Successful treatment of rectal varices with antegrade transvenous sclerotherapy via the splenorenal shunt from the transjugular approach.

A 74-year-old patient presented with hematochezia and a history of liver cirrhosis with repeated bleeding from esophageal and rectal varices. Endoscopic examination revealed multiple rectal varices with positive red color signs. Ascites, severe portosystemic thrombosis and a splenorenal shunt were diagnosed on a contrast-enhanced dynamic computed tomography examination. From a transjugular approach, we circumvented thrombosed regions by maneuvering double balloon catheters through the shunt and dilated left colic marginal vein. We managed to successfully obliterate the varices.

Splenic Vein Diameter is a Risk Factor for the Portal Venous System Thrombosis After Partial Splenic Artery Embolization.

PURPOSE: Portal venous system thrombosis is a complication of partial splenic artery embolization, and pre-treatment risk assessment is thus important. The purpose of this study was to identify the risk factors for portal venous system thrombosis after partial splenic artery embolization. MATERIALS AND METHODS: We retrospectively analyzed 67 consecutive patients who underwent contrast-enhanced computed tomography before and after first partial splenic artery embolization between July 2007 and October 2018. As risk factors, we investigated age, sex, hematological data, liver function, steroid use, heparin use, and findings from pre- and post-treatment computed tomography. Uni- and multivariate analyses were performed to evaluate the relationship between thrombus appearance or growth and these factors. Values of p < 0.05 were considered significant. RESULTS: Partial splenic artery embolization was technically successful in all 67 patients. Nine patients showed appearance or growth of thrombus. Univariate analysis showed maximum diameter of the splenic vein before treatment (p = 0.0076), percentage of infarcted spleen (p = 0.017), and volume of infarcted spleen (p = 0.022) as significant risk factors. Multivariate analysis showed significant differences in maximum diameter of the splenic vein before treatment (p = 0.041) and percentage of infarcted spleen (p = 0.023). According to receiver operating characteristic analysis, cutoffs for maximum diameter of the splenic vein and percentage of infarcted spleen for distinguishing the appearance or growth of thrombus were 17 mm and 58.2%. CONCLUSION: Large maximum diameter of the splenic vein before partial splenic artery embolization and high percentage of infarcted spleen after partial splenic artery embolization were identified as risk factors for portal venous system thrombosis. LEVEL OF EVIDENCE: Level 4, Case Series.

[Spontaneous Splenic Rupture with Angioimmunoblastic T-Cell Lymphoma Successfully Treated Using Transcatheter Arterial Embolization].

A 75-year-old woman presented to our hospital with a history of fever, cervical lymphadenopathy, and fatigue. Computed tomography(CT)revealed systemic lymphadenopathy with prominent splenomegaly. Axillary lymph node biopsy results revealed diffuse proliferation of atypical lymphoid cells with arborizing high endothelial venules. Immunohistochemical staining was positive for CD3, CD5, and CD10, but negative for CD20 and CD79a. Given these findings, a diagnosis of angioimmunoblastic T-cell lymphoma(AITL)was made. Due to the extremely high tumor burden, pre-therapy with corticosteroids was initiated. However, the patient suddenly went into hemorrhagic shock. Contrast-enhanced CT revealed abdominal bleeding due to splenic rupture. Bleeding was rapidly controlled using transcatheter arterial embolization(TAE). Five days after TAE, mini-CHOP therapy was initiated. Splenomegaly is common in hematologic disease. Owing to the lethality of the condition, in cases of progressive anemia with splenomegaly in patients with hematologic disease, the possibility of splenic rupture should be considered. Since TAE carries no risk of post-splenectomy infection and allows timely resumption of chemotherapy, it could be considered as one of the preferred treatment choices for splenic rupture in hemodynamically unstable patients.

A Case of Localized Malignant Peritoneal Mesothelioma With Lung Cancer Detected by 18F-FDG PET/CT.

A 62-year-old woman was referred for cough and lower abdominal pain. F-FDG PET/CT showed strong uptake not only in the left lung mass and hilar and mediastinal lymph nodes, but also a huge lower abdominal mass. All lesions were initially thought to be multiple metastases because bronchial biopsy of the lung mass showed poorly differentiated adenocarcinoma. However, the abdominal mass was found to be malignant peritoneal mesothelioma after surgical resection. It was difficult to diagnose this case correctly before resection because localized malignant peritoneal mesothelioma is rare.

Therapeutic Effect of Rapamycin on Aortic Dissection in Mice.

Aortic dissection (AD) is a serious clinical condition that is unpredictable and frequently results in fatal outcome. Although rapamycin, an inhibitor of mechanistic target of rapamycin (mTOR), has been reported to be effective in preventing aortopathies in mouse models, its mode of action has yet to be clarified. A mouse AD model that was created by the simultaneous administration of ß-aminopropionitrile (BAPN) and angiotensin II (AngII) for 14 days. Rapamycin treatment was started either at day 1 or at day 7 of BAPN+AngII challenge, and continued throughout the observational period. Rapamycin was effective both in preventing AD development and in suppressing AD progression. On the other hand, gefitinib, an inhibitor of growth factor signaling, did not show such a beneficial effect, even though both rapamycin and gefitinib suppressed cell cycle activation in AD. Rapamycin suppressed cell cycle-related genes and induced muscle development-related genes in an AD-related gene expression network without a major impact on inflammation-related genes. Rapamycin augmented the activation of Akt1, Akt2, and Stat3, and maintained the contractile phenotype of aortic smooth muscle cells. These findings indicate that rapamycin was effective both in preventing the development and in suppressing the progression of AD, indicating the importance of the mTOR pathway in AD pathogenesis.

Genetic Deletion of Socs3 in Smooth Muscle Cells Ameliorates Aortic Dissection in Mice.

Aortic dissection (AD) is the acute destruction of aortic wall and is reportedly induced by inflammatory response. Here we investigated the role of smooth muscle Socs3 (a negative regulator of Janus kinases/signal transducer and activator of transcription signaling) in AD pathogenesis using a mouse model generated via ß-aminopropionitrile and angiotensin II infusion. Socs3 deletion specifically in smooth muscle cells yielded a chronic inflammatory response of the aortic wall, which was associated with increased fibroblasts, reinforced aortic tensile strength, and less-severe tissue destruction. Although an acute inflammatory response is detrimental in AD, smooth muscle-regulated inflammatory response seemed protective against AD.

MRTF-A promotes angiotensin II-induced inflammatory response and aortic dissection in mice.

Aortic dissection (AD) is a major cause of acute aortic syndrome with high mortality due to the destruction of aortic walls. Although recent studies indicate the critical role of inflammation in the disease mechanism of AD, it is unclear how inflammatory response is initiated. Here, we demonstrate that myocardin-related transcription factor A (MRTF-A), a signal transducer of humoral and mechanical stress, plays an important role in pathogenesis of AD in a mouse model. A mouse model of AD was created by continuous infusion of angiotensin II (AngII) that induced MRTF-A expression and caused AD in 4 days. Systemic deletion of Mrtfa gene resulted in a marked suppression of AD development. Transcriptome and gene annotation enrichment analyses revealed that AngII infusion for 1 day caused pro-inflammatory and pro-apoptotic responses before AD development, which were suppressed by Mrtfa deletion. AngII infusion for 1 day induced pro-inflammatory response, as demonstrated by expressions of Il6, Tnf, and Ccl2, and apoptosis of aortic wall cells, as detected by TUNEL staining, in an MRTF-A-dependent manner. Pharmacological inhibition of MRTF-A by CCG-203971 during AngII infusion partially suppressed AD phenotype, indicating that acute suppression of MRTF-A is effective in preventing the aortic wall destruction. These results indicate that MRTF-A transduces the stress of AngII challenge to the pro-inflammatory and pro-apoptotic responses, ultimately leading to AD development. Intervening this pathway may represent a potential therapeutic strategy.

Utility of low-dose gelatin sponge particles and 5% ethanolamine oleate iopamidol mixture in retrograde transvenous obliteration (GERTO) for gastric varices.

OBJECTIVE: To determine the utility of low-dose gelatin sponge particles and 5% ethanolamine oleate iopamidol (EOI) mixture in retrograde transvenous obliteration (GERTO) for gastric varices (GV). METHODS: 57 consecutive patients who underwent balloon-occluded retrograde transvenous obliteration (B-RTO) for GV were divided into three groups with Hirota's grade by balloon-occluded retrograde transvenous venography. Hirota's Grade 1 patients were assigned to G1 group and underwent treatment with 5% EOI. Grade ≥ 2 patients prior to August 2015 were G ≥ 2 group treated with 5% EOI, and those treated thereafter were GERTO group. The amount of EOI used per unit GV volume (EOI/GV ratio), the times to embolization and recurrence rate of GV were evaluated. RESULTS: The EOI/GV ratio was 0.66 ± 0.19 in G1, 1.5 ± 0.8 in G ≥ 2, and 0.58 ± 0.23 in GERTO (G ≥ 2 vs GERTO, p < 0.0001). The times to embolization were 26.5 ± 10.5 min for G1, 39.2 ± 26.8 for G ≥ 2, and 21.4 ± 9.4 for GERTO (G ≥ 2 vs GERTO, p = 0.005). The recurrence rate was not significantly different in any of the groups. CONCLUSION: GERTO was performed in lower amount of sclerosants and in less time compared to conventional B-RTO in Hirota's grade ≥2. ADVANCES IN KNOWLEDGE: Feasibility of low-dose gelatin sponge particles and 5% EOI mixture as sclerosants for GV.

High Salt Intake Worsens Aortic Dissection in Mice: Involvement of IL (Interleukin)-17A-Dependent ECM (Extracellular Matrix) Metabolism.

OBJECTIVE: Aortic dissection (AD) is a fatal disease that occurs suddenly without preceding clinical signs or symptoms. Although high salt intake is a proposed risk factor for cardiovascular diseases, the relationship between AD and high salt intake has not been clarified. We examined the effect of high-salt challenge on a mouse AD model. Approach and Results: AD was induced in male mice by continuous infusion of ß-aminopropionitrile and Ang II (angiotensin II). High-salt challenge exacerbated aortic wall destruction in AD. Deletion of Il17a (IL-17KO [IL (interleukin)-17A knockout]) did not affect the AD phenotype at baseline, but it abolished the high salt-induced worsening of the aortic destruction. Unexpectedly, aortas of IL-17KO mice exhibited global changes in ECM (extracellular matrix)-related genes without alteration of proinflammatory genes, altered architecture of collagen fibers, and reduced stiffness before AD induction. The aortas of IL-17KO mice were less sensitive to AD-inducing stimuli, as shown by the induction of phenotypic modulation markers SMemb and vimentin, suggesting a reduced stress response. The aortas of IL-17KO mice had a higher population of smooth muscle cells with nuclear-localized phosphorylated Smad2, indicative of TGFß (transforming growth factor-beta) signal activation. Consistently, pretreatment of smooth muscle cells in culture with IL-17A blunted the activation of Smad2 by TGFß1. CONCLUSIONS: These findings indicate that high salt intake has a worsening effect on AD in the context of high aortic wall stiffness, which is under the control of IL-17A through ECM metabolism. Therefore, salt restriction may represent a low-cost and practical way to reduce AD risk.

Indomethacin reduces rates of aortic dissection and rupture of the abdominal aorta by inhibiting monocyte/macrophage accumulation in a murine model.

Aortic dissection is a life-threatening condition, which is characterised by separation of the constituent layers of the aortic wall. We have recently shown that monocyte/macrophage infiltration into the aortic wall is a pathogenic mechanism of the condition. In the present study, we investigated whether the anti-inflammatory agent, indomethacin, could inhibit monocyte/macrophage accumulation in the aortic wall and ensuing dissection. Indomethacin was administered (from 3 days prior with daily oral administration) to mice in which aortic dissection was induced using beta-aminopropionitrile (BAPN) and angiotensin II (Ang II) infusion (2 weeks). Indomethacin prevented death from abdominal aortic dissection and decreased incidence of aortic dissection by as high as 40%. Histological and flow cytometry analyses showed that indomethacin administration resulted in inhibition of monocyte transendothelial migration and monocyte/macrophage accumulation in the aortic wall. These results indicate that indomethacin administration reduces rate of onset of aortic dissection in a murine model of the condition.

Usefulness of Venous Pressure Measurement in Endovascular Treatment of Budd-Chiari Syndrome: A Retrospective Cohort Study.

Objective Therapeutic predictors derived from the venous pressure before therapy have not been identified for Budd-Chiari syndrome (BCS). The aim of this study was to determine whether or not measuring the distal pressure or pressure gradient was useful for predicting treatment efficacy in BCS. Methods We retrospectively analyzed seven consecutive patients diagnosed with symptomatic BCS at our hospital between 2008 and 2017. Distal and proximal venous pressures at occlusion sites of BCS were measured before treatment in all cases. The pressure gradient was defined as the difference between distal and proximal venous pressures. A receiver operating characteristics (ROC) analysis was performed for venous pressures. Results Percutaneous old balloon angioplasty (POBA) was performed in seven cases, with technical success achieved in all cases (100%). No complications were encountered. The median primary patency was 574 (interquartile range, 439.5-1,056.5) days. The 1-year primary patency rate was 71.73%. Six cases (85.7%) showed resolution of symptoms, representing clinical success. The ROC analysis revealed a high distal pressure (area under the ROC curve = 0.83, cut-off=12 mmHg) as a predictor of treatment efficacy of POBA for symptomatic BCS. In addition, the pressure gradient was considered significant from a clinical perspective, because the 6 successful cases with resolution of symptoms showed a large pressure gradient (range, 8-21 mmHg) before treatment, whereas the failed case showed a relatively small pressure gradient (7 mmHg). Conclusion High distal pressure and a large pressure gradient might predict the treatment efficacy of balloon angioplasty for symptomatic BCS.

Risk factors for local recurrence of hepatocellular carcinoma after transcatheter arterial chemoembolization with drug-eluting beads (DEB-TACE).

PURPOSE: To identify the risk factors for local recurrence in hepatocellular carcinoma (HCC) patients treated with transcatheter arterial chemoembolization (TACE) with drug-eluting beads (DEB-TACE). MATERIALS AND METHODS: In this retrospective study, 35 patients (27 males, 8 females; median age 73 years) with 116 tumors (median size 14 mm) treated with DEB-TACE from May 2014 to September 2018 were evaluated. Age, sex, etiology, Child-Pugh class, alpha-fetoprotein, des-gamma-carboxyprothrombin, previous conventional TACE, tumor location, tumor size, tumor number, contact with the liver surface, level of embolization, corona enhancement on CT during hepatic arteriography, vascular lakes, additional embolization with gelatin sponge particles, and supplying vessels on digital subtraction angiography (DSA) after embolization were analyzed. RESULTS: Univariate analysis showed that advanced age, female, large tumor, contact with the liver surface, and residual supplying vessels were significant risk factors for local recurrence (p = 0.012, 0.0013, 0.0023, 0.025, and < 0.001, respectively). On multivariate logistic analysis, large tumor, contact with the liver surface, and residual supplying vessels on DSA were significant risk factors for local recurrence (p = 0.0026, 0.038, and < 0.001, respectively). CONCLUSION: Large tumor size, contact with the liver surface, and residual supplying vessels on DSA were significant risk factors associated with local recurrence after DEB-TACE for HCC.

Selective Balloon-occluded Retrograde Transvenous Obliteration for Gastric Varices.

Objective Balloon-occluded retrograde transvenous obliteration (B-RTO) for gastric varices (GV) is associated with drawbacks including a postoperative increase in portal pressure and the risk of subsequent worsening of esophageal varices (EV). Selective B-RTO that embolizes only the varices may have the potential to minimize such risks. The aim of this study is to retrospectively compare the postoperative course of patients after selective B-RTO (Group S) and conventional B-RTO (Group B). Methods One hundred four patients treated from January 2007 to April 2012 were classified into Groups S (n=5) and B (n=99). In the univariate analysis, the volume of 5% ethanolamine oleate iopamiodol (EOI) administered at baseline and the GV blood flow on endoscopic ultrasound after B-RTO were considered as covariates. The rates of GV recurrence and EV aggravation was also compared between Groups B and S. Results In Group S, the volume of 5% EOI was significantly lower (Group S vs. Group B: 14.6±5.5 vs. 28.5±16.4 mL; p=0.0012) and the rate of EV aggravation was lower in comparison to Group B (p=0.045). However, in Group S, the rate of complete eradication of GV blood flow was significantly lower (Group S vs. Group B: 0% vs. 89.9%; p<0.001) and the rate of re-treatment for GV was higher in comparison to Group B (Group S vs. Group B: 60% vs. 1.0%; p<0.001). Conclusion Selective B-RTO for GV could minimize the risk of a worsening of EV or reduce the amount of sclerosants; however, the rate of recurrence was high in comparison to conventional B-RTO.

Optimal blood pressure targets for patients with hypertension: a systematic review and meta-analysis.

Optimal blood pressure (BP) targets for hypertension have been an important clinical issue but have been elusive. The Systolic Blood Pressure Intervention Trial (SPRINT) showed significant benefits of intensive BP-lowering treatment with a target systolic BP level of < 120 mm Hg on major cardiovascular (CV) events and mortality, whereas there was a modest increase in renal events related to BP-lowering treatment. We searched the PubMed, Cochrane CENTRAL, and ICHUSHI databases for randomized trials that assigned participants to intensive versus usual BP-lowering treatment with different BP targets. The outcomes were major CV events, all-cause death, myocardial infarction, stroke, heart failure, renal events, and adverse events. Nineteen trials that enrolled a total of 55,529 participants with a mean follow-up duration ranging from 1.6 to 12.2 years were included in the present analysis. There was a significant reduction in major CV events, myocardial infarction, and stroke and a trend toward a reduction in heart failure associated with intensive BP-lowering treatment, but no differences in the risks of all-cause death, renal events, or adverse events were observed between the randomized groups. Subgroup analyses indicated that intensive BP-lowering treatment with a target of < 130/80 mm Hg and/or achievement of BP < 130/80 mm Hg were associated with a significant reduction in major CV events compared with the usual group. In conclusion, intensive BP-lowering treatment reduces the risk of CV events. A target BP level of < 130/80 mm Hg appears to be optimal for CV protection in patients with hypertension.

Visually-Rated Medial Temporal Lobe Atrophy with Lower Educational History as a Quick Indicator of Amnestic Cognitive Impairment after Stroke.

BACKGROUND: Time and resource limitations prevent cognitive assessment in acute-to-subacute settings, even in comprehensive stroke centers. OBJECTIVE: To assess cognitive function in acute stroke patients undergoing routine clinical, laboratory, and radiological investigations, with a view to improving post-stroke care and treatment. METHODS: Sixty-nine patients (72.6±11.1 years; 65% male) were prospectively enrolled within 14 days of acute ischemic stroke. Patients with altered consciousness, aphasia, or dysarthria were excluded. Clinical features including modified Rankin and NIH stroke scales, and vascular risk factors were assessed, as well as neuroimaging parameters by semi-quantitative evaluation of medial temporal lobe atrophy (MTLA) using MRA source images, FLAIR images for white matter changes (Fazekas scores), and T2∗ images for cerebral microbleeds. Neuropsychological screening was conducted using the Montreal Cognitive Assessment (MoCA) test. Univariate and multivariate analyses were used to evaluate the influence of variables on MoCA total and subscale scores. RESULTS: Lower MoCA scores of 22 or less were associated with MTLA [OR (95% CI), 5.3 (1.0-27.5); p = 0.045], education years [OR (95% CI), 0.71 (0.55-0.91); p = 0.007], and modified Rankin scale at discharge [OR (95% CI), 2.4 (1.3-4.5); p = 0.007]. The delayed recall MoCA score was correlated with MTLA (r = - 0.452, p < 0.001), periventricular (r = - 0.273, p = 0.024), and deep (r = - 0.242, p = 0.046), white matter changes. CONCLUSIONS: MTLA, together with lower educational history, are quick indicators of amnestic cognitive impairment after stroke. The association between cognitive impairment and physical disability at discharge may signify the importance of earlier cognitive assessment.

The Use of Bromocriptine for Peripartum Cardiomyopathy after Twin Delivery via Oocyte Donation.

Peripartum cardiomyopathy (PPCM) is rare but life-threatening. We herein report the case of a 48-year-old woman with PPCM after oocyte donation and delivery of twins. Two weeks after delivery, she suffered from severe symptoms of heart failure [orthopnea, New York Heart Association (NYHA) class IV, pulmonary edema and a reduced left ventricular ejection fraction of 18%]. Although standard heart failure therapy was effective for diminishing the congestion, it was not sufficient to improve her symptoms or left ventricular systolic dysfunction. During admission, we added bromocriptine. A year later after the onset, she was in a good state with an improved left ventricular systolic function.

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.

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.

The role of IL-6 in pathogenesis of abdominal aortic aneurysm in mice.

Although the pathogenesis of abdominal aortic aneurysm (AAA) remains unclear, evidence is accumulating to support a central role for inflammation. Inflammatory responses are coordinated by various soluble cytokines of which IL-6 is one of the major proinflammatory cytokines. In this study we examined the role of IL-6 in the pathogenesis of experimental AAA induced by a periaortic exposure to CaCl2 in mice. We now report that the administration of MR16-1, a neutralizing monoclonal antibody specific for the mouse IL-6 receptor, mildly suppressed the development of AAA. The inhibition of IL-6 signaling provoked by MR16-1 also resulted in a suppression of Stat3 activity. Conversely, no significant changes in either NFκB activity, Jnk activity or the expression of matrix metalloproteinases (Mmp) -2 and -9 were identified. Transcriptome analyses revealed that MR16-1-sensitive genes encode chemokines and their receptors, as well as factors that regulate vascular permeability and cell migration. Imaging cytometric analyses then consistently demonstrated reduced cellular infiltration for MR16-1-treated AAA. These results suggest that IL-6 plays an important but limited role in AAA pathogenesis, and primarily regulates cell migration and infiltration. These data would also suggest that IL-6 activity may play an important role in scenarios of continuous cellular infiltration, possibly including human AAA.