Raison d'etre of Tibial Artery Bypass for Intermittent Claudication in the Era of Endovascular Therapy.

BACKGROUND: There is currently no positive opinion regarding infrapopliteal revascularization for intermittent claudication (IC) in any guidelines. The aim of this study was to analyze the outcomes of infragenicular bypass and verify the adequacy of tibial artery bypass for IC. METHODS AND RESULTS: Over a 21-year period, 58 below-knee popliteal artery (BKPOP) bypasses and 35 tibial artery bypasses were performed for IC caused by arteriosclerosis obliterans. Graft patency and major amputation (MA) were examined as primary endpoints and the predictor of each outcome was estimated by multivariate analysis. The primary patency (PP), secondary patency (SP), and freedom from MA (ffMA) rates of a prosthetic/vein graft in all cases at 5 years were 19/68%, 22/86%, and 78/100% (P<0.01 in all). Limited to vein graft cases, PP and SP rates of popliteal/tibial bypass at 5 years were 73/62% (P=0.32) and 92/80% (P=0.22), respectively. In tibial artery bypass with a vein graft, the PP and SP rates of a single saphenous vein/spliced vein graft at 5 years were 71/46% (P=0.11) and 89/61% (P=0.03). A prosthetic graft was a common negative predictor for graft patency and MA by multivariate analysis. CONCLUSIONS: Tibial artery bypass is an acceptable treatment option for IC when a single saphenous vein can be harvested as a graft conduit. (Circ J 2016; 80: 1460-1469).

Arteriovenous malformation arising on persistent sciatic vessels.

BACKGROUND: A persistent sciatic artery is a rare congenital anomaly, and an arteriovenous malformation arising on persistent sciatic vessels is extremely rare. METHODS: This report presents the case of a 30-year-old female with persistent sciatic vessels complicated with an arteriovenous malformation in the right buttock. It was surgically inaccessible, and a three-staged transcatheter embolization using 20% N-butyl-cyanoacrylate/80% lipiodol was performed. RESULTS: The arteriovenous malformation was shown to have been extinguished by multidetector computed tomography. CONCLUSIONS: This report presents the first case of persistent sciatic vessels complicated with an arteriovenous malformation treated by transcatheter embolization.

Hypereosinophilic syndrome accompanying gangrene of the toes with peripheral arterial occlusion--a case report.

The authors herein report the case of a teenage boy who presented with peripheral arterial occlusion of both upper and lower extremities associated with hypereosinophilia. During a 10-year follow-up, corticosteroid therapy was continued for the treatment of hypereosinophilia. The patient underwent bilateral lumbar sympathectomies because of severe ischemia of the bilateral lower extremities with gangrene of the toes. Based on the progress of his disease over the past 10 years, he was suspected to have idiopathic hypereosinophilic syndrome (HES) accompanied by peripheral arterial obstruction. Idiopathic HES is a disease characterized by unexpected hypereosinophilia, which may lead to organ damage. This is a very rare case of peripheral arterial occlusion associated with idiopathic HIS.

[Gastrointestinal stromal tumor of the omentum: report of a case].

A 69-year old man was found a mass becoming larger in abdominal computed tomography. The mass consisted of intermingling solid and cystic component was located below the liver. Abdominal angiography showed tumor staining supplied from right gastroepiploic artery. We considered the mass cystadenoma, lymphangioma, cystic mesothelioma, or gastrointestinal stromal tumor (GIST) preoperatively, and then surgical resection was performed. The tumor was found localized in the greater omentum. Pathological examination showed the tumor composed of proliferation of atypical sort spindle cells and tumor cells were immunohistochemically positive for C-KIT and CD34, identifying the tumor as a primary GIST of the greater omentum.

Serum protein acrolein adducts: utility in detecting oxidant stress in hemodialysis patients and reversal using a vitamin E-bonded hemodialyzer.

Accumulating evidence indicates that protein modification by acrolein is one of the major hallmarks of atherosclerosis. The purpose of the present study was to evaluate the serum acrolein-modified protein adduct (Acr) level in end-stage renal disease (ESRD), and to elucidate the efficacy of vitamin E-bonded hemodialyzer in reducing Acr in a crossover trial. A significant increase in Acr was found in ESRD patients compared with healthy controls (p <.001). In ESRD, the Acr level of those patients with type 2 diabetes mellitus (DM) was significantly higher compared with the non-DM group (p <.05). Forty-one ESRD patients who exhibited Acr levels higher than the mean value in ESRD were treated by vitamin E-bonded hemodialyzer for 6 months. After 6 months of treatment, Acr levels were decreased to those found in healthy individuals (p <.001). When hemodialyzers were switched back from vitamin E bonded to the original regular ones, Acr levels increased to nearly their initial levels after 3 months (p <.001), compared with the 6 month time point. These results suggest the potential of Acr as an oxidative stress marker in ESRD, and that vitamin E-bonded hemodialyzer treatment is a reasonable approach to reduce oxidative stress in ESRD.

Fibroblast growth factor-2 gene transfer can stimulate hepatocyte growth factor expression irrespective of hypoxia-mediated downregulation in ischemic limbs.

Hepatocyte growth factor (HGF) is a potent angiogenic polypeptide that stimulates angiogenesis. Transcriptional regulation of HGF, however, has not been fully defined, with the exception of the hypoxia-mediated downregulation in cultured cells. In the present study, we report that angiogenic growth factors, including HGF, were upregulated in a murine model of critical limb ischemia in vivo, a finding that was in conflict with previous in vitro data. Mice deficient in basic fibroblast growth factor-2 (FGF-2) showed reduced induction of HGF protein in ischemic muscles, and overexpression of FGF-2 via gene transfer stimulated endogenous HGF, irrespective of the presence of ischemia. In culture, FGF-2 rapidly stimulated HGF mRNA, and a sustained expression was evident in the time course in vascular smooth muscle cells and fibroblasts. FGF-2-mediated induction of HGF was fully dependent on the mitogen-activated protein kinase pathway yet was not affected by either hypoxia or a protein kinase A inhibitor. In the early expression, FGF-2 directly stimulated HGF mRNA without the requirement of new protein synthesis, whereas sustained induction of HGF in the later phase was partly mediated by platelet-derived growth factor-AA. Furthermore, in vivo overexpression of FGF-2 significantly improved the blood perfusion, and the effect was abolished by systemic blockade of HGF in ischemic limbs. This is the first demonstration of a regulational mechanism of HGF expression via FGF-2 that was independent of the presence of hypoxia. The harmonized therapeutic effects of FGF-2, accompanied with the activity of endogenous HGF, may provide a beneficial effect for the treatment of limb ischemia.

Angiogenic gene therapy for experimental critical limb ischemia: acceleration of limb loss by overexpression of vascular endothelial growth factor 165 but not of fibroblast growth factor-2.

Recent studies suggest the possible therapeutic effect of intramuscular vascular endothelial growth factor (VEGF) gene transfer in individuals with critical limb ischemia. Little information, however, is available regarding (1) the required expression level of VEGF for therapeutic effect, (2) the related expression of endogenous angiogenic factors, including fibroblast growth factor-2 (FGF-2), and (3) the related adverse effects due to overexpression of VEGF. To address these issues, we tested effects of overexpression of VEGF165 using recombinant Sendai virus (SeV), as directly compared with FGF-2 gene transfer. Intramuscular injection of SeV strongly boosted FGF-2, resulting in significant therapeutic effects for limb salvage with increased blood perfusion associated with enhanced endogenous VEGF expression in murine models of critical limb ischemia. In contrast, VEGF165 overexpression, 5-times higher than that of baseline on day 1, also strongly evoked endogenous VEGF in muscles, resulting in an accelerated limb amputation without recovery of blood perfusion. Interestingly, viable skeletal muscles of either VEGF165- or FGF-2-treated ischemic limbs showed similar platelet-endothelial cell adhesion molecule-1-positive vessel densities. Maturation of newly formed vessels suggested by smooth muscle cell actin-positive cell lining, however, was significantly disturbed in muscles with VEGF. Further, therapeutic effects of FGF-2 were completely diminished by anti-VEGF neutralizing antibody in vivo, thus indicating that endogenous VEGF does contribute to the effect of FGF-2. These results suggest that VEGF is necessary, but should be delicately regulated to lower expression to treat ischemic limb. The therapeutic effect of FGF-2, associated with the harmonized angiogenic effects seen with endogenous VEGF, provides important insights into therapeutic angiogenesis.