[A Case of Subphrenic Lymph Node Metastasis from Gastric Cancer in Which FDG-PET/CT Was Useful for Diagnosis].

A 70-year-old man was admitted for lymph node metastasis detected by FDG-PET/CT showing a mass 10mm in diameter. He had a history of a distal gastrectomy for advanced gastric cancer and was administered postoperative adjuvant chemotherapy consisting of 2 courses of TS-1 with CDDP and TS-1 only for 1 year. Lymph node recurrence was diagnosed and resected 4 years after the initial surgery. Histological examination revealed lymph node metastasis of the gastric cancer. He was administered adjuvant chemotherapy using TS-1 and has been followed-up without recurrences for 17 months after the second operation. We reported a case in which FDG-PET/CT was potentially beneficial for the diagnosis of the postoperative small lymph node metastasis.

Thoracic endovascular aortic repair with homemade stent grafts: early and mid-term outcomes.

PURPOSE: We reviewed our experience with homemade stent grafts in the repair of a variety of thoracic aortic lesions. The objective of this study was to assess the early and mid-term outcomes of this therapy. METHODS: From 1999 to 2007, homemade stent grafts were inserted in 88 patients with an atherosclerotic aneurysm, dissection, pseudoaneurysm, trauma, or rupture in the thoracic aorta. The endoprostheses were stainless steel Z-stents covered by a polyester graft, and were custom-designed for each patient. RESULTS: Placement of stent grafts was technically successful in 81 of the 88 patients (92%). Within 30 days after treatment, 3 patients died, 3 had a cerebral infarction, and 3 had onset of paraplegia or paraparesis. Primary endoleaks were observed in 8 patients (9%). During the mean follow-up period of 32 ± 26 months, 7 patients had persistent endoleaks and 7 had stent-graft migration. The aneurysm-related mortality rate was 7%. The rate of freedom from open-surgery conversion at 32 months was 89.0%. CONCLUSIONS: Our early experience with elective and emergency thoracic endovascular aortic repair using homemade stent grafts provided therapeutic benefits to high-risk patients. Endoleaks and stent-graft migrations were the factors most commonly responsible for secondary intervention in the mid-term period. Careful follow-up of patients treated with this approach is needed to avoid major complications in the long term.

[Long-term outcomes of thoracic endovascular aortic repair with homemade stent-grafts].

We reviewed our experience with homemade stent-grafts in the repair of thoracic aortic lesions. The objective of this study was to assess the long-term outcomes of this therapy. From 1999 to 2008, homemade stent-grafts were inserted in 94 patients with various thoracic diseases. The endoprostheses were stainless steel Z-stents covered with polyester graft and were custom designed for each patient. Placement of the stent-grafts was technically successful in 85 of the 94 patients (90%). Within 30 days after the treatment, 4 patients died, 3 had cerebral infarction, and 3 had the onset of paraplegia or paraparesis. Primary endoleaks were observed in 10 patients (11%). During the mean follow-up period of 43 +/- 29 months, 10 patients had endoleaks and 8 had stent-graft migration. The aneurysm-related mortality rate was 12%. Our early outcomes of elective and emergency thoracic endovascular aortic repair with homemade stent-grafts demonstrated their therapeutic effectiveness in high-risk patients with various thoracic diseases. Endoleaks and migration were, however, the factors most responsible for secondary intervention in the mid-term period. Careful follow-up of the treated patients is needed to avoid the major complication in the long-term period.

Mitral stenosis due to pannus overgrowth after rigid ring annuloplasty.

Although mitral stenosis (MS) due to pannus overgrowth after mitral valve repair for rheumatic mitral regurgitation (MR) is not uncommon, it is extremely rare in relation to non-rheumatic mitral regurgitation. Whilst it has been suggested that the rigid annuloplasty ring induces pannus overgrowth in the same manner as the flexible ring, to date only in cases using the flexible ring has pannus formation been confirmed by a pathological examination after redo surgery. The case is described of a woman who had undergone mitral valve repair using a 28 mm rigid ring three years previously because of non-rheumatic MR, and subsequently suffered from MS due to pannus formation over the annuloplasty ring. To the present authors' knowledge, this is the first report of MS due to pannus formation after mitral valve repair using a rigid annuloplasty ring to treat non-rheumatic MR documented at reoperation.

Spontaneous dissection of the iliac artery in a patient with fibromuscular dysplasia.

A 49-year-old man was referred to our hospital at 10 days after the onset of sudden intermittent claudication of the right lower limb and with right lower abdominal pain. Diagnosis by computed tomography scan and pelvic angiography was dissection from the common iliac artery to peripheral external iliac artery with thrombosed false lumen. Replacement of the common and external iliac artery was performed using a 10-mm Dacron prosthesis. A pathological examination of the right common iliac artery revealed an arterial disorder caused by fibromuscular dysplasia.

Obstruction of St. Jude medical valves in the aortic position: plasma transforming growth factor type beta 1 in patients with pannus overgrowth.

The study investigated the hypothesis that plasma transforming growth factor type beta 1 (TGF-beta1) initiated pannus overgrowth in cases with aortic prosthetic valve dysfunction (PVD). Patients with obstruction of an aortic St. Jude Medical valve in 26 cases (PVD group) and without obstruction in 48 cases (control group) were studied. Plasma TGF-beta1, the intensity of the prothrombin time-international normalized ratio (PT-INR), and the interruption of an oral anticoagulant medicine were conducted. Plasma TGF-beta1 levels in the PVD group (87.7 +/- 29.2 ng/mL) were significantly higher (P < 0.05) than in the control group (73.7 +/- 25.2 ng/mL). The interruption of an oral anticoagulant medicine in 54% of the PVD group versus 12% of the control group was identified (P < 0.001). The mean value of the PT-INR in the PVD group (1.75 +/- 0.30) and control group (1.75 +/- 0.30) was not significantly different (P = 0.82). In conclusion, elevated levels of plasma TGF-beta1 may play a role in pannus overgrowth.

Pannus overgrowth after mitral valve replacement with a Carpentier-Edwards pericardial bioprosthesis.

A Carpentier-Edwards pericardial (CEP) bioprosthesis was explanted from an 81-year-old woman due to nonstructural dysfunction 9 years after mitral valve replacement. The nonstructural dysfunction produced severe regurgitation in the mitral position. During the surgery, excessive pannus overgrowth was seen on the left ventricular side of the CEP bioprosthesis. Pannus overgrowth was prominent on one leaflet. That leaflet was stiff and shortened due to the excessive overgrowth of pannus. In this patient, the distortion of one leaflet was the main reason for transvalvular leakage of the CEP bioprosthesis in the mitral position. A new CEP bioprosthesis was implanted in the mitral position. Pathological analysis revealed fibrotic pannus with a small amount of cellular material over the leaflets of the resected CEP valve. This change was marked on the distorted leaflet.

STAT3 Activation Correlates with Adventitial Neutrophil Infiltration in Human Aortic Dissection.

Objective: Aortic dissection (AD) is a fatal disease that is caused by the rapid destruction of the aortic wall. Although recent studies in animal models indicate an important relationship between inflammation and tissue destruction, activation status of inflammatory signaling and its relation to the inflammatory cell infiltration are poorly characterized in human AD. Materials and Methods: We examined the activation of inflammatory signaling molecules NFκB and STAT3, and neutrophil infiltration in AD tissue samples that were obtained during the surgical repair within 24 h after AD onset. Results: Activation of NFκB was observed mainly in the intima both in AD samples and in aortic samples without AD. Activation of STAT3 was observed in AD samples, but not in the aortic sample without AD. Neutrophil infiltration was observed predominantly in the adventitial layer of AD samples. Histological analysis revealed that STAT3 was activated in cells other than neutrophils. Notably, STAT3 activation and neutrophil infiltration showed positive correlation in adventitial layer of AD tissue. Conclusion: These findings demonstrated that adventitial STAT3 activation was associated with neutrophil infiltration, suggesting their importance in AD pathogenesis.

Abdominal Aortic Aneurysm Caused by Aortic Fibromuscular Dysplasia: A Case Report.

Fibromuscular dysplasia (FMD) mainly develops in medium-sized arteries, including renal, extracranial, and extremity arteries, but it rarely causes abdominal aortic aneurysm (AAA). A 69-year-old woman with AAA diagnosed on ultrasonography by a home doctor visited our hospital. Contrast-enhanced computed tomography revealed a saccular aneurysm of terminal abdominal aorta. We performed abdominal aortic replacement and resected the section with aneurysm. Pathological examination of the wall tissue of the resected aneurysm revealed findings that are consistent with FMD. We report this case of AAA caused by aortic FMD because of its rarity.

Cytokine Profile of Human Abdominal Aortic Aneurysm: Involvement of JAK/STAT Pathway.

Objective: Abdominal aortic aneurysm (AAA) is characterized by inflammation and destruction of normal tissue architecture. The present study aimed to evaluate the inflammatory signaling cascade by analyzing the cytokines of AAA tissue. Materials and Methods: We analyzed the comprehensive cytokine secretion profiles of 52 cytokines from human AAA in four patients with AAA using fluorescent beads-based multiplex assay. Further, the effect of janus kinase (JAK) inhibition by pyridone 6 on cytokine profiles was also evaluated. Results: Cytokine secretion profiles were found to be similar among the four patients. A high level of JAK/signal transducers and activator of transcription (STAT) pathway activity in AAA tissue in culture was maintained, which may be attributed to the secretion of endogenous JAK-activating cytokines. Inhibition of JAK by pyridone 6 resulted in the suppression of STAT3 phosphorylation and secretion of a subset of chemokines and JAK-activating cytokines. However, the inhibition of JAK had no effect on the secretion of matrix metalloproteinase (MMP)-2, MMP-9, or TGF-ß family that is responsible for the metabolism of extracellular matrix. Conclusion: The findings of the present study suggested that AAA tissue exhibits a stereotypical profile of cytokine secretion, where JAK/STAT pathway may play a role in regulating a subset of cytokines. Identification of such a cytokine profile may reveal potential diagnostic markers and therapeutic targets for AAA.

Role of Macrophage Socs3 in the Pathogenesis of Aortic Dissection.

BACKGROUND: Aortic dissection (AD) is a life-threatening medical emergency caused by the abrupt destruction of the intimomedial layer of the aortic walls. Given that previous studies have reported the involvement of proinflammatory cytokine interleukin-6 in AD pathogenesis, we investigated the role of signal transduction and activator of transcription 3 signaling, a downstream pathway of interleukin-6 in macrophages in pathogenesis of AD. METHODS AND RESULTS: We characterized the pathological and molecular events triggered by aortic stress, which can lead to AD. Aortic stress on the suprarenal aorta because of infrarenal aorta stiffening and angiotensin II infusion for 1 week caused focal medial rupture at the branching point of the celiac trunk and superior mesenteric artery. This focal medial rupture healed in 6 weeks in wild-type (WT) mice, but progressed to AD in mice with macrophage-specific deletion of Socs3 gene (mSocs3-KO). mSocs3-KO mice showed premature activation of cell proliferation, an inflammatory response, and skewed differentiation of macrophages toward the tissue-destructive phenotype. Concomitantly, they showed aberrant phenotypic modulation of smooth muscle cells and transforming growth factor beta signaling, which are likely to participate in tissue repair. Human AD samples revealed signal transduction and activator of transcription 3 activation in adventitial macrophages adjacent to the site of tissue destruction. CONCLUSIONS: These findings suggest that AD development is preceded by focal medial rupture, in which macrophage Socs3 maintains proper inflammatory response and differentiation of SMCs, thus promoting fibrotic healing to prevent tissue destruction and AD development. Understanding the sequence of the pathological and molecular events preceding AD development will help predict and prevent AD development and progression.

Characterization of SMAD2 Activation in Human Thoracic Aortic Aneurysm.

Objective: Thoracic aortic aneurysm (TAA) reflects the local expansion of the thoracic aorta; the underlying causal molecular mechanism of TAA is not well understood. Recent studies have shown the importance of transforming growth factor beta (TGFß) signaling in Marfan and Loeys-Dietz syndromes; however, its role in non-familial, non-syndromic TAA remains unclear. Materials and Methods: We performed histochemical and immunohistochemical analyses for activated (phosphorylated) SMAD2 (P-SMAD2) as an indicator of TGFß signaling activities in the ascending TAA tissue as well as in the ascending aortic tissue with a normal diameter obtained from 7 patients without any clinical findings suggesting familial or syndromic TAA. Results: TAA samples showed a higher P-SMAD2-positive area than samples with a normal diameter. P-SMAD2 signal was higher in the outer zone of the aortic and TAA walls. Within the TAA tissue, P-SMAD2 staining showed the following two distinct patterns: layer-like staining at the border of the medial layer and the thickened intima and a spot-like staining within the medial layer surrounding the microvessels. Conclusion: These findings suggested that TGFß signaling is activated in several distinct histopathological contexts in TAA, suggesting a complex role of TGFß.

Involvement of B Cells, Immunoglobulins, and Syk in the Pathogenesis of Abdominal Aortic Aneurysm.

BACKGROUND: Abdominal aortic aneurysm (AAA) is a potentially life-threatening disease that is common in older individuals. Currently, therapeutic options are limited to surgical interventions. Although it has long been known that AAA tissue is enriched in B cells and immunoglobulins, their involvement in AAA pathogenesis remains controversial. METHODS AND RESULTS: We investigated the role of B cells and immunoglobulins in a murine model of AAA, induced with a periaortic application of CaCl2, and in human AAA. Both human and mouse AAA tissue showed B-cell infiltration. Mouse AAA tissue showed deposition of IgG and activation of Syk, a key molecule in B-cell activation and immunoglobulin function, which were localized to infiltrating cells including B cells and macrophages. B-cell-deficient muMT mice showed suppression of AAA development that was associated with reduced activation of Syk and less expression of matrix metalloproteinase-9. Administration of exogenous immunoglobulins restored the blunted Syk activation and AAA development in muMT mice. Additionally, exogenous immunoglobulins induced interleukin-6 and metalloproteinase-9 secretions in human AAA tissue cultures. Furthermore, administration of R788, a specific Syk inhibitor, suppressed AAA expansion, reduced inflammatory response, and reduced immunoglobulin deposition in AAA tissue. CONCLUSIONS: From these results, we concluded that B cells and immunoglobulins participated in AAA pathogenesis by promoting inflammatory and tissue-destructive activities. Finally, we identified Syk as a potential therapeutic target.

Coil embolization of splenic artery aneurysm with preservation of the parent artery using a neck remodeling technique.

We describe a case of a large and wide neck splenic artery aneurysm, treated by coil embolization using a balloon neck remodeling technique. The patency of the splenic artery was preserved without technical complications. This method should be considered as an alternative method for transcatheter management of splenic artery aneurysms.

A case of unilateral leg edema due to abdominal aortic aneurysm with aortocaval fistula.

Aortocaval fistula (ACF) is a rare complication of abdominal aortic aneurysm (AAA), and its preoperative diagnosis is often difficult. A 71-year-old woman was admitted to our hospital due to unilateral leg edema. Abdominal computed tomography (CT) showed an abdominal aortic aneurysm (AAA), a common iliac aortic aneurysm (CIAA) and ACF was suspected. Digital subtraction angiography (DSA) was performed, enabling us to identify the region of ACF with AAA preoperatively. ACF is associated with high mortality because it is difficult to control venous bleeding from ACF. Detailed preoperative diagnosis of ACF can provide many advantages to control bleeding from ACF during an operation.

Embolic myocardial infarction and left ventricular rupture due to mitral valve endocarditis.

A left ventricular rupture due to embolic myocardial infarction is extremely rare. A 72-year-old woman developed an acute embolic myocardial infarction and mitral regurgitation due to infective endocarditis. Two days after the infarction, a left ventricular free wall rupture occurred after transesophageal echo examination. She received an epicardial patch and mitral valve replacement. Perioperatively, an intra-aortic balloon pump and long-term antibiotics were used. The postoperative course was uneventful, and she is doing well 10 months after surgery.

Moderate cerebral venous congestion induces rapid cerebral protection via adenosine A1 receptor activation.

Stroke is a devastating complication in cardiovascular surgery, and neuronal damage is worsened by intracranial pressure elevation caused by cerebral venous circulatory disturbances (CVCD). However, we have previously reported that CVCD before cerebral ischemia decreases the infarct area. In the present study, focal cerebral ischemia was induced in spontaneously hypertensive rats by filament insertion through the carotid artery. Rats were divided into the following four groups: sham-operated, mild or severe venous congestion (VC), and DPCPX. The DPCPX group received the adenosine A1 receptor antagonist 8-cyclopentyl-1,3-dipropylxanthine (DPCPX) prior to mild VC. Behavior, infarct volume, edema and S-100 protein were evaluated among the four groups. The infarct volume rates in mild VC and severe VC groups were significantly less than that in sham-operated and DPCPX groups. However, the mortality of the severe VC group worsened in a time-dependent manner. We observed a significant decrease in edema in the mild VC group compared to the DPCPX group. Behavioral scores also indicated that the mild VC group had fewer neurological deficits than the other three groups, including the DPCPX group. We were able to induce rapid cerebral protection via adenosine A1 receptor activation by administering an appropriate degree of VC prior to cerebral ischemia produced by middle cerebral artery occlusion. Our work suggests possible mechanisms by which such effective VC may lead to cerebral protection and adenosine A1 receptor activation.

Aortic valve replacement after esophagectomy with substernal gastric tube reconstruction.

A 67-year-old woman with a history of esophagectomy with substernal gastric tube (GT) reconstruction and left lower lobectomy required aortic valve replacement (AVR) for aortic valve regurgitation and stenosis. Through a median sternotomy (MS) with cardiopulmonary bypass (CPB), we performed AVR without injury to the GT. Careful peeling of the GT and detailed information of the operative field by multidetector-row computed tomography (MDCT) scan enabled us to carry out the operation safely in the usual operative view.

The impact of preoperative identification of the Adamkiewicz artery on descending and thoracoabdominal aortic repair.

OBJECTIVE: To investigate the impact of preoperative identification of the Adamkiewicz artery (AKA) on prevention of spinal cord injury (SCI) through the multicenter Japanese Study of Spinal Cord Protection in Descending and Thoracoabdominal Aortic Repair (JASPAR) registry. METHODS: Between January 2000 and October 2011, 2435 descending/thoracoabdominal aortic repairs were performed, including 1998 elective repairs and 437 urgent repairs, in 14 major centers in Japan. The mean patient age was 67 ± 13 years, and 74.2% were males. There were 1471 open repairs (ORs), including 748 descending and 137 thoracoabdominal extent [Ex] I, 136 Ex II, 194 Ex III, 115 Ex IV, and 138 Ex V, and 964 endovascular repairs (EVRs). Of the 2435 patients, 1252 (51%) underwent preoperative magnetic resonance or computed tomography angiography to identify the AKA. RESULTS: The AKA was identified in 1096 of the 1252 patients who underwent preoperative imaging (87.6%). Hospital mortality was 9.2% (n = 136) in those who underwent OR and 6.4% (n = 62) in those who underwent EVR. The incidence of SCI was 7.3% in the OR group (descending, 4.2%; Ex I, 9.4%; Ex II, 14.0%; Ex III, 14.4%; Ex IV, 4.2 %; Ex V, 7.2%) and 2.9% in the EVR group. The risk factors for SCI in ORs were advanced age, extended repair, emergency, and occluded bilateral hypogastric arteries. In ORs of the aortic segment involving the AKA, having no AKA reconstruction was a significant risk factor for SCI (odds ratio, 2.79, 95% confidence interval, 1.14-6.79; P = .024). CONCLUSIONS: In descending/thoracoabdominal aortic repairs, preoperative AKA identification with its adequate reconstruction or preservation, especially, in ORs of aortic pathologies involving the AKA, would be a useful adjunct for more secure spinal cord protection.