Use of Edoxaban for the Treatment of Heparin-Induced Thrombocytopenia.

Heparin-induced thrombocytopenia (HIT) is a life-threatening adverse drug reaction of heparin therapy, which increases a patient's risk of developing venous and/or arterial thromboembolism. HIT should be treated through discontinuation of heparin and administration of nonheparin anticoagulants such as argatroban. For long-term anticoagulation, parenteral nonheparin anticoagulants are generally converted to oral treatment with a vitamin K antagonist such as warfarin. Although administration of warfarin is recommended to overlap with a nonheparin anticoagulant for a minimum of 5 days, overlapping with argatroban and warfarin presents high risks of bleeding. We describe a case of HIT treated with edoxaban. A 78-year-old man underwent surgery for esophageal cancer and was administered heparin perioperatively. After surgery, he was diagnosed with HIT and venous thromboembolism. We immediately stopped heparin and initiated parenteral argatroban. The patient was subsequently started on edoxaban without any overlap between the two drugs. The treatment was successful. The treatment of edoxaban following argatroban for HIT could reduce bleeding complications and shorten the length of hospital stay. To the best of our knowledge, this is the first report of the use of edoxaban for HIT treatment.

The Role of Syk in Inflammatory Response of Human Abdominal Aortic Aneurysm Tissue.

Objective: Inflammatory response is central to pathogenesis of abdominal aortic aneurysm (AAA). Recently, we reported that Syk, a signaling molecule in inflammatory cells, promotes AAA development in a mouse model. In this study, we aimed to investigate the role of Syk in human AAA pathogenesis. Materials and Methods: We obtained human AAA wall samples during open surgical aortic repair at Kurume University Hospital. Immunohistochemical analyses of AAA samples were performed for Syk activation and cell type markers. Ex vivo culture of human AAA tissue was utilized to evaluate the effect of P505-15, a Syk inhibitor, on secretions of interleukin-6 (IL-6) and matrix metalloproteinases (MMPs). Results: Immunohistochemical analysis showed infiltration of B cells, T cells, and macrophages in AAA samples. Syk activation was localized mainly in B cells and part of macrophages. AAA tissue in culture secreted IL-6, MMP-9, and MMP-2 without any stimulation. The unstimulated secretions of IL-6, MMP-9, and MMP-2 were insensitive to P505-15. Secretions of IL-6 and MMP-9 were enhanced by exogenous normal human immunoglobulin G (IgG), which was suppressed by P505-15, whereas secretion of MMP-2 was insensitive to IgG or P505-15. Conclusion: These results demonstrate an important role of Syk for IgG-dependent inflammatory response in human AAA.

Aortic Dissection Associated with Autosomal Dominant Polycystic Kidney Disease

A 78-year-old man who had been diagnosed with autosomal dominant polycystic kidney disease (ADPKD) and hypertension presented with chest pain. His family history was positive for ADPKD. Chest computed tomography (CT) revealed a type A aortic dissection with thrombotic occlusion of a false lumen and an ulcer-like projection in the ascending aorta, an aneurysm of the ascending aorta, and pericardial effusion. Abdominal CT showed multiple renal and hepatic cysts. At surgery, aortic dissection with thrombotic occlusion of the false lumen and an intimal tear in the distal ascending aorta were observed. Hemiarch replacement including the intimal tear was performed. The patient is doing well without requiring dialysis and without recurrence of aortic dissection or aneurysm under strict antihypertensive therapy 3 years after the operation. Pathological examination of aortic wall specimens revealed no degenerative abnormality. ADPKD should be kept in mind as one of the causative disorders of aortic dissection.

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.

Usefulness of three-dimensional transesophageal echocardiography for diagnosis of hemolytic anemia due to inverted internal felt strip after surgery for aortic dissection.

Felt strips are widely used for reinforcement of the aortic stump in surgery for aortic dissection (AD). Postoperative hemolytic anemia (HA) due to an inverted internal felt strip at the aortic stump fixation for AD is extremely rare. A 70-year-old woman underwent ascending aorta replacement for acute type A AD, where both proximal and distal anastomotic sites were reinforced with Teflon felt strips. A week later, macroscopic hematuria and HA emerged. Three-dimensional transesophageal echocardiography (3D-TEE) demonstrated that the proximal inner felt strip turned up and protruded into the aortic inner lumen. At redo surgery, which was performed 2 weeks after the initial surgery, the findings of 3D-TEE were confirmed, and the inverted internal felt strip was replaced with a bovine pericardial strip. The findings of HA disappeared immediately after the second surgery. 3D-TEE is a very informative, valuable modality for accurate diagnosis that leads to a safe surgery.