Background and Purpose: This study aimed to evaluate the treatment effect of intraarterial versus intravenous tirofiban during endovascular thrombectomy in acute ischemic stroke. Methods: This study retrospectively examined 503 patients with acute ischemic stroke with large vessel occlusion who received endovascular thrombectomy within 24 hours of stroke onset. Patients were divided into 3 groups: no tirofiban (n=354), intraarterial tirofiban (n=79), and intravenous tirofiban (n=70). The 3 groups were compared in terms of recanalization rate, symptomatic intracerebral hemorrhage, in-hospital death rate, 3-month death, and 3-month outcomes measured by modified Rankin Scale score (good clinical outcome of 0–2, poor outcome of 5–6). The comparison was statistically assessed by propensity score matching, followed by Freidman rank-sum test and pairwise Wilcoxon signed-rank test with Bonferroni correction. Results: The propensity score matching resulted in 92 matched triplets. Compared with the no-tirofiban group, the intravenous tirofiban group showed significantly increased recanalization (96.7% versus 64.1%, P <0.001), an increased rate of 3-month good outcome (69.5% versus 51.2%, P =0.034), and a lower rate of 3-month poor outcome (12.2% versus 41.4%, P <0.001). There was no significant difference between the tirofiban intravenous and no-tirofiban groups in terms of symptomatic intracerebral hemorrhage (2.2% versus 0%, P =1.000). However, symptomatic intracerebral hemorrhage was significantly increased in the intraarterial-tirofiban group compared with the no-tirofiban group (19.1% versus 0%, P <0.001), with an increased rate of in-hospital death (23.6% versus 0% P <0.001), and increased rate of 3-month death (26.8% versus 11.1%, P =0.021). The intraarterial-tirofiban and no-tirofiban group showed no significant difference in recanalization rate (66.3% versus 64.1%, P =1.000). Conclusions: As an adjunct to endovascular thrombectomy, intravenous tirofiban is associated with high recanalization rate and good outcome, whereas intraarterial tirofiban is associated with high hemorrhagic rate and death rate.

Background and Purpose— This study aimed to explore safety of tirofiban in endovascular treatment of acute ischemic stroke. Methods— Two hundred eighteen ischemic stroke patients receiving endovascular thrombectomy were prospectively recruited, with 94 treated with intra-arterial tirofiban and 124 were not. The 2 groups were compared in terms of symptomatic intracranial hemorrhage (ICH) and fatal ICH rate by the χ 2 test and logistic regression. Results— Patients treated with tirofiban compared with those without tirofiban had significantly higher rate of symptomatic ICH (14.6% versus 5.7%; P =0.027) and fatal ICH (8.8% versus 1.6%; P =0.014). Tirofiban-treated patients had increased odds of symptomatic ICH by 2.9-fold (95% CI, 1.1–7.5), and odds of fatal ICH increased by 5.9-fold (95% CI, 1.2–28.4). Conclusions— Tirofiban treatment increases risk of major ICH after endovascular thrombectomy for acute ischemic stroke in this nonrandomized study.

Caspases are an evolutionarily conserved family of proteases responsible for mediating and initiating cell death signals. In the past, the dysregulated activation of caspases was reported to play diverse but equally essential roles in neurodegenerative diseases, such as brain injury and neuroinflammatory diseases. A subarachnoid hemorrhage (SAH) is a traumatic event that is either immediately lethal or induces a high risk of stroke and neurological deficits. Currently, the prognosis of SAH after treatment is not ideal. Early brain injury (EBI) is considered one of the main factors contributing to the poor prognosis of SAH. The mechanisms of EBI are complex and associated with oxidative stress, neuroinflammation, blood-brain barrier disruption, and cell death. Based on mounting evidence, caspases are involved in neuronal apoptosis or death, endothelial cell apoptosis, and increased inflammatory cytokine-induced by apoptosis, pyroptosis, and necroptosis in the initial stages after SAH. Caspases can simultaneously mediate multiple death modes and regulate each other. Caspase inhibitors (including XIAP, VX-765, and Z-VAD-FMK) play an essential role in ameliorating EBI after SAH. In this review, we explore the related pathways mediated by caspases and their reciprocal regulation patterns after SAH. Furthermore, we focus on the extensive crosstalk of caspases as a potential area of research on therapeutic strategies for treating EBI after SAH.

Background: Atrial Fibrillation (AF) is associated with poorer functional outcomes in acute stroke patients. It has been hypothesized that this is due to poor collateral recruitment. Aims: This study aimed to investigate the relationship between AF and collaterals with outcome in thrombectomy patients. Methods: This retrospective cohort study identified 1036 acute ischemic patients from the INternational Stroke Perfusion Imaging REgistry. The cohort was divided into two groups: 432 with AF and 604 without AF. Patients were stratified by collateral grades as good, moderate, and poor. Within each collateral grade, the prediction of AF vs. No AF for good outcome (3-month modified Rankin Scale of 0-2) was determined. Then, within each collateral grade, perfusion was compared between those with and AF and without AF. Results: AF was negatively associated with good outcome in patients with poor collaterals (26.7% vs. 51.2% for AF vs. No AF, odds ratio=0.32 [95% CI 0.22, 0.50], p<0.001), but not in patients with good (50.9% vs 58.1% for AF vs. No AF, odds ratio=0.75 [0.46, 1.23], p=0.249) or moderate collaterals (43.6% vs 50.9% for AF vs. No AF, odds ratio=0.75 [0.47, 1.18], p=0.214). AF was associated with severe hypoperfusion only in patients with poor collateral flow (54.0 vs. 35.5 ml for AF vs. No AF, p<0.001). Conclusions: AF-related stroke is associated with more severe hypoperfusion and worse outcome in those with poor collaterals.