Purpose: To evaluate the effect of vessel calcification on in-stent restenosis (ISR) after drug-coated stent (DCS) placement in the femoropopliteal segment. Materials and Methods: A retrospective multicenter study was undertaken involving 220 consecutive symptomatic patients (mean age 73.1±8.3 years; 175 men) with femoropopliteal lesions in 230 limbs treated with the Zilver PTX DCS and having duplex surveillance after the endovascular procedures. Mean lesion length was 16.4±9.8 cm (range 2–40); there were 104 (45.2%) total occlusions and 68 (29.6%) in-stent restenoses (ISR). Twenty (8.7%) vessels had no runoff. The majority of lesions (148, 64.3%) were calcified according to the peripheral arterial calcium scoring system (PACSS). Primary patency was evaluated by duplex. Lesions were classified as either PACSS 0–2 (none or unilateral wall calcification) or PACSS 3 and 4 (bilateral wall calcification). Multivariate analysis was performed to identify variables associated with ISR; the results are given as the hazard ratio (HR) and 95% confidence interval (CI). Results: The 1-, 2-, and 5-year primary patency and freedom from clinically-driven target lesion revascularization estimates were 75.9%, 63.6%, and 45.0%, and 84.7%, 73.7%, and 54.2%, respectively. Major amputations were performed on 4 limbs during follow-up. In multivariate analysis, vessel calcification (adjusted HR 1.718, 95% CI 1.035 to 2.851, p=0.036) was significantly correlated with the occurrence of ISR, along with lesion length (adjusted HR 1.041, 95% CI 1.013 to 1.070, p=0.003), and cilostazol administration (adjusted HR 0.476, 95% CI 0.259 to 0.876, p=0.017). Conclusion: This study suggested that bilateral vessel wall calcification was an independent risk factor for ISR in complex femoropopliteal lesions after Zilver PTX DCS placement, along with lesion length; cilostazol administration had a protective effect.

No abstract

IntroductionType II endoleak (EL) is frequently seen after endovascular aneurysm repair (EVAR) for abdominal aortic aneurysm (AAA) and is often considered responsible for aneurysm sac enlargement if it persists. In order to reduce type II EL and consequent sac enlargement, pre-emptive embolisation of the inferior mesenteric artery (IMA), which is a main source for persistent type II EL, has been introduced in many vascular centres. At present, there is a lack of robust evidence to support the efficacy of pre-emptive embolisation of IMA on reduction of persistent type II EL with subsequent sac shrinkage.Method and analysisThis multicentre, randomised controlled trial will recruit 200 patients who have fusiform AAA ≥50 mm/rapidly enlarging fusiform AAA, with patent IMA, and randomly allocate them either to a pre-emptive IMA embolisation group or non-embolisation control group in a ratio of 1:1. The primary endpoint is the difference of aneurysm sac volume change assessed by CT scans between the pre-emptive IMA embolisation group and the control group at 12 months after EVAR. The secondary endpoints are defined as change of aneurysm sac volume in both groups at 6 and 24 months, freedom from sac enlargement at 12 and 24 months after EVAR, prevalence of type II EL at 1, 6, 12 and 24 months evaluated by contrast-enhanced CT, reintervention rate, aneurysm related mortality, overall survival, perioperative morbidity, volume of contrast media used during EVAR and dosage of radiation.Ethics and disseminationThe protocol has been reviewed and approved by the ethics committee of Nara Medical University (No. 2113). The findings of this study will be communicated to healthcare professionals, participants and the public through peer-reviewed publications, scientific conferences and the University Hospital Medical Information Network Clinical Trials Registry home page.Trial registration numberUMIN000035502.

Background: Abdominal aortic aneurysms (AAA) with iliac artery occlusive diseases are not uncommon. When an occlusion extends from iliac artery to common femoral artery (CFA), adjunctive procedures such as endareterectomy of CFA and angioplasty of iliac artery are performed prior to endovascular aneurysm repair (EVAR). Alternatively, aorto-uni-iliac stentgrafting with femoro-femoro bypass surgery could be performed. If run off vessels such as superficial femoral artery (SFA) and profunda femoris artery (PFA) are both occluded in addition to the CFA, surgical procedures may become extremely complex, with much longer procedure time. We present an unusual case of AAA with arterial occlusion ranging from external iliac artery (EIA) to superficial and profunda femoris arteries, which was fully managed with endovascular means. Case presentation: The patient was a 76 year old male who was found incidentally to have a fusiform infrarenal AAA, the size of which was 55 mm in maximal transverse diameter. Despite the occlusions of left EIA, CFA and proximal parts of SFA and PFA, he did not have ischemic symptoms in his left leg due to the development of abundant collateral networks from left internal iliac artery. The patient had a past history of endarterectomy of left CFA. Since a repeated endarterectomy or interposition grafting of the CFA were deemed extremely difficult, without any patent runoff vessel, EVAR was performed using the occluded vessel simply as a conduit for the delivery of the endograft, without revascularizing the vessel. An angioplasty balloon was delivered from right CFA to the occluded left CFA through a subintimal space. A percutaneous puncture of the expanded balloon was done at the occluded left CFA under fluoroscopy, inserting the guidewire into the punctured balloon, finally establishing the through and through wire. EVAR was successfully performed using AFX unibody stentgraft without any complication. Conclusion: AAA with access vessel occlusions from EIA to SFA was successfully treated with EVAR with the aid of the balloon oriented percutaneous puncture technique. Having the technique as an armamentarium can broaden the application of EVAR for AAA with the complicated access.