Surgical Treatment of Cystic Adventitial Disease of the Popliteal Artery: Five Case Reports

Cystic adventitial disease (CAD) is a rare cause of intermittent claudication and nonatherosclerotic conditions in middle-aged men without cardiovascular risk factors. The etiology of CAD is unclear; however, the direct communication between a cyst and a joint is presumed to be a cause. We herein report a case series of CAD of the popliteal artery (CADPA), in which patients were treated with surgical resection and vascular reconstruction. Although less invasive treatment modalities, including percutaneous cyst aspiration and percutaneous transluminal angioplasty, have been the subject of recent reports, these treatments have had a higher recurrence rate. Therefore, all of the CAPDA cases in the present series were treated surgically, which lead to good outcomes

Clinical Study Relationship of Inflammatory Biomarkers with Severity of Peripheral Arterial Disease

Objective. The pentraxin family, including high-sensitivity C-reactive protein (hs-CRP), serum amyloid P (SAP), and pentraxin 3 (PTX3), has been identified as playing a key role in inflammatory reactions such as in atherosclerosis and cardiovascular disease. In this study, we examined the relationship between peripheral arterial disease (PAD) and serum levels of pentraxins. Methods. This study was undertaken via a retrospective review of PAD patients with surgical intervention for lesions of the common femoral artery. We evaluated the preoperative patient conditions, hemodynamic status, such as ankle brachial index (ABI), and clinical ischemic conditions according to Rutherford classification. Preoperatively, we collected blood samples for determining the serum levels of hs-CRP, SAP, and PTX3. Results. Twelve PAD patients with common femoral arterial lesions were treated and examined. The hemodynamic severity of PAD was not negatively correlated with hs-CRP, SAP, or PTX3. The clinical severity evaluated by Rutherford classification was significantly positively correlated with the serum level of PTX3 ( = 0.019). Conclusion. We demonstrated that PTX3 might be a better marker of PAD than hs-CRP and SAP. Furthermore, PTX3 might be a prognostic marker to evaluate the severity of PAD

Endothelial Dysfunction of Patients with Peripheral Arterial Disease Measured by Peripheral Arterial Tonometry

Objective. Endothelial dysfunction plays a key role in atherosclerotic disease. Several methods have been reported to be useful for evaluating the endothelial dysfunction, and we investigated the endothelial dysfunction in patients with peripheral arterial disease (PAD) using peripheral arterial tonometry (PAT) test in this study. Furthermore, we examined the factors significantly correlated with PAT test. Methods. We performed PAT tests in 67 patients with PAD. In addition, we recorded the patients’ demographics, including comorbidities, and hemodynamical status, such as ankle brachial pressure index (ABI). Results. In a univariate analysis, the ABI value (r=0.271, P=0.029) and a history of cerebrovascular disease (r=0.208, P=0.143) were found to significantly correlate with PAT test, which calculated the reactive hyperemia index (RHI). In a multivariate analysis, only the ABI value significantly and independently correlated with RHI (β=0.254, P=0.041). Conclusion. This study showed a significant correlation between RHI and ABI. The PAT test is a useful tool for evaluating not only endothelial dysfunction but also the hemodynamical state in patients with PAD

The Infrapopliteal Arterial Occlusions Similar to Buerger Disease: Report of Two Cases

We herein present two cases that required the differential diagnosis of Buerger disease. Case 1 involved a 55-year-old male with a smoking habit who was admitted with ulcers and coldness in his fingers and toes. Angiography showed blockage in both the radial and posterior tibial arteries, which led to an initial diagnosis of Buerger disease. However, a biopsy of the right posterior tibial artery showed pathological findings of fibromuscular dysplasia (FMD). Case 2 involved a 28-year-old male with intermittent claudication who was examined at another hospital. Angiography showed occlusion of both popliteal and crural arteries, and the patient was suspected to have Buerger disease. However, computed tomography disclosed an abnormal slip on both sides of the popliteal fossa, and we diagnosed him with bilateral popliteal artery entrapment syndrome (PAES). These cases illustrate that other occlusive diseases, such as FMD and PAES, may sometimes be misdiagnosed as Buerger disease

Osteoclast-Like Cells in Aneurysmal Disease Exhibit an Enhanced Proteolytic Phenotype

Abdominal aortic aneurysm (AAA) is among the top 20 causes of death in the United States. Surgical repair is the gold standard for AAA treatment, therefore, there is a need for non-invasive therapeutic interventions. Aneurysms are more closely associated with the osteoclast-like catabolic degradation of the artery, rather than the osteoblast-like anabolic processes of arterial calcification. We have reported the presence of osteoclast-like cells (OLCs) in human and mouse aneurysmal tissues. The aim of this study was to examine OLCs from aneurysmal tissues as a source of degenerative proteases. Aneurysmal and control tissues from humans, and from the mouse CaPO4 and angiotensin II (AngII) disease models, were analyzed via flow cytometry and immunofluorescence for the expression of osteoclast markers. We found higher expression of the osteoclast markers tartrate-resistant acid phosphatase (TRAP), matrix metalloproteinase-9 (MMP-9), and cathepsin K, and the signaling molecule, hypoxia-inducible factor-1α (HIF-1α), in aneurysmal tissue compared to controls. Aneurysmal tissues also contained more OLCs than controls. Additionally, more OLCs from aneurysms express HIF-1α, and produce more MMP-9 and cathepsin K, than myeloid cells from the same tissue. These data indicate that OLCs are a significant source of proteases known to be involved in aortic degradation, in which the HIF-1α signaling pathway may play an important role. Our findings suggest that OLCs may be an attractive target for non-surgical suppression of aneurysm formation due to their expression of degradative proteases