Journal of vascular surgery
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Comparative Study
A morphologic study of chronic type B aortic dissections and aneurysms after thoracic endovascular stent grafting.
The long-term results of treating chronic aortic dissections and aneurysms in association with dissections with thoracic endovascular aortic repair (TEVAR) are unknown, and the timing for intervention is uncertain. We evaluated the morphology of stent graft and aorta remodeling and the volumetric changes in these patients after successful TEVAR. ⋯ Aortic remodeling after TEVAR in chronic dissection is a continuous process. There were no significant differences between chronic dissections and aneurysms in all volumetric parameters. Treating chronic dissections early, before aneurysm formation, did not appear to have a morphologic advantage.
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Endovascular techniques have shown to be useful in the management of vascular injuries because they transform a complex and potentially dangerous procedure into a safe one. We present the case of a 39-year-old man with congestive heart failure and abdominal bruit 11 years after an abdominal gunshot wound. ⋯ Symptoms resolved, and follow-up imaging showed patency of the graft and closure of the arteriovenous communication. To our knowledge, this is the first report of a nonaneurysmal disease treated with this device.
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Venous hypoxia has been postulated to contribute to varicose vein (VV) formation. Direct measurements of vein wall oxygen tension have previously demonstrated that the average minimum oxygen tensions were significantly lower in VVs compared with non-varicose veins (NVVs). Hypoxia-inducible factors (HIFs) are nuclear transcriptional factors that regulate the expression of several genes of oxygen homeostasis. This study aimed to investigate if hypoxia was associated with VVs by assessing the expression of HIF-1α, HIF-2α, HIF target genes, and upstream HIF regulatory enzymes in VVs and NVVs, and their regulation by hypoxia. ⋯ The study concluded, we believe for the first time, an increased activation of the HIF pathway, with upregulation of the expression of HIF-1α and HIF-2α transcription factors, and HIF target genes, in VVs compared with NVVs. Exposure of VVs and NVVs to hypoxic conditions was associated with increased expression of HIF-1α and HIF-2α protein and HIF target genes. The data suggest that the HIF pathway may be associated with several pathophysiologic changes in the VV wall, and that hypoxia may be a feature contributing to VV pathogenesis.
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In patients with Marfan syndrome, the complications of aortic degeneration, including dissection, aneurysm, and rupture represent the main cause of mortality. Although contemporary management of ascending aortic disease requires open surgical reconstruction, endovascular repair is now available for management of descending thoracic and abdominal aortic pathology (ie, thoracic endovascular aortic repair [TEVAR], endovascular aneurysm repair [EVAR]). The short- and long-term benefit of endovascular repair in Marfan patients remains largely unproven. We examine our outcomes after EVAR in this patient population. ⋯ Aortic disease associated with Marfan syndrome is a complex clinical problem and many patients require remedial procedures. Endovascular therapy can provide a useful adjunct or bridge to open surgical treatment in selected patients. However, failure of endovascular therapy is common, and its use should be judicious with close follow-up to avoid delay if open surgical repair is required.
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Type II endoleak (T2EL) with aneurysm expansion is believed to place patients at risk for aneurysm-related mortality (ARM). Treatment with glue and/or coil embolization of the aneurysm sac, inferior mesenteric artery (IMA), and lumbar branches via translumbar or transarterial approaches has been utilized to ablate such endoleaks, and thus decrease ARM. We evaluated the midterm results of percutaneous endovascular treatment of T2EL with aneurysm expansion. ⋯ In this series, percutaneous endovascular intervention for type II endoleak with aneurysm sac growth does not appear to alter the rate of aneurysm sac growth, and the majority of patients display persistent/recurrent endoleak. However, diagnostic angiographic evaluation may reveal unexpected type I and III endoleaks and is therefore recommended for all patients with T2EL and sac growth. While coil and glue embolization of aneurysm sac and selected branch vessels does not appear to yield benefit in our series, the diagnosis and subsequent definitive treatment of previously occult type I and III endoleaks may explain the absence of delayed rupture and ARM in our series.