Enterprise stents versus low-profile visualized intraluminal support stents for stent-assisted coiling of unruptured paraclinoid aneurysms.

BACKGROUND: The microsurgical treatment of paraclinoid aneurysms can be challenging due to the anatomical structures that surround them. OBJECTIVE: This study compared the clinical and angiographic outcomes of unruptured paraclinoid aneurysms treated with enterprise (EP) stents and low-profile visualized intraluminal support (LVIS) stents. METHODS: A retrospective analysis of the clinical and radiological data from 133 patients with 139 unruptured paraclinoid aneurysms, who received an EP or an LVIS stent between January 2017 and June 2021 at Taizhou People's Hospital, was performed. Immediate postoperative and follow-up angiographic results were analyzed retrospectively using the Raymond-Roy occlusion classification (RROC). Any complications following the procedure and the patients' clinical outcomes were noted. RESULTS: Enterprise stents were used for stent-assisted coiling in 64 patients with 68 aneurysms and LVIS stents were used in 69 patients with 71 aneurysms. Both groups exhibited an increase in the proportion of aneurysms meeting the criteria for RROC class I, but the LVIS group demonstrated a higher rate of aneurysms meeting the class I criteria compared with the EP group, both on immediate postoperative angiography (45.1% vs. 11.8%, p< 0.001) and on follow-up angiography (94.9% vs. 80.6%, p= 0.025). Procedure-related complications were experienced by 9.4% of patients in the EP group (one coil prolapse, two parent artery occlusions, and three thromboembolic events), and 8.7% of patients in the LVIS group (three stent-related thrombosis and three thromboembolic events). There were no statistically significant differences between the two groups in relation to perioperative complications (p= 0.746) or favorable clinical outcomes (p= 0.492). CONCLUSION: A greater proportion of aneurysms in the LVIS group met the criteria for RROC class I compared with the EP group. There is no significant difference in procedural complications or clinical outcomes between EP and LVIS stents. Although no aneurysm recurrence was observed during the short follow-up period, continued monitoring is required.

Chronic angiotensin-converting enzyme inhibition up-regulates mouse kidney growth arrest specific-6 protein and the AXL subfamily of receptor tyrosine kinases.

INTRODUCTION: Growth arrest specific-6 (GAS-6), a vitamin K-dependent protein, is a potential mediator in progressive and chronic renal disease, specifically as a mediator of abnormal mesangial cell proliferation. Nitric oxide and angiotensin II affect mesangial cell proliferation. However, an association between nitric oxide synthase or angiotensin II on GAS-6 expression in the kidney has not previously been examined. Thus, our aim was to examine the effects of antihypertensive angiotensin-converting enzyme inhibitors and chronic nitric oxide synthase inhibition on the kidney expression of GAS-6 and its receptors AXL, MER and RSE. METHODS: Four groups of adult male C57BL/6J mice were studied: group 1, untreated controls (tap water for six weeks); group 2, treated orally with a nitric oxide synthase inhibitor, N-nitro-L-arginine methyl ester (L-NAME, 0.325 mg/ml for six weeks); group 3, treated orally with captopril (0.6875 mg/ml for six weeks); group 4, co-treated orally with L-NAME and captopril (same doses for six weeks). At the end of the study, kidneys were placed in fixative and processed to paraffin for immunohistochemical staining. RESULTS: GAS-6 and its receptors were not present in control and L-NAME-treated mice. Positive GAS-6 staining was detectable only in those mice receiving some form of chronic dosing with captopril, whether they were treated with captopril only or with captopril and L-NAME. Immunohistochemical detection across cases for MER and RSE was rare, whereas AXL-positive staining in the kidney mirrored GAS-6 staining/expression. The staining of GAS6 and AXL was predominantly localised to the renal tubular cells. CONCLUSIONS: These findings suggest that GAS-6 may not be a final common pathway for nitric oxide synthase inhibition-induced renal disease. Renal tubular GAS-6 expression following captopril treatment was unexpected and could be beneficial in preventing tubular atrophy following the onset of persistent systemic hypertension.