Predictors and prognosis of early neurological outcomes on patients with Vertebrobasilar artery occlusion undergoing endovascular treatment.

BACKGROUND: This research explored the factors influencing early neurological outcomes (ENO) in patients who had vertebrobasilar artery occlusion (VBAO) and received endovascular treatment (EVT), as well as examining the causal influence of ENO on the prognosis of VBAO patients. METHODS: A retrospective review was carried out on patients from 65 Chinese stroke centers, all within 24 hours of the estimated occlusion time. ENO includes early neurological improvement (ENI) and early neurological deterioration (END), defined as a decrease or an increase of at least 4 points in NIHSS score between baseline and 24 hours after EVT. Death within 24 hours after EVT also consider as END. END was further divided into explainable END and unexplainable END (unEND). Independent predictors of ENO and the association between ENO and outcomes in patients with VBAO were determined using center-adjusted analyses. The study developed a multivariate logistic regression model to examine the comparative risk of unEND versus explainable END on the clinical outcomes in VBAO patients. RESULTS: A total of 2257 patients were included. Glasgow Coma Scale (GCS) (OR 1.16, 95% CI 1.03-1.30) and successful reperfusion (OR 1.15, 95% CI 1.02-1.30) were associated with ENI. Baseline NIHSS (OR 0.60, 95% CI 0.53-0.68), successful reperfusion (OR 0.79, 95% CI 0.71-0.89) and puncture to reperfusion time (OR 1.17, 95% CI 1.03-1.33) were associated with END. When examining three-month prognostic indexes, both END and ENI were found to be linked to the three-month outcomes, but in opposite directions. A subgroup analysis of END suggested that unexplained END typically demonstrated a more favorable prognosis compared to explained END, although the prognosis remained generally unfavorable. CONCLUSIONS: ENO, whether they manifested as early improvement or deterioration, were linked to the prognosis of VBAO patients undergoing EVT. The outcomes after unEND were more favorable than those following explained END.

Rescue stenting after failure of endovascular thrombectomy for acute vertebrobasilar artery occlusion: data from the PERSIST registry.

BACKGROUND: Among acute vertebrobasilar artery occlusion (VBAO) patients, successful reperfusion is a strong predictor of favorable outcomes. However, failed reperfusion (FR) with endovascular thrombectomy (EVT) in VBAO was observed to occur in 18-50% of cases. We aim to evaluate the safety and efficacy of rescue stenting (RS) for VBAO after failed EVT. METHODS: Patients with VBAO who received EVT were enrolled retrospectively. Propensity score matching was performed as the primary analysis to compare the outcomes between patients with RS and FR. Furthermore, a comparison between using the self-expanding stent (SES) and balloon-mounted stent (BMS) in the RS group was also conducted. The primary and secondary outcomes were defined as a 90-day modified Rankin Scale (mRS) score 0-3, and a 90-day mRS score 0-2, respectively. Safety outcomes included all-cause mortality at 90 days and symptomatic intracranial hemorrhage (sICH). RESULTS: The RS group showed a significantly higher rate of 90-day mRS score 0-3 (46.6% vs 20.7%; adjusted OR (aOR) 5.06, 95% CI 1.88 to 13.59, P=0.001) and a lower rate of 90-day mortality (34.5% vs 55.2%; aOR 0.42, 95% CI 0.23 to 0.90, P=0.026) than the FR group. The rates of 90-day mRS score 0-2 and sICH were not significantly different between the RS group and FR group. There were no differences in all outcomes between SES and BMS groups. CONCLUSIONS: RS appeared to be a safe and effective rescue approach in patients with VBAO who failed EVT, and there was no difference between using SES and BMS.

The safety and effectiveness of endovascular treatment for patients with vertebrobasilar artery occlusions: according to the BEST and BASICS criteria.

Background: Whether endovascular treatment (EVT) is safe and effective for vertebrobasilar artery occlusion (VBAO) is yet incompletely understood. Two RCTs, the endovascular treatment versus standard medical treatment for vertebrobasilar artery occlusion (BEST) trail and the Basilar Artery International Cooperation Study (BASICS), concentrating on this field were recently reported. Objective: We use real-world registry data of VBAO to compare the outcome of EVT inside and outside the inclusion and exclusion criteria of the BEST and BASICS study to testify the feasibility of the selection paradigms of VBAO in these trials. Methods: Consecutive patients with VBAO receiving EVT involving 21 stroke centers were retrospectively included. The safety outcomes [3-month mortality, symptomatic intracranial hemorrhage (sICH), and effectiveness outcomes (the proportion of 3-month functional independence (mRS of 0-2) and favorable outcome (mRS of 0-3)] were compared between VBAO patients who meet or failed to meet the BEST/BASICS selection criteria for EVT. Results: Our study cohort consisted of 577 VBAO patients who underwent EVT. Of them, 446 patients had pc-ASPECTS ≧8. Successful reperfusion (mTICI 2b or 3) was achieved in 85.4% (n = 493). There were 418 patients fulfilling the BEST criterion for EVT and 194 fulfilling the BASICS criterion. Regression analysis indicated that adherence to BEST or BASICS criterion for EVT was not independently related to most of the safety and effectiveness outcome except that adherence to BEST was significantly associated with the 3-month favorable outcome (ORBEST: 1.742, 95% CI: 1.087-2.790). However, when we put pc-ASPECTS into both criteria with a cut-off value of 8, meeting both BEST criterion plus pc-ASPECTS and BASICS criterion plus pc-ASPECTS was independently related to 3-month functional independence (ORBEST: 1.687, 95% CI: 1.077-2.644; ORBASIC: 1.653, 95% CI: 1.038-2.631) and favorable outcome (ORBEST: 2.280, 95% CI: 1.484-3.502; ORBASIC: 2.153, 95% CI: 1.372-3.378). Conclusion: Our study indicated that, based on real-world data of EVT, adherence to BEST or BASICS criterion for EVT was not independently associated with the safety and effectiveness outcome except that adherence to BEST was significantly related to the 3-month favorable outcome. However, the BEST or BASICS selection criterion and pc-ASPECTS ≧8 might be better paradigms for EVT patient selection.

LINC00839 Regulates Proliferation, Migration, Invasion, Apoptosis and Glycolysis in Neuroblastoma Cells Through miR-338-3p/GLUT1 Axis.

BACKGROUND: Long noncoding RNAs (lncRNAs) are related to the development and treatment of neuroblastoma. The lncRNA LINC00839 is dysregulated in neuroblastoma, while its function and mechanism in neuroblastoma development remain largely unclear. METHODS: The tumor and adjacent noncancerous tissues were collected from 48 neuroblastoma patients. LINC00839, glucose transporter 1 (GLUT1) and microRNA-338-3p (miR-338-3p) abundances were examined via quantitative reverse transcription polymerase chain reaction or Western blot. Cell proliferation, apoptosis, migration, invasion and glycolysis were assessed via Cell Counting Kit-8, colony formation, flow cytometry, wound healing, transwell, glucose uptake and lactate production. The target relationship of miR-338-3p and LINC00839 or GLUT1 was tested via dual-luciferase reporter analysis and RNA immunoprecipitation. The function of LINC00839 on neuroblastoma cell growth in vivo was tested via a xenograft model. RESULTS: LINC00839 and GLUT1 abundances were increased in neuroblastoma tissues and cell lines. The high expression of LINC00839 and GLUT1 indicated the lower overall survival. LINC00839 interference constrained neuroblastoma cell proliferation, migration, invasion and glycolysis, and facilitated apoptosis. GLUT1 overexpression or miR-338-3p knockdown could mitigate the influence of LINC00839 silence on neuroblastoma cell processes. LINC00839 could regulate GLUT1 expression via miR-338-3p. LINC00839 knockdown reduced neuroblastoma cell growth in xenograft model. CONCLUSION: LINC00839 silence repressed neuroblastoma cell proliferation, migration, invasion and glycolysis and promoted apoptosis via regulating miR-338-3p/GLUT1 axis.