Paclitaxel drug-coated balloon angioplasty for the treatment of failing arteriovenous fistulas: a single-center experience.

Objectives: To report our experience of angioplasty with Lutonix (Bard Peripheral Vascular, Inc., Tempe, AZ) drug-coated balloon (DCB) for the treatment of failing arteriovenous fistulas (AVF).Materials and methods: Retrospective, single-center analysis consisting of 14 patients treated with Lutonix paclitaxel DCBs in the period from July 2015 through April 2017. We analyzed technical success, clinical success, primary patency of the target lesion, primary patency of the dialysis circuit, and the rate of complications. Regular follow-up of AVF patency was realized by clinical examination and duplex ultrasonography. The Kaplan-Meier survival method was applied to determine the cumulative primary patency of the target lesion and the dialysis circuit.Results: Technical success was 100% and clinical success 92.9%. There were no major or minor complications. Cumulative target lesion primary patency after DCB was 69.2% at 6 months and 31.6% at 12 months. Cumulative vascular circuit primary patency was 61.5% at 6 months and 31.6% at 12 months.Conclusion: Compared to results reported in literature with plain old balloon angioplasty (POBA), Lutonix paclitaxel DCB angioplasty proved a short-term patency benefit in treatment of dialysis AVF stenosis.

TEVAR for Ruptured type B Aortic Dissection in a Patient with Turner Syndrome.

TEVAR has replaced open surgical repair as preferred treatment for complicated acute type B aortic dissection. But the literature on thoracic endovascular aortic repair (TEVAR) for ruptured type B dissection is scarce. Patients with Turner syndrome are at risk for aortic dissection and rupture at a young age with an immediate mortality rate of 63%. Only a few cases have been described and the best treatment is not yet established. We present a case of a 49 year-old woman with Turner syndrome who suffered from a ruptured aortic dissection Stanford type B. A TEVAR procedure was performed, but the life of the patient could not be saved. In this case report we discuss the lessons we learned as well as some unsolved questions about TEVAR for ruptured type B aortic dissection.

Stent Graft Dislocation after EVAR Treated with an Endostapling Fixation System.

Stent-graft migration and type I endoleak are major complications after endovascular aneurysm repair (EVAR). We present a case of an 88-year-old female patient with a 56-mm-diameter progredient infrarenal AAA, with severely angulated proximal aneurysm neck and iliac arteries. EVAR was performed using a Gore Excluder stent-graft. -Computed tomography angiography (CTA) at one week postoperatively demonstrated a dislocation of the stent-graft and a proximal Type I endoleak. Placement of a proximal cuff with the use of 6 endostaples resulted in proximal neck seal and exclusion of the endoleak. CTA 2 years postoperatively showed no signs of a proximal type I endoleak. Use of an endostapling fixation system is a viable treatment option in cases of stent-graft dislocation resulting from angulation of the proximal neck.

A painless neck swelling and von Recklinghausen.

BACKGROUND: Von Recklinghausen's disease, an autosomal dominant genetic disorder, may occasionally present with unusual localizations of neurofibromas. CLINICAL CASE: A 46-year old woman, known with Von Recklinghausen's disease, reported a swelling and a feeling of pressure and globus sensation. Clinical examination revealed multiple large nodi on the right side of the neck. Laboratory testing including thyroid-stimulating hormone (TSH) was normal. An MRI showed a 1 x 3 x 10 centimeter sausage-like structure compressing the right jugular vein. At surgical exploration a string-like tumour firmly attached to the right vagal and recurrent laryngeal nerve was found. The tumor and both nerves were macroscopically curative resected. Histopathological examination demonstrated a plexiform cervical vagus nerve neurofibroma without malignancy. CONCLUSION: Patients with Von Recklinghausen's disease presenting with painless neck swellings may harbour cranial nerve neurofibromas.

Fenestrated stent-grafts for salvage of prior endovascular abdominal aortic aneurysm repair.

OBJECTIVES: To review our experience with fenestrated endovascular aneurysm repair (F-EVAR) to treat complications after previous standard infrarenal endovascular aneurysm repair (EVAR). METHODS: A prospectively maintained database including all consecutive patients with juxtarenal abdominal aortic aneurysm that were treated with F-EVAR after failed previous EVAR within the period March 2002 to November 2012 at the University Medical Center of Groningen, Netherlands (up to October 2009), and the Klinikum Nürnberg Süd, Germany (from November 2009) was analyzed. Evaluated outcomes included initial technical success, operative mortality and morbidity, and late procedure-related events with regard to survival, target vessel patency, endoleak, renal function, and reintervention. RESULTS: A total of 26 patients (24 male, mean age 73.2 ± 6.5 years) were treated. All patients had proximal anatomies precluding endovascular reintervention with standard techniques. In 23 patients a fenestrated proximal cuff was used, and in three patients a bifurcated fenestrated stent graft. Technical success was achieved in 24 (92.3%) patients. One patient required on-table open conversion because of impossibility to retrieve the top cap as a result of twist of the ipsilateral limb. In the second patient the right kidney was lost due to inadvertent stenting in a smaller branch of the renal artery. Catheterization difficulties, all related to the passage through the limbs or struts of the previous stent graft, were encountered in 11 (42.3%) cases, including five (19.2%) patients with iliac access problems and six (23.1%) with challenging renal catheterization. Operative target vessel perfusion success rate was 94.6% (70/74). Operative mortality was 0%. Mean follow-up was 26.8 ± 28.5 months. No proximal type I endoleak was present on first postoperative CTA. The mean aneurysm maximal diameter decreased from 73 ± 20 mm to 66.7 ± 21 mm (p < .05). There were six late deaths, one of them aneurysm related. Estimated survival rates at 1 and 2 years were 94.1 ± 5.7% and 87.4 ± 8.4%, respectively. Patency during follow-up for the target vessels treated successfully with a fenestrated stent graft was 100% (70/70). Reintervention was required in four cases, including one acute conversion due to rupture, one for iliac limb occlusion and two for type Ib and II endoleak. Renal function deterioration was observed solely in the two cases of primary technical failure. CONCLUSIONS: F-EVAR represents a feasible option for the repair of juxtarenal abdominal aortic aneurysm after prior EVAR failure. It is advantageous in terms of mortality and less morbid than open surgery, but is associated with increased technical challenges because of the previously placed stent graft. Outcome seems related to initial technical success.

Stent graft infection in the lower limb.

BACKGROUND: Poor wound healing can occur after limb amputation. CASE REPORT: We describe the case of a patient with a persistent fistula after below-knee amputation. The fistula is maintained due to an infected stent graft. After removal of the stent graft and adequate antibiotic treatment the wounds healed and extended amputation was avoided. CONCLUSION: The diagnosis of stent graft infection is challenging and requires aggressive treatment to prevent further amputation.

Thromboxane synthase inhibitor, UK 38485, prevents renal injury in the rabbit isolated perfused kidney exposed to cold ischemia.

Recent studies have indicated that, the administration of thromboxane A2 (TxA2) inhibitors improved renal functions in experimental renal allograft transplantation. Thus TxA2, a vasoconstrictor metabolite of arachidonic acid, may play a role in renal function and blood flow during hypothermic storage. The aim of the present study was to evaluate the cytoprotective effect of TxA2 synthase inhibitor, UK 38485, on altered renal function due to cold ischemia for 24 and 72 h. Experiments were performed in isolated perfused kidney from adult rabbits. Kidneys were perfused with Euro-Collins (EC) containing UK 38485 and incubated with the same solution in a beaker exposed to cold ischemia for 24 and 72 h. The same procedure was applied to the control kidneys in EC solution alone. Vascular responses and urinary output to noradrenaline, angiotensin II, endothelin-1, acetylcholine, and sympathetic stimulation were assessed as the functional activity of kidney. The addition of UK 38485 to EC solution increased the preservation time of kidney and protects the vascular endothelial regulatory functions and urine excretion when compared to EC alone. The results of the present study can be taken as an evidence of the cytoprotective effect of the UK 38485 and might be useful for kidney preservation.

The endothelium-derived relaxing factor-mediated acetylcholine response of the arterial perfusion pressure after cold storage of the isolated rabbit kidney.

The vasodilatation induced by acetylcholine (ACh) in a rabbit isolated perfused kidney was abolished when the tissue was exposed to cold ischemia for 72 h in Euro-Collins (EC) solution. This vasodilatation is due to the release of endothelium-derived relaxing factor (EDRF) from renal vasculature as evidenced by the attenuation following methylene blue pretreatment. When kidneys were preserved in EC solution containing UK 38485, a thromboxane synthase inhibitor, or nicardipine, a calcium channel blocker, ACh-induced vasodilatation persisted after 72 h of cold ischemia. These results were taken as evidence of tissue protective activity of UK 38485 and nicardipine and have promising implications for cadaveric kidney transplantation.

The effect of nicardipine on renal functions following 72-hour cold ischemia.

The aim of the study was to investigate the cytoprotective effect of a calcium channel blocker, nicardipine, on altered renal function due to cold ischemia for 72 h. The experiments were performed on isolated perfused kidneys from adult rabbits. Kidneys were perfused with either standard Euro-Collins (EC) solution (n = 7) or EC containing nicardipine (n = 6) and then incubated with the same preservation solutions in a beaker exposed to cold ischemia for 72 h at +4 degrees C. In the control group the same procedure was applied to untreated kidneys (n = 6) which were exposed to cold ischemia for 30 min. Vascular responses and urinary output to noradrenaline, angiotensin II, endothelin-1, acetylcholine and sympathetic stimulation were assessed as the functional activities of the kidney. The responses of the preserved kidneys were compared following cold ischemic conditions. The results indicate that the addition of nicardipine to EC solution protects the vascular endothelial regulatory function and urine excretion; therefore, dihydropyridine calcium channel blockers might be useful for kidney preservation.

The effects of endothelin peptides in the rabbit isolated perfused kidney.

1. Endothelin-1 (21-amino acids) and pre-pro endothelin-1 (39-amino acids) produced a concentration-dependent increase in perfusion pressure when infused through the renal artery of rabbit isolated perfused kidney. Addition of phosphoramidon to the medium caused a potentiation in the vasoconstrictor response to endothelin-1 and greatly, but not completely, inhibited vasoconstriction induced by pre-pro-endothelin-1. 2. Addition of indomethacin to the medium did not alter the vasoconstrictor effects of the peptides. 3. Methylene blue in the medium caused a highly significant potentiation in the vasoconstrictor response to endothelin-1. 4. A short-term infusion of endothelin-1 through the renal artery elicited a decrease in urine flow which returned to control levels after perfusing the kidney with Krebs buffer, but prolonged infusion of the peptide produced an irreversible increase in urine flow. 5. Phosphoramidon, methylene blue and indomethacin failed to alter the effect of endothelin-1 on urine flow. 6. From these results it was concluded that phosphoramidon-sensitive endothelin-converting enzyme, probably localized in microvasculature of the kidney, can convert pre-pro-endothelin-1 to endothelin-1 which is responsible for the vasoconstrictor effect of pre-pro-endothelin-1 in addition to its possible direct vasoconstrictor effect on kidney vasculature. Moreover, the endothelin-1 degradating enzyme in kidney should be a phosphoramidon-sensitive metalloproteinase(s). The results also indicated the release of EDRF but not prostanoids by endothelin-peptides in the rabbit isolated perfused kidney.

Endothelin-1-induced oedema in rat and guinea-pig isolated perfused lungs.

Endothelin-1 caused an increase in perfusion pressure, bronchial resistance, lung weight and tracheal effusion when infused through the pulmonary artery of rat and guinea-pig isolated lungs. In contrast to vasoconstriction, the effects of endothelin-1 on bronchial resistance, lung weight and tracheal effusion were not concentration-dependent. Recovery from vasoconstriction occurred within 15-30 min when the lung was further perfused with Krebs buffer. Increases in lung weight, bronchial resistance and tracheal effusion induced by endothelin-1 were irreversible when infused at concentrations above 10(-10) M. UK 38,485, a thromboxane A2 synthesis inhibitor, partly prevented the increase in lung weight and tracheal effusion without altering the vasoconstriction induced by endothelin-1. Such an antagonism was not seen in guinea-pig lung at the concentration used. Iloprost, a stable analogue of prostacyclin, antagonized the effects of endothelin-1 on perfusion pressure and lung weight without reducing tracheal effusion in both rat and guinea-pig lungs. Pretreatment with allopurinol did not alter the effects of endothelin-1. These results were taken as evidence for the potent lung oedema-producing effect of the peptide which seems to be partially mediated by the secondary release of thromboxane A2.

Further studies on the potent positive chronotropic effect of (15S)-15-methyl-prostaglandin E1 on the guinea-pig isolated spontaneously beating right atrium.

1. 15-Me-PGE1 (10(-14)-10(-11) M) elicited a concentration-dependent and long-lasting increase in heart rate without an effect on contractility of the isolated spontaneously beating guinea-pig right atria. 2. Noradrenaline, histamine and PGE1 produced a concentration-dependent increase in both heart rate and contractility with relatively higher concentrations. 3. beta-Adrenoceptor blocker propranolol and histamine H2-receptor blocker cimetidine inhibited the effects of noradrenaline and histamine respectively without altering the positive chronotropic effect of 15-Me-PGE1. 4. Prazosin and lidocaine partially inhibited the effect of 15-Me-PGE1, while reducing Na+ concentration in the medium to 50 mM almost completely inhibited the positive chronotropic effect of the analog. 5. Calcium channel blocker, nicardipine, decreased the positive chronotropic effect of 15-Me-PGE1 in a concentration-dependent manner. 6. These results were taken as an evidence for the specific and unique effect of 15-Me-PGE1 in the guinea-pig sinoatrial node interacting with Na+ and Ca2+ fluxes probably through their specific exchangers.