General Anesthesia-Related Drop in Diastolic Blood Pressure May Impact the Long-Term Outcome in Stroke Patients Undergoing Thrombectomy.

Background: Several factors affect the efficacy of endovascular thrombectomy (EVT); however, the anesthesia-related factors have not been fully explored. We aimed to identify independent predictors of outcome by analyzing procedural factors based on a multicentric stroke registry. Methods: Data of consecutive patients with acute ischemic stroke (AIS) were extracted from the prospective STAY ALIVE stroke registry. Demographic, clinical, and periprocedural factors including hemodynamic values were analyzed in patients undergoing thrombectomy with either general anesthesia (GA) or conscious sedation (CS). Independent predictors of outcome both at 30 and 90 days based on the modified Rankin Scale (mRS: 0−2 as favorable outcome) were also explored. Results: A total of 199 patients (GA: 76 (38%) vs. CS: 117 (59%); in addition, six patients were converted from CS to GA) were included. The minimum value of systolic, diastolic, and mean arterial pressure was significantly lower in the GA compared to the CS group, and GA was associated with a longer onset to EVT time and a higher drop in all hemodynamic variables (all, p < 0.001). A higher drop in diastolic blood pressure (DBP) was even independently associated with a poor 90-day outcome (p = 0.024). Conclusion: A GA-related drop in DBP may independently predict a poor long-term outcome in stroke patients undergoing thrombectomy.

Fatty Acid-Binding Protein 3 and CXC-Chemokine Ligand 16 are Associated with Unfavorable Outcome in Aneurysmal Subarachnoid Hemorrhage.

BACKGROUND: Aneurysmal subarachnoid hemorrhage (aSAH) is associated with activation of the inflammatory cascade contributing to unfavorable outcome and secondary complications, such as delayed cerebral ischemia (DCI). Both fatty acid-binding protein 3 (FABP3) and CXC-chemokine ligand 16 (CXCL-16) have been linked to vascular inflammation and cellular death. The authors aimed to assess the 30-day prognostic value of serum levels of FABP3 and CXCL-16 and explore their associations with DCI in aSAH patients. METHODS: A total of 60 patients with aSAH were prospectively enrolled. Sampling for markers was done at 24 hours after the index event. FABP3 and CXCL-16 serum concentrations were determined by MilliPlex multiplex immunoassay method. The primary endpoint was unfavorable outcome at Day 30 based on the modified Rankin Scale. RESULTS: Both FABP3 and CXCL-16 levels were significantly elevated in patients with unfavorable outcome compared to those with favorable outcome after aSAH (FABP3: 2133 pg/mL, IQR: 1053-4567 vs. 3773, 3295-13116; p<0.003 and CXCL-16: 384 pg/mL, 313-502 vs. 498, 456-62, p<0.001). The area under the curve (AUC) for serum CXCL-16 levels as a predictor of unfavorable outcome at Day 30 was 0.747 (95% CI =0.622-0.871; p<0.001). Based on binary logistic regression analysis, serum CXCL-16 with a cut-off level >446.7 ng/L independently predicted Day 30 unfavorable outcome with a sensitivity of 81% and a specificity of 62%. Neither CXCL-16 nor FABP3 showed a significant correlation with DCI. CONCLUSION: Early FABP3 and CXCL-16 levels are significantly associated with poor 30-day outcome in patients with aSAH.

Risk analysis of post-procedural intracranial hemorrhage based on STAY ALIVE Acute Stroke Registry.

BACKGROUND: Intracranial hemorrhages (ICH) are classified as symptomatic or asymptomatic according to the presence of clinical deterioration. Here, we aimed to find predictive factors of symptomatic intracranial bleeding in a registry-based stroke research. METHODS: Data of consecutive patients with acute ischemic stroke (AIS) were extracted from the prospective STAY ALIVE stroke registry. Analysis of the total population and treatment sugroups such as endovascular thrombectomy (EVT), intravenous thrombolysis (IVT), or their combination (IVT+EVT) were also done. Outcome measures were ICH, 30- and 90-day clinical outcome based on the modified Rankin Scale (mRS:0-2 as favorable outcome). The hemorrhage was captured by a non-enhanced CT of the skull within 24 h after procedure. RESULTS: A total of 355 patients (mean age: 68±11; female N=177 (49.9%); EVT n=131 (36.9%); IVT n=157 (44.2%); IVT+EVT n=67 (18.9%) were included in the analysis. The total number of ICH was 47 (13%), symptomatic (sICH) 12 (3.4%) and asymptomatic (aICH) 35 (9.9%) in the whole population. NIHSS ≥15.5 at 24 post stroke hours predicted sICH with a sensitivity of 100% and a specificity of 92% (p<0.001). Furthermore, lower age, good collateral circulation on initial CT angiography and lower NIHSS score measured at 24 h independently associated with a favorable 90-day outcome, whereas baseline NIHSS and ASPECT score were not. CONCLUSION: Although partial recanalization, ASPECT< 6, and poor collaterals were significantly associated with sICH, the only independent predictor was NIHSS ≥15.5 at 24 post stroke hours. This suggests a careful evaluation of patients with worsening NIHSS despite an adequate therapy.

Prostaglandin E2, a postulated mediator of neurovascular coupling, at low concentrations dilates whereas at higher concentrations constricts human cerebral parenchymal arterioles.

There is considerable controversy regarding the vasoactive action of prostaglandin E2 (PGE2). On the one hand, indirect evidence implicates that astrocytic release of PGE2 contributes to neurovascular coupling responses mediating functional hyperemia in the brain. On the other hand, overproduction of PGE2 was also reported to contribute to cerebral vasospasm associated with subarachnoid hemorrhage. The present study was conducted to resolve this controversy by determining the direct vasoactive effects of PGE2 in resistance-sized human cerebral parenchymal arterioles. To achieve this goal PGE2-induced isotonic vasomotor responses were assessed in parenchymal arterioles isolated from fronto-temporo-parietal cortical tissues surgically removed from patients and expression of PGE2 receptors were examined. In functionally intact parenchymal arterioles lower concentrations of PGE2 (from 10-8 to 10-6 mol/l) caused significant, endothelium-independent vasorelaxation, which was inhibited by the EP4 receptor blocker BGC201531. In contrast, higher concentrations of PGE2 evoked significant EP1-dependent vasoconstriction, which could not be reversed by the EP4 receptor agonist CAY10598. We also confirmed previous observations that PGE2 primarily evokes constriction in intracerebral arterioles isolated from R. norvegicus. Importantly, vascular mRNA and protein expression of vasodilator EP4 receptors was significantly higher than that of vasoconstrictor EP1 receptors in human cerebral arterioles. PGE2 at low concentrations dilates whereas at higher concentrations constricts human cerebral parenchymal arterioles. This bimodal vasomotor response is consistent with both the proposed vasodilator role of PGE2 during functional hyperemia and its putative role in cerebral vasospasm associated with subarachnoid hemorrhage in human patients.

Subacute Elevation of Plasma Level of Caspase-Cleaved Cytokeratin-18 is Associated with Hemorrhagic Transformation and Functional Outcome in Ischemic Stroke.

BACKGROUND: Caspase-cleaved cytokeratin-18 (CCCK-18) is an apoptosis marker. Here, we analyzed the relationship between plasma level of CCCK-18 in the acute and subacute stage of ischemic stroke and early and late functional outcome. Besides, correlation among CCCK-18 and complications, such as hemorrhagic transformation (HT) were also explored. METHODS: Plasma concentration of CCCK-18 was investigated in 54 patients at admission and poststroke 72 hours. HT was evaluated by CT scans on 24 poststroke hours. Outcome measures were assessed by modified Rankin scale at hospital discharge and 6-month later. Receiver operating characteristics (ROC) analysis was used to determine the best cut-off values of CCCK-18 as a predictor of unfavorable functional outcome. RESULTS: Significantly elevated CCCK-18 level was observed at 72 hours after onset of stroke, in nonsurviving compared to surviving patients (331 ± 191 ng/L versus 251 ± 164 ng/L, P = .01). Based on ROC analysis, the cut-off value of plasma CCCK-18 levels >223 ng/L at 72 poststroke hours predicted 6-month unfavorable stroke outcome with a sensitivity of 84.4% and a specificity of 77.3% (area under the curve: .851, 95% confidence interval = .745-.955, P < .001). The rate of complications such as HT and in-hospital infection was significantly higher in patients presented with a plasma CCCK-18 level above the cut-off value. CONCLUSIONS: The association between high serum CCCK-18 levels and unfavorable early and late stroke outcome in an unselected study population was first described here. Besides, the apoptosis marker CCCK-18 might be a predictor of further complication such as HT and in-hospital infection.

[Nebivolol in treatment of multiple cerebral aneurysms]. / Nebivolol alkalmazása többszörös agyi aneurysmák esetén.

INTRODUCTION: We examined the effect of nebivolol on blood pressure control after subarachnoidal hemorrhage in three patients with multiple aneurysms. PATIENTS AND METHODS: Endovascular intervention was applied to treat the bleeding aneurysms of all patients, and the silent aneurysms were followed-up. In all patients nebivolol was used as long-term anti-hypertensive medication. RESULTS: With nebivolol treatment the blood pressure in our patients was maintained in the normal range with no unexpected shoot-ups. The size of the silent aneurysms did not increase and the endovascularly treated aneurysms demonstrated acceptable morphology on follow-up catheter-angiography. DISCUSSION: After endovascular treatment of the bleeding aneurysm, strict blood pressure control is essential in those with multiple aneurysms to prevent the rupture of silent aneurysms. Antihypertensive medications with a 24-hour effect are preferable. Nebivolol seemed to be an appropriate medication for this purpose in all of our patients.

The use of covered stents for the endovascular treatment of extracranial internal carotid artery stenosis: a prospective study with a 5-year follow-up.

OBJECTIVES: To evaluate the safety and feasibility of the use of covered stents for the treatment of extracranial carotid artery stenosis caused by highly embologenic plaques, and to study the long-term outcome of patients receiving such covered stents. METHODS: Between 2002 and 2007, 46 patients (63% symptomatic, 78.3% male, 67 +/- 8.6 years old) with internal carotid artery stenosis caused by embologenic plaques or restenosis were treated with self-expanding covered stents (Symbiot, Boston Scientific). Pre-dilatation or protecting devices were not used. Post-dilatation was applied in every patient. Each patient was followed long-term. The outcome measures were the occurrence of neurological events, and the development of in-stent restenosis, as detected by clinical examination and duplex ultrasound. RESULTS: The technical success rate of stenting was 100%. There were no neurological complications in the peri-procedural period. The mean follow-up period was 34.3 +/- 27.7 months (the rate of patients lost to follow-up was 15.2%) during which no stroke or stroke-related deaths occurred. Restenosis was detected in 3 patients (6.5%). CONCLUSION: Covered stents provide efficient peri- and post-procedural protection against neurological complications due to embolisation from high-risk plaques during carotid artery stenting. Restenosis of covered stents appears to be infrequent during long-term follow-up.

Favorable early outcome of carotid artery stenting without protection devices.

BACKGROUND AND PURPOSE: Protection devices are increasingly used in carotid artery stenting. However, no randomized trial has been conducted to evaluate the efficacy of such devices, and arguments have also been formulated against their routine use. We set out to investigate the complication rates associated with carotid artery stenting performed without protection devices. Applicability of covered stents in the carotid system was also evaluated. METHODS: Between January 2001 and July 2003, 245 consecutive patients (260 hemispheres) underwent carotid artery stenting. No protection devices were applied. Covered stents were implanted in 31 (12.1%) cases. The incidence of complications during the intervention and the subsequent 30-day follow-up period was recorded. RESULTS: The technical success rate was 98.8%. One postprocedural nonneurological death (0.4%) occurred. Neurological complications (inclusive of transient ischemic attacks) were observed in 14 cases (5.4%). The rate of major complications (death, major stroke, and myocardial infarction) was 1.6% among the symptomatic and 1.5% among the asymptomatic cases. The rate of minor strokes was 3.2% in the symptomatic and 1.5% in the asymptomatic group. Of the neurological complications, 64.3% occurred postprocedurally. No ipsilateral neurological complications were detected in the subgroup treated with covered stents. CONCLUSIONS: Carotid artery stenting without protection devices appears to be safe. Most of the neurological complications could not have been prevented with protection devices, because they occurred after the intervention. The application of covered stents may reduce the rate of embolization-related complications in the periprocedural period.