Survival is not improved by elective repair of abdominal aortic aneurysms smaller than 5.5 cm, even when operative mortality is low.

Given the encouraging study results and the significant burden of DFU, use of this mat may result in significant reductions in morbidity, mortality, and resource utilization.

Abstract-Cilostazol is an antiplatelet agent and vasodilator marketed in Japan for treatment of ischemic symptoms of peripheral vascular disease. It is currently being evaluated in the United States for treatment of symptomatic intermittent claudication (IC). Cilostazol has been shown to improve walking distance in patients with IC. In addition to its reported vasodilator and antiplatelet effects, cilostazol has been proposed to have beneficial effects on plasma lipoproteins. We examined the effect of cilostazol versus placebo on plasma lipoproteins in 189 patients with IC. After 12 weeks of therapy with 100 mg cilostazol BID, plasma triglycerides decreased 15% (PϽ0.001). Cilostazol also increased plasma high density lipoprotein cholesterol (HDL-C) (10%) and apolipoprotein (apo) A1 (5.7%) significantly (PϽ0.001 and PϽ0.01, respectively). Both HDL 3 and HDL 2 subfractions were increased by cilostazol; however, the greatest percentage increase was observed in HDL 2 . Individuals with baseline hypertriglyceridemia (Ͼ140 mg/dL) experienced the greatest changes in both HDL-C and triglycerides with cilostazol treatment. In that subset of patients, HDL-C was increased 12.2% and triglycerides were decreased 23%. With cilostazol, there was a trend (3%) toward decreased apoB as well as increased apoA1, resulting in a significant (9.8%, PϽ0.002) increase in the apoA1 to apoB ratio. ilostazol is a vasodilator and platelet aggregation inhibitor that has been marketed since 1988 in Japan for treatment of ischemic symptoms of peripheral vascular disease. Cilostazol {6[4-(1-cyclohexyl-1H-tetrazol-5-yl)butoxy]-3,4-dihydro-2-(1H)-quinolinone} is a 2-oxoquinolone derivative (molecular weight, 369.47) that has a plasma half-life of 10.5Ϯ4.4 hours after oral administration (Figure 1). Cilostazol inhibits both primary and secondary platelet aggregation in response to ADP, collagen, epinephrine, and arachidonic acid.1,2 The antiplatelet and vasodilator properties of cilostazol have been attributed to its ability to elevate intracellular levels of cAMP.3 Cilostazol is currently being evaluated in the United States for treatment of symptomatic intermittent claudication (IC). Japanese studies performed in diabetic patients have indicated that, in addition to its vasodilator and antiplatelet properties, cilostazol may also favorably modify plasma lipoproteins by increasing HDL cholesterol (HDL-C) and reducing triglycerides. 4 The purpose of the present study was to determine whether cilostazol favorably modifies plasma lipoproteins in a general population of patients with stable IC. Methods Patient PopulationThe study included subjects with documented chronic, stable, symptomatic IC secondary to peripheral arterial disease (PAD). PAD was defined as an ankle-brachial index (ABI) Յ0.90; termination of walking on a variable-load, constant-speed treadmill due to IC (Ͼ54 and Ͻ805 m); and a Doppler-measured drop of Ն10 mm Hg in blood pressure of 1 ankle after the treadmill test. For patients without a qualifying ABI, a 20 -mm Hg drop in postexe...

SummaryBackgroundClostridium difficile infection is the most common health-care-associated infection in the USA. We assessed the safety and efficacy of ridinilazole versus vancomycin for treatment of C difficile infection.MethodsWe did a phase 2, randomised, double-blind, active-controlled, non-inferiority study. Participants with signs and symptoms of C difficile infection and a positive diagnostic test result were recruited from 33 centres in the USA and Canada and randomly assigned (1:1) to receive oral ridinilazole (200 mg every 12 h) or oral vancomycin (125 mg every 6 h) for 10 days. The primary endpoint was achievement of a sustained clinical response, defined as clinical cure at the end of treatment and no recurrence within 30 days, which was used to establish non-inferiority (15% margin) of ridinilazole versus vancomycin. The primary efficacy analysis was done on a modified intention-to-treat population comprising all individuals with C difficile infection confirmed by the presence of free toxin in stool who were randomly assigned to receive one or more doses of the study drug. The study is registered with ClinicalTrials.gov, number NCT02092935.FindingsBetween June 26, 2014, and August 31, 2015, 100 patients were recruited; 50 were randomly assigned to receive ridinilazole and 50 to vancomycin. 16 patients did not complete the study, and 11 discontinued treatment early. The primary efficacy analysis included 69 patients (n=36 in the ridinilazole group; n=33 in the vancomycin group). 24 of 36 (66·7%) patients in the ridinilazole group versus 14 of 33 (42·4%) of those in the vancomycin group had a sustained clinical response (treatment difference 21·1%, 90% CI 3·1–39·1, p=0·0004), establishing the non-inferiority of ridinilazole and also showing statistical superiority at the 10% level. Ridinilazole was well tolerated, with an adverse event profile similar to that of vancomycin: 82% (41 of 50) of participants reported adverse events in the ridinilazole group and 80% (40 of 50) in the vancomycin group. There were no adverse events related to ridinilazole that led to discontinuation.InterpretationRidinilazole is a targeted-spectrum antimicrobial that shows potential in treatment of initial C difficile infection and in providing sustained benefit through reduction in disease recurrence. Further clinical development is warranted.FundingWellcome Trust and Summit Therapeutics.

Age, gender, race, and body size have statistically significant but small effects on IAD. Use of these parameters to define AAA may not offer sufficient advantage over simpler definitions (such as an IAD > or = 3.0 cm) to be warranted.

A 10 mm woven Dacron axillofemoral bypass graft was removed from a 65-year-old patient during redo surgery after an implant period of 26 months, because of a large seroma that surrounded the entire length of the graft. Tissue blocks were taken from representative areas along the entire length of the graft surface and evaluated by light microscopy with hematoxylin and eosin and Masson trichrome staining, scanning electron microscopy, transmission electron microscopy, and immunocytochemical staining. Paraffin-embedded sections were stained with smooth muscle cell alpha-actin, which demonstrated smooth muscle cells in the pseudointima, and Ham 56 stain to identify macrophages. Endothelial factor VIII/von Willebrand factor and Ulex europaeus agglutinin identified human endothelial cells on the flow surface, in areas far removed from the anastomoses to the native vessels. This is the first definitive proof in a human of endothelialization of a synthetic arterial graft beyond the pannus ingrowth zone.

Abbreviations: ABI ϭ ankle/brachial index, OR ϭ odds ratio, UK ϭ urokinase PURPOSE: To improve the patency rate for angioplasty in chronic occlusion of the superficial femoral artery by deploying stents after angioplasty. MATERIALS AND METHODS:Angioplasty and stent placement were performed in 61 arteries in 48 male patients. The mean occlusion length was 13.5 cm and the mean stent length was 30 cm. Patency rates were analyzed at 6 months and at 1, 2, 3, and 4 years. The predictors of restenosis were analyzed by univariate and multiple logistic regression.RESULTS: Patency rates were 87% at 6 months, consisting of 74% primary, 6% primary assisted, and 7% secondary; 79% at 1 year, consisting of 47% primary, 19% primary assisted, and 13% secondary; 72% at 2 years, consisting of 36% primary, 26% primary assisted, and 10% secondary; 70% at 3 years, consisting of 26% primary, 22% primary assisted, and 22% secondary; and 63% at 4 years, consisting of 25% primary, 0% primary assisted, and 38% secondary. There was a 15% morbidity rate and one mortality as a result of retroperitoneal bleeding. Better patency rates were noted at all time intervals in diabetic limbs, 7-mm-diameter versus 10-mmdiameter stents, shorter obstructions and shorter stents, nonsmokers, in limbs in which urokinase was not necessary after stent deployment, and in limbs with an International Society of Cardiovascular Surgery (ISCVS) classification under 3. Patency rates were not affected by age, race, number of trifurcation vessels patent, experience in performing the procedures, and procedures requiring less time. By multivariate logistic analysis, the independent predictors of patency at 6 months were postprocedure ankle/brachial index (ABI) and shorter stent length; at 1 year, preprocedure ABI, shorter stent length, and the presence of diabetes; at 2 years, preprocedure ABI and the presence of diabetes; and at 3 years, the preprocedure ABI. CONCLUSIONS:The techniques used to reestablish antegrade flow in these superficial femoral arteries yielded a high success rate. In addition, the use of angioplasty with stents may improve patency rates over angioplasty without stents.A common cause of lower extremity claudication is arteriosclerotic occlusion of the superficial femoral artery. A recent analysis of leg arteriograms on 1,000 consecutive patients with lower extremity claudication from our medical center revealed that in patients with no previous surgical or radiologic intervention in the arteries of the

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