitia, with reduced amounts in the outer adventitia of aged vein grafts. Aged veins had reduced eNOS membrane targeting and colocalization with caveolin-1 as well as reduced eNOS protein expression in comparison to young adult veins. In an exchange model between young and aged animals, heterogeneous vein grafts (Yo(Ag) and Ag-Yo) showed significantly thicker neointima compared with young (Yo(Yo)) controls, and had Notch-4-positive cells, but not DII-4-positive cells, diminished in the adventitia. Vein grafts that were air-denuded of endothelium did not show any adaptation to the arterial environment and also lacked both DII-4 and Notch-4 expression at 3 wk. Conclusions. During vein graft adaptation to the arterial environment, both DII-4 and Notch-4 expression are down-regulated in an aged, but not a young, background. Loss of Notch-4 is associated with loss of attenuation of neointima. The delta-Notch signaling pathway may be active during vein graft adaptation. Published by Elsevier Inc.

Arterial tissue-engineering techniques that have been reported previously typically involve long waiting times of several months while cells from the recipient are cultured to create the engineered vessel. In this study, we developed a different approach to arterial tissue engineering that can substantially reduce the waiting time for a graft. Tissue-engineered vessels (TEVs) were grown from banked porcine smooth muscle cells that were allogeneic to the intended recipient, using a biomimetic perfusion system. The engineered vessels were then decellularized, leaving behind the mechanically robust extracellular matrix of the graft wall. The acellular grafts were then seeded with cells that were derived from the intended recipient-either endothelial progenitor cells (EPC) or endothelial cell (EC)-on the graft lumen. TEV were then implanted as end-to-side grafts in the porcine carotid artery, which is a rigorous testbed due to its tendency for graft occlusion. The EPC- and EC-seeded TEV all remained patent for 30 d in this study, whereas the contralateral control vein grafts were patent in only 3/8 implants. Going along with the improved patency, the cell-seeded TEV demonstrated less neointimal hyperplasia and fewer proliferating cells than did the vein grafts. Proteins in the mammalian target of rapamycin signaling pathway tended to be decreased in TEV compared with vein grafts, implicating this pathway in the TEV's resistance to occlusion from intimal hyperplasia. These results indicate that a readily available, decellularized tissue-engineered vessel can be seeded with autologous endothelial progenitor cells to provide a biological vascular graft that resists both clotting and intimal hyperplasia. In addition, these results show that engineered connective tissues can be grown from banked cells, rendered acellular, and then used for tissue regeneration in vivo.

Eph-B4 determines mammalian venous differentiation in the embryo but is thought to be a quiescent marker of adult veins. We have previously shown that surgical transposition of a vein into the arterial environment is characterized by loss of venous identity, as indicated by the loss of Eph-B4, and intimal thickening. We used a mouse model of vein graft implantation to test the hypothesis that Eph-B4 is a critical determinant of venous wall thickness during postsurgical adaptation to the arterial environment. We show that stimulation of Eph-B4 signaling, either via ligand stimulation or expression of a constitutively active Eph-B4, inhibits venous wall thickening and preserves venous identity; conversely, reduction of Eph-B4 signaling is associated with increased venous wall thickness. Stimulated Eph-B4 associates with caveolin-1 (Cav-1); loss of Cav-1 or Eph-B4 kinase function abolishes inhibition of vein graft thickening. These results show that Eph-B4 is active in adult veins and regulates venous remodeling. Eph-B4-Cav-1-mediated vessel remodeling may be a venous-specific adaptive mechanism. Controlled stimulation of embryonic signaling pathways such as Eph-B4 may be a novel strategy to manipulate venous wall remodeling in adults.

Background. There are few predictors of limb salvage in patients with critical limb ischemia (CLI). We evaluated the accuracy of correlation of skin perfusion pressure (SPP) measurements in response to vasodilation to clinical outcome. Methods. Patients with CLI were evaluated by SPP at baseline. After injection of the vasodilator alprostadil, SPP was re-evaluated at 120 min and at day 7. Results. Patients showing clinical improvement demonstrated increased SPP in response to vasodilation (120 min: 34.12 +/- 2.44 to 48.33 +/- 3.41 mm Hg, P &lt; 0.01; day 7: 33.13 +/- 3.14 to 45.83 +/- 3.79 mm Hg, P &lt; 0.01), whereas patients who clinically deteriorated demonstrated no increase in SPP (120 min: 30.00 +/- 2.67 to 35.00 +/- 2.31 mm Hg, P = 0.086; day 7: 35.00 +/- 3.54 to 27.5 +/- 4.33 mm Hg, P = 0.22). Conclusions. Prognosis for limb salvage correlated with SPP improvement post-vasodilator treatment after both early and late time points. Measurement of SPP after vasodilator treatment may be clinically useful in the treatment of patients with CLI. A multi-center trial of SPP in response to vasodilators is warranted. (C) 2010 Elsevier Inc. All rights reserved.

The purpose of this study was to evaluate the technical and mid-term results of primary stent placement for chronic total occlusions (CTO) of the iliac artery, in comparison to stent placement for iliac artery stenosis. A retrospective study was carried out on 114 consecutive limbs with 24 CTOs and 90 stenoses of the iliac artery that underwent primary stent placement. Primary, assisted primary patency, and limb salvage rates were determined in accordance with the Society for Vascular Surgery guidelines. Angiographic and intravascular ultrasonographic success was achieved in all 114 limbs (100%). Three major complications, including 1 distal embolism and 2 arterial ruptures, occurred in the CTO group. The 2-year primary patency rate in the CTO group was as high as that observed in the stenosis group (91% vs 89%). There were also no significant differences in the assisted primary patency, limb salvage, and survival rates between the two groups. Our results indicate that primary stent placement is a safe and effective treatment for iliac CTOs. However, major complications, including distal embolization and iliac artery rupture, remain a significant problem, and caution should therefore be exercised when performing this technique for iliac CTOs.

Arterial reconstructions for lower-extremity ischemia, comprising aortoiliac, aortofemoral, and femoropopoliteal bypasses, and other procedures, have an intrinsic tendency to fail as time elapses. Surgical approaches to arteries in patients who have failed bypass grafts are often rendered more difficult, or even impossible to use, by surgical scarring or infection. The authors report two cases in which the diseased native arteries treated with failed aortoiliac and femoropopliteal bypass grafts were successfully recanalized with primary stent placement. Our cases show that stent placement of the diseased native arteries can represent a possible option for the treatment of failed bypass grafts.

We report a case that was successfully treated by primary stent placement without thrombolysis or thrombectomy for graft thrombosis after aortoiliac reconstructive surgery. A 79-year-old man presented with a 2-month history of severe intermittent claudication of the right leg. He had undergone a surgical repair of abdominal aortic aneurysm with a bifurcated polyester graft 3 years before presentation. Digital subtraction angiography revealed total occlusion of the right limb of the graft. He underwent primary stent placement on the lesion, and completion angiography showed revascularization of the right limb. Primary stent placement can be performed to decrease the risks of surgery and increase the salvage of a graft with chronic total occlusion.

Venous and arterial identity is predetermined in the embryo, with embryonic vessels expressing Eph-B4 differentiating into veins and vessels expressing ephrin-B2 differentiating into arteries. The specialized membrane organelles lipid rafts and caveolae serve as localized domains for proteins to interact with one another and play a role in signal transduction and vesicular trafficking. Several tyrosine kinase membrane receptors, including Eph-B1, have been colocalized to caveolae. These data suggest that caveolae and Eph receptors may have coordinated roles in determining vessel identity, not only during embryogenesis but perhaps also during adult vascular remodeling and angiogenesis.

Although anomalies of the inferior vena cava (IVC) are seen frequently in a clinical setting, congenital absence of the IVC (AIVC) is rare. However, anomalies of the IVC should be considered in young patients suffering from recurrent and idiopathic DVT. We report a case of DVT possibly caused by AIVC in a 27-year-old man, and discuss the clinical features, diagnosis, and treatment of this unusual entity.

To investigate whether cilostazol, a cyclic adenosine monophosphate (cAMP) phosphodiesterase inhibitor, suppresses intimal hyperplasia in canine vein grafts, and to elucidate its mechanisms in terms of cell proliferation and apoptosis. Bilateral reversed jugular vein interposition grafts of the common carotid artery were performed in 12 beagle dogs. Starting from 7 days before surgery, either cilostazol (30 mg/day; n = 6) or a placebo (n = 6) was given orally twice daily. Vein grafts were harvested at 1 or 4 weeks, and fixed under pressure for histological examination. By 1 week after implantation, the cilostazol group showed significantly less cell proliferation than the placebo group. By 4 weeks after implantation, intimal and medial thickness was significantly thinner in the cilostazol group than in the placebo group. There was significantly more apoptosis in the placebo group than in the cilostazol group at both time points. Cilostazol suppressed the development of intimal hyperplasia in canine autogenous vein grafts. Thus, it may be associated with the modulation of cell proliferation and apoptosis.

To report the preliminary results of primary stenting of the superficial femoral artery (SFA) in high-risk patients with symptomatic SFA occlusive disease. Between February 2005 and April 2007, a collective 30 lower limbs in 28 high-risk patients with SFA occlusive disease were treated by primary stenting. Hemodynamic improvement was assessed by ankle brachial pressure index (ABI), before and after the procedure. Primary and primary-assisted patency and limb salvage were measured in concordance with the Society for Vascular Surgery guidelines. The technical success rate was 97%. The average ABI before and after stent placement increased significantly, from 0.41 +/- 0.33 to 0.82 +/- 0.20 (P &lt; 0.001). The primary and primary-assisted patency rates were 86% and 90% at 6 months, 86% and 90% at 12 months, and 68% and 90% at 24 months, respectively. The limb salvage rate was 92% at 6, 12, and 24 months and the survival rate was 95% at 6, 12, and 24 months. Our results suggest that the primary stenting of SFA lesions is a feasible, safe, and effective procedure for high-risk patients with SFA occlusive disease.

Autogenous vein and arterial grafts, such as great saphenous veins and internal mammary and radial arteries, remain the gold standard conduits for vascular reconstruction. Expanded polytetrafluoroethylene (PTFE) grafts, which exhibit little inflammatory and thrombogenic reactivity, are the most commonly used material of choice for small diameter vascular grafts when autogenous grafts are not available. Several modifications of the basic graft have been attempted to enhance graft healing of expanded PTFE grafts, and little but definite experimental and clinical improvement has been achieved so far. The technique of vascular tissue engineering, in combination with stem cell research, may hold the key for the creation of a practical and successful small diameter prosthetic graft.

Pulmonary artery sarcoma is a rare malignant tumor. The disease is frequently misdiagnosed as chronic pulmonary thromboembolism because of the similar clinical and radiologic findings. We present a case of primary pulmonary artery sarcoma that was misdiagnosed as chronic pulmonary thromboembolism, and discuss the clinical presentation, diagnosis, and outcome.

Percutaneous transluminal angioplasty and endovascular stent placement are becoming common techniques for iliac artery stenosis and obstruction that are intended to reduce the need for surgical bypass procedures. The usual complications include acute or subacute thrombosis, distal embolization, dissection, and extravasation. Although stent infection is very rare after stent replacement, it is reportedly associated with a high risk of morbidity and mortality, and the use of prophylactic antibiotics should be considered. We present a case of rupture of an infected pseudoaneurysm at the site of the external iliac artery that occurred 4 months after an uneventful percutaneous transluminal angioplasty and stent placement.

We performed pulmonary thromboendarterectomy under deep hypothermic intermittent circulatory arrest in 18 patients with chronic pulmonary thromboembolism from August 2001 to January 2004. In some of these cases, reperfusion pulmonary edema prevented a satisfactory improvement in hemodynamic data soon after the surgery. Here we report two cases of chronic pulmonary thromboembolism in which we successfully prevented postoperative persistent pulmonary hypertension and hypoxia caused by severe reperfusion pulmonary edema by the use of a percutaneous cardiopulmonary support device.

Left ventricular free-wall rupture is a well recognized complication of myocardial infarction and a frequent cause of death. The appropriate surgical management varies significantly depending on the condition of the tear and the presence of concomitant lesions. We present a case of oozing type postinfarction cardiac rupture that was treated successfully by a sutureless patch technique using a fibrin tissue-adhesive collagen fleece (Tacho-Comb [Torii Pharmaceutical, Tokyo, Japan]). This represents a quick, effective, and safe option for dealing with oozing type myocardial rupture due to myocardial infarction. (c) 2005 by The Society of Thoracic Surgeons

Although vein graft aneurysms have been described to be atherosclerotic in nature, it has been hypothesized that vein graft aneurysms may be a part of a systemic dilating process. In the case reported here, histopathologic exnamination of vein graft aneurysms demonstrates aneurysmal degeneration with no atherosclerotic changes and do support the hypothesis that vein graft aneurysms may be a manifestation of a systemic dilating process.