Search

To identify the risk factors associated with patency loss after bailout stenting with third-generation hybrid heparin-bonded nitinol stent of the femoropopliteal segment. Prospective, multicenter, single-arm registry including 156 patients (50 females, mean age 72 ± 11 years) subjected, from February 2017 to December 2018, to provisional stenting with Gore Tigris vascular stent of the distal superficial femoral artery, with or without involvement of the popliteal artery, in 9 different centers. The 194 lesions, with Rutherford score ≥ 3, were stented in case of recoil, dissection or residual stenosis not responding to percutaneous trans-luminal angioplasty (PTA). The follow-up (FU) was performed with clinical evaluation and duplex ultrasound (DUS) at 1, 6 and 12 months. The primary patency rate was 99(95%CI 98–100)% at 1 month, 86(80–92)% at 6 months and 81(74–88)% at-12 months. After patency loss, 13/23 (56.5%) patients were re-treated, yielding a primary assisted patency of 91(86–96)% at 6 months and 88(82–94)% at 12 months and a secondary patency of 94(90–98)% at 6 months and 90(84–95)% at 12 months. Rutherford score ≥ 4 (p = 0.03) and previous severe treatments (p = 0.01) were identified as risk factors for early patency loss during FU. The involvement of the popliteal artery was not an independent risk factor for loss of patency. The bailout stenting of the femoropopliteal segment with third-generation nitinol stents is a safe and effective option in case of recoil, dissection or residual stenosis not responding to PTA. Critical limb ischemia and history of previous major treatment at the same level are significant prognostic factors for patency loss during FU.

The aim of our study is to assess the effectiveness of popliteal artery aneurysm (PAA) endovascular treatment. We retrospectively evaluated 48 high-surgical-risk patients that presented at our three departments with evidence of popliteal artery aneurysms, both symptomatic and asymptomatic, and were therefore treated by deployment of stent graft. Immediate technical success was 100%. No periprocedural complications occurred. During a mean follow-up of 24.5 months (range 6–72), 12/48 occlusions of stent graft occurred, five of which occurred in the first 30 days after the procedure while other seven occurred during long-term follow-up. Primary stent patency rate was 70.8% and secondary stent patency rate was 89.6% at 1 year. No limb amputation was witnessed. According to our experience, endovascular approach appeared as an effective treatment for popliteal artery aneurysms, as it appeared affected by a low rate of peri- and post-procedural complications. It could be proposed as treatment of choice in patients with high surgical risk.

Background Intraprocedural aneurysm sac embolization (embo-EVAR) during endovascular abdominal aneurysm repair (EVAR) using coils and fibrin glue is a technique for preventing type II endoleak (EII). Our aim is to evaluate feasibility, safety and clinical outcome of this promising approach. Materials and Methods A retrospective clinical case analysis of 72 patients who underwent EVAR during the period 2011–2014. Two groups were compared at 6 and 12 months follow-up with contrast media computed tomography scan and contrast-enhanced ultrasound (CEUS) imaging: consecutively, 36 patients (group A) treated with classic EVAR and 36 patients (group B) treated with embo-EVAR. Coils were released filling better as possible the aneurysm sac; the embolization was completed by injecting fibrin glue. Device and materials used, differential systemic and sac pressures, presence of any endoleak, and complication were registered. Results In our experience, we had 100% technical success without surgical conversion. Embo-EVAR was performed, after endograft deployment, in group B patients, all with ratio of Δ-pressures (obtained from Δ-sac pressure/Δ-differential pressure) > 0.16. No early or late complications occurred and mortality was nil. Follow-up was performed with computed tomography-angiography and CEUS at 6 and 12 months. We observed 9 type II and 1 type Ia endoleak in group A and 2 type II and 1 type Ib endoleaks in group B. Mean radiation exposure time was 30.3 min in group A and 43.3 min in group B. EVAR procedure average cost was 9,000 €. The average cost of sac embolization was 1,500€. Conclusions Although a randomized study is necessary, embo-EVAR may be a valid approach to prevent type II endoleaks and further complications. Mild costs and exposure-dose increase could be accepted to avoid reinterventions, and in our experience, it could be routinely performed with excellent results.

The possibility of detecting segment-specific injury of the proximal tubule by means of urinary enzymes was investigated in rats. Urinary glutamine synthetase, an enzyme exclusively localized in the S3 segment, and N-acetyl-beta-D-glucosaminidase, prevalently a S1-S2, but S3 enzyme also, were determined after single treatment with 100 mg/kg body wt. of hexachloro-1:3-butadiene (HCBD; i.p.), toxic for the S3 segment, or 25 mg/kg body wt. of potassium dichromate (s.c.), toxic for the S1-S2 segments. Excretion of total urinary proteins was also measured. In addition, a dose-response relationship was determined between three doses (50, 100 and 200 mg/kg body wt.) of HCBD and glutamine synthetase activity in urine. Glutamine synthetase activity, measured according to a new assay for urine based on modification of methods developed for organs, increased in the urine only when the S3 segment of the proximal tubule was damaged, as demonstrated by histological findings of the kidneys. HCBD caused early excretion of the enzyme related to the necrosis of the S3 segment, whereas potassium dichromate caused a slight increase only when the resulting lesion to this segment (vacuolization) began to develop. On the contrary, N-acetyl-beta-D-glucosaminidase activity showed the peak of excretion 24 and 34 h after treatment with HCBD or potassium dichromate, respectively, according to the histological findings of necrosis of the S3 segment (the former) and vacuolization of the S1-S2 segments (the latter). Excretion of total urinary proteins reached the peak 24 h (HCBD) and 48 h (potassium dichromate) after treatment. HCBD at 200 mg/kg body wt, caused a peak of glutamine synthetase activity in urine 10 h after injection, whereas the peak caused by doses of 50 and 100 mg/kg body wt. occurred 24 h following treatment. The peak of enzyme activity in urine significantly increased with the dose. The results suggest that the measurement of urinary activity of S3 segment-specific enzyme as glutamine synthetase allows us to detect early S3 segment-specific injury of the proximal tubule. In addition, the method for urinary enzyme activity appears sensitive, simple and fast.

Glutamine transaminase K(GTK) excretion assessed in urine and by kidney histology was evaluated in rats after single treatment with 1.0 mg/kg i.p. of mercuric chloride, 100 mg/kg i.p. of hexachloro-1:3-butadiene (both S3, pars recta, segment-specific nephrotoxicants) and 25 mg/kg s.c. of potassium dichromate (S1–S2, pars convoluta, segment-specific nephrotoxicant). The aim was to correlate segment-specific injury and enzyme excretion in order to assess, using non-vasive methods, localization of GTK along the proximal tubule. Mercuric chloride and hexachloro-1:3-butadiene produced early focal damage in the pars recta (focal necrosis was shown 10 h after treatment, and diffuse necrosis appeared later at 34 and 24 h after treatment). Changes of the pars convoluta were occasional and delayed (72 h after treatment for both substances). On the contrary, potassium dichromate induced damage of the pars convoluta (vacuolar degeneration and focal necrosis were evident 24 h and 48 h after treatment, respectively), whereas the pars recta was affected later (focal vacuolar degeneration was observed 72 h after treatment). Increase urinary GTK excretion was early after treatment with mercuric chloride and hexachloro-1:3-butadiene (significant increase was observed within 10 h), with a peak for both substances 24␣h after treatment, in agreement with the necrosis of the pars recta. Potassium dichromate induced a significant increase of enzyme excretion in urine also 24 h after injection, according to histological features showing vacuolar degeneration of the pars convoluta; the peak of excretion was reached 48 h after treatment (delay was due, probably, to s.c. administration). The results show that GTK increased in urine after treatment with S3 and S1–S2 specific nephrotoxicants; the combination of histological examination and urinary enzyme supports the evidence that the enzyme is distributed along the whole of the proximal tubule.