6 research outputs found

    Deficiency of interleukin-1 receptor antagonist causes spontaneous femoral artery aneurysms

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    Interleukin (IL) -1, a proinflammatory cytokine, increases in aneurysm, and the IL-1 receptor antagonist (IL-1Ra) modulates IL-1 activity endogenously. We show here that IL-1Ra-deficiency in hematopoietic cells disrupts immune system homeostasis and causes spontaneous femoral artery aneurysms in mice lacking interventions such as drugs or surgery. Thus, IL-1Ra-deficient mice provide easy observations with age and diminish mortality that typically follows surgical procedures. Furthermore, since IL-1Ra-deficient mice contain the entire spectrum of lesions observed during inflammatory aneurysm, this mouse model likely will provide numerous opportunities to study the pathogenesis and therapy of inflammatory aneurysm

    Macrophage Notch Ligand Delta-Like 4 Promotes Vein Graft Lesion Development, Implications for the Treatment of Vein Graft Failure

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    Objective—Despite its large clinical impact, the underlying mechanisms for vein graft failure remain obscure and no effective therapeutic solutions are available. We tested the hypothesis that Notch signaling promotes vein graft disease. Approach and Results—We used 2 biotherapeutics for Delta-like ligand 4 (Dll4), a Notch ligand: (1) blocking antibody and (2) macrophage- or endothelial cell (EC)–targeted small-interfering RNA. Dll4 antibody administration for 28 days inhibited vein graft lesion development in low-density lipoprotein (LDL) receptor-deficient (Ldlr−/−) mice, and suppressed macrophage accumulation and macrophage expression of proinflammatory M1 genes. Dll4 antibody treatment for 7 days after grafting also reduced macrophage burden at day 28. Dll4 silencing via macrophage-targeted lipid nanoparticles reduced lesion development and macrophage accumulation, whereas EC-targeted Dll4 small-interfering RNA produced no effects. Gain-of-function and loss-of-function studies suggested in vitro that Dll4 induces proinflammatory molecules in macrophages. Macrophage Dll4 also stimulated smooth muscle cell proliferation and migration and suppressed their differentiation. Conclusions—These results suggest that macrophage Dll4 promotes lesion development in vein grafts via macrophage activation and crosstalk between macrophages and smooth muscle cells, supporting the Dll4–Notch axis as a novel therapeutic target.United States. National Institutes of Health (R01HL107550)American Heart Association (0655878T)American Heart Association (12GRNT9510001)American Heart Association (12GRNT1207025)Good Samaritan FoundationShapiro Family Foundatio

    Pulmonary intravascular lymphoma diagnosed by 18-fluorodeoxyglucose positron emission tomography-guided transbronchial lung biopsy in a man with long-term survival: a case report

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    <p>Abstract</p> <p>Introduction</p> <p>18-Fluorodeoxyglucose positron emission tomography can detect the pulmonary involvement of intravascular lymphoma that presents no abnormality in a computed tomography scan.</p> <p>Case presentation</p> <p>We report the case of a 61-year-old Japanese man who had pulmonary intravascular lymphoma and no computed tomography abnormality. We were able to make an antemortem diagnosis of pulmonary intravascular lymphoma by transbronchial lung biopsy according to 18-fluorodeoxyglucose positron emission tomography findings. He is free of recurrent disease 24 months after chemotherapy.</p> <p>Conclusions</p> <p>To the best of our knowledge, this is the first reported case of a long-term survivor of pulmonary intravascular lymphoma diagnosed by transbronchial lung biopsy under the guide of 18-fluorodeoxyglucose positron emission tomography.</p

    Successful healing of aneurysmal false lumen using a second-generation drug-eluting stent in spontaneous coronary artery dissection: a case report

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    Abstract Background According to 2023 ESC Guideline, conservative medical management is generally recommended for the treatment of spontaneous coronary artery dissection (SCAD) except for patients with signs of ongoing myocardial ischemia. However, in some cases, invasive treatment (coronary artery bypass graft surgery or percutaneous coronary intervention (PCI)) is performed because of the progression of aneurysm in SCAD. Although there is no established strategy for the management of coronary aneurysm in SCAD, we report a case of successful healing of aneurysmal false lumen (AFL) using a second-generation drug-eluting stent (DES) in SCAD. Case presentation A 44-year-old woman without any cardiovascular risk factors was transferred to our hospital due to inferior myocardial infarction. Coronary angiography (CAG) showed multiple SCADs in the coronary artery. We performed PCI to the distal right coronary artery (RCA) because the RCA showed severe stenosis (99%) with bradycardia. Six days after the first PCI, SCAD relapsed in the mid left anterior descending artery (LAD). Furthermore, AFL was observed by intravascular ultrasound imaging. To avoid enlargement of the AFL and progression of the dissection toward the proximal site of the LAD, we performed PCI to the mid LAD to seal the entry tear of the dissection using a second-generation DES. CAG revealed that the AFL in the mid LAD completely diminished at 1 year after PCI. Conclusions The implantation of a second-generation DES might be one of therapeutic options for sealing AFL in SCAD patients
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