Hemorrhagic Transformation Research Articles

Clinical value of thromboelastography in predicting the risk of recurrence of acute ischemic stroke.

Thromboelastography (TEG) can objectively reflect the formation, development and rupture process of thrombosis in patients, but there are limited data on whether TEG can be used as a predictive tool for recurrence in patients with acute ischemic stroke. To explore the TEG risk of recurrence in patients with acute ischemic stroke predictive value. A total of 441 patients with acute ischemic stroke who met the research criteria in the First Affiliated Hospital of Henan University of Traditional Chinese Medicine from January 2020 to December 2021 were selected as the research objects. TEG was measured in all patients, and the main parameters of TEG (R value, indicating coagulation reaction time; K value and Angle, the rate of blood clot formation; MA value, indicating the maximum amplitude). The primary outcome of this study was ischemic stroke recurrence. Recurrent events included cerebral infarction, cerebral hemorrhage, TIA, and were determined by combining imaging events and clinical events. Logistic regression analysis was used to explore the influencing factors of recurrence in patients with acute ischemic stroke. Fifty-six patients (12.7%) had recurrence. Multivariate Logistic regression analysis showed that: Age [OR = 1.078, 95%CI(1.024, 1.135)], triglyceride [OR = 1.541, 95%CI(1.033, 2.298)], glycosylated hemoglobin [OR = 1.401, 95%CI(1.097, 1.790)], history of hypertension [OR = 16.046, p < 0.05], 95%CI(4.726, 54.489), R value [OR = 0.533, 95%CI(0.351, 0.809)], MA value [OR = 1.399, 95%CI(1.004, 1.949)] were independent influencing factors for hemorrhagic transformation in patients with acute ischemic stroke. TEG has some value in predicting recurrence in patients with acute ischemic stroke, and the MA value in TEG [AUC = 0.806 (95%CI:0.747-0.867), with a sensitivity of 78.6% and a specificity of 70.4%], predicted the most significant efficiency of AIS recurrence.

Advances in the Mechanisms of Hemorrhagic Transformation and Therapeutic Agents after Intravenous Thrombolysis in Ischemic Stroke

Advances in the Mechanisms of Hemorrhagic Transformation and Therapeutic Agents after Intravenous Thrombolysis in Ischemic Stroke

“Hemorrhagic Transformation Following Thrombolytic Therapy in Acute Ischemic Stroke: A Case Series of 5 Patients”

Stroke stands as a global health menace, causing substantial disability and mortality. Timely intervention, specifically within the critical "Golden Hour" following acute ischemic stroke, is imperative. Thrombolytic agents like tissue plasminogen activators (tPA) are pivotal for clot dissolution and blood flow restoration, yet their use introduces the risk of hemorrhagic transformation (HTF).In a recent case series involving five patients receiving thrombolytic therapy for acute ischemic stroke, we illuminate the occurrence of post-treatment HTF, its clinical ramifications, and the intricate challenges in its management. Early intervention in acute ischemic stroke aims to safeguard at-risk brain tissue, with thrombolytic therapy, notably tPA, serving as a primary treatment avenue. However, the associated risk of HTF hovers around 30%–35%, influenced by factors like age, comorbidities, and infarct size. The vulnerable ischemic penumbra, marked by a compromised blood-brain barrier and free radical generation, is particularly susceptible. Treatment decisions, guided by the National Institutes of Health Stroke Scale (NIHSS), pivot on stroke severity assessment, emphasizing the need for vigilant post-treatment monitoring. In conclusion, navigating the delicate balance between the benefits of early thrombolysis and the risks of HTF remains a persistent challenge in optimizing outcomes for acute ischemic stroke patients.

Emerging diagnostic markers and therapeutic targets in post-stroke hemorrhagic transformation and brain edema.

Stroke is a devastating condition that can lead to significant morbidity and mortality. The aftermath of a stroke, particularly hemorrhagic transformation (HT) and brain edema, can significantly impact the prognosis of patients. Early detection and effective management of these complications are crucial for improving outcomes in stroke patients. This review highlights the emerging diagnostic markers and therapeutic targets including claudin, occludin, zonula occluden, s100β, albumin, MMP-9, MMP-2, MMP-12, IL-1β, TNF-α, IL-6, IFN-γ, TGF-β, IL-10, IL-4, IL-13, MCP-1/CCL2, CXCL2, CXCL8, CXCL12, CCL5, CX3CL1, ICAM-1, VCAM-1, P-selectin, E-selectin, PECAM-1/CD31, JAMs, HMGB1, vWF, VEGF, ROS, NAC, and AQP4. The clinical significance and implications of these biomarkers were also discussed.

Drugs/agents for the treatment of ischemic stroke: Advances and perspectives.

Ischemic stroke (IS) poses a significant threat to global human health and life. In recent decades, we have witnessed unprecedented progresses against IS, including thrombolysis, thrombectomy, and a few medicines that can assist in reopening the blocked brain vessels or serve as standalone treatments for patients who are not eligible for thrombolysis/thrombectomy therapies. However, the narrow time windows of thrombolysis/thrombectomy, coupled with the risk of hemorrhagic transformation, as well as the lack of highly effective and safe medications, continue to present big challenges in the acute treatment and long-term recovery of IS. In the past 3 years, several excellent articles have reviewed pathophysiology of IS and therapeutic medicines for the treatment of IS based on the pathophysiology. Regretfully, there is no comprehensive overview to summarize all categories of anti-IS drugs/agents designed and synthesized based on molecular mechanisms of IS pathophysiology. From medicinal chemistry view of point, this article reviews a multitude of anti-IS drugs/agents, including small molecule compounds, natural products, peptides, and others, which have been developed based on the molecular mechanism of IS pathophysiology, such as excitotoxicity, oxidative/nitrosative stresses, cell death pathways, and neuroinflammation, and so forth. In addition, several emerging medicines and strategies, including nanomedicines, stem cell therapy and noncoding RNAs, which recently appeared for the treatment of IS, are shortly introduced. Finally, the perspectives on the associated challenges and future directions of anti-IS drugs/agents are briefly provided to move the field forward.

The role of neuro-inflammatory in the pathogenesis of brain edema and hemorrhagic transformation in ischemic stroke: mechanisms and therapeutic target

Acute cerebrovascular accident is one of the leading causes of disability and death worldwide. Given the significant increase in life expectancy of the population, stroke will remain a serious medical and social problem in the next few decades. Among the various causes of stroke, ischemic brain damage predominates. Ischemic stroke is based on a decrease in the intensity of blood supply to the brain tissues, as a result of which there is a decrease in the delivery to neurons of the required amount of glucose and oxygen, which are required to ensure the normal function of this organ. At the same time, in many cases, spontaneous or medical restoration of blood flow after a period of ischemia is accompanied by a paradoxical increase in damage, and therefore it is advisable to consider the process of damage to brain tissue during circulatory disorders in the context of ischemic-reperfusion injury (IRI). One of the key mechanisms of brain IRP is the inflammatory response. In the process of secondary immune damage to the brain, both mechanisms of innate immunity, manifested by leukocyte infiltration of the damaged brain area, and antigen-dependent reactions of adaptive immunity are involved. One of the most important manifestations of neuroinflammation in cerebral IRI is an increase in transand paracellular permeability of the blood-brain barrier, which underlies the development of vasogenic cerebral edema and hemorrhagic transformation of the focus. This review considers current ideas about the molecular mechanisms that link aseptic inflammation, edema, and hemorrhagic transformation.

Prognostic Burden of Hemorrhagic Transformation in Acute Ischemic Stroke: A Brief Report from the Real Life

Introduction: Hemorrhagic Transformation (HT) represents one of the main complications of acute ischemic stroke, affecting its management and prognosis. Few data exists on prognosis of HT in the real world. Aim of this study was to evaluate the prognostic impact of HT in a real world cohort of patients hospitalized for acute ischemic stroke. Methods: We retrospectively analyzed the clinical data of patients with acute ischemic stroke consecutively admitted to our Stroke Unit. Patients with HT were compared with those without HT. Modified Rankin Scale (mRS) at hospital discharge and at 90 days were the study outcomes. Poor prognosis was defined as mRS≥4. A multivariate logistic regression analysis was performed to identify independent predictors of outcomes. Results: The study population consisted of 564 patients with mean age 77.5±11.8 years. Fifty-two patients (9.2%) showed HT on brain CT. Length of hospitalization, in-hospital mortality, median mRS at discharge, percentage of patients with mRS≥4 at discharge, percentage of HT patients discharged without secondary antiplatelet or anticoagulant prophylaxis and median 90- day mRS were significantly higher in patients with HT than in those without. The presence of HT was predictive of mRS≥4 at discharge and at 90 days (AUC 0.720 and 0.776, respectively). The presence of HT was an independent predictor of poor outcome, increasing the risk by about four times both at discharge (OR 3.64, 95% 1.46-9.06) and at 90 days (OR 4.26, 95% 1.07-16.88). Conclusions: HT is associated with a poor outcome in terms of mortality and severe residual disability both in the acute phase and at 90 days.

A weakly supervised deep learning model integrating noncontrasted computed tomography images and clinical factors facilitates haemorrhagic transformation prediction after intravenous thrombolysis in acute ischaemic stroke patients

BackgroundHaemorrhage transformation (HT) is a serious complication of intravenous thrombolysis (IVT) in acute ischaemic stroke (AIS). Accurate and timely prediction of the risk of HT before IVT may change the treatment decision and improve clinical prognosis. We aimed to develop a deep learning method for predicting HT after IVT for AIS using noncontrast computed tomography (NCCT) images.MethodsWe retrospectively collected data from 828 AIS patients undergoing recombinant tissue plasminogen activator (rt-PA) treatment within a 4.5-h time window (n = 665) or of undergoing urokinase treatment within a 6-h time window (n = 163) and divided them into the HT group (n = 69) and non-HT group (n = 759). HT was defined based on the criteria of the European Cooperative Acute Stroke Study-II trial. To address the problems of indiscernible features and imbalanced data, a weakly supervised deep learning (WSDL) model for HT prediction was constructed based on multiple instance learning and active learning using admission NCCT images and clinical information in addition to conventional deep learning models. Threefold cross-validation and transfer learning were performed to confirm the robustness of the network. Of note, the predictive value of the commonly used scales in clinics associated with NCCT images (i.e., the HAT and SEDAN score) was also analysed and compared to measure the feasibility of our proposed DL algorithms.ResultsCompared to the conventional DL and ML models, the WSDL model had the highest AUC of 0.799 (95% CI 0.712–0.883). Significant differences were observed between the WSDL model and five ML models (P < 0.05). The prediction performance of the WSDL model outperforms the HAT and SEDAN scores at the optimal operating point (threshold = 1.5). Further subgroup analysis showed that the WSDL model performed better for symptomatic intracranial haemorrhage (AUC = 0.833, F1 score = 0.909).ConclusionsOur WSDL model based on NCCT images had relatively good performance for predicting HT in AIS and may be suitable for assisting in clinical treatment decision-making.

Cerebral microbleeds and asundexian in non-cardioembolic ischemic stroke: Secondary analyses of the PACIFIC-STROKE randomized trial.

Cerebral microbleeds are magnetic imaging resonance (MRI) markers of hemorrhage-prone cerebral small vessel disease that predict future risk of ischemic stroke and intracranial hemorrhage (ICrH). There exist concerns about the net benefit of antithrombotic therapy in patients with microbleeds. We aimed to investigate the effects of an oral factor-XIa inhibitor (asundexian), that is hypothesized to inhibit thrombosis without compromising hemostasis, on the development of new microbleeds over time and interactions between microbleeds and asundexian treatment on clinical outcomes. We additionally assessed associations between baseline microbleeds and the risks of clinical and neuroimaging outcomes in patients with non-cardioembolic ischemic stroke. This is a secondary analysis of the PACIFIC-STROKE, international, multi-center Phase 2b double-blind, randomized clinical trial. PACIFIC-STROKE enrolled patients aged ⩾ 45 years with mild-to-moderate non-cardioembolic ischemic stroke who presented within 48 h of symptom onset for whom antiplatelet therapy was intended. Microbleeds were centrally adjudicated, and participants with an interpretable T2*-weighted sequence at their baseline MRI were included in this analysis. Patients were randomized to asundexian (10/20/50 mg daily) versus placebo plus standard antiplatelet treatment. Regression models were used to estimate the effects of (1) all pooled asundexian doses and (2) asundexian 50 mg daily on new microbleed formation on 26-week MRIs. Cox proportional hazards or regression models were additionally used to estimate interactions between treatment assignment and microbleeds for ischemic stroke/transient ischemic attack (TIA) (primary outcome), and ICrH, all-cause mortality, hemorrhagic transformation (HT), and new microbleeds (secondary outcomes). Of 1746 participants (mean age, 67.0 ± 10.0; 34% female) with baseline MRIs, 604 (35%) had microbleeds. During a median follow-up of 10.6 months, 7.0% (n = 122) had ischemic stroke/TIA, 0.5% (n = 8) ICrH, and 2.1% (n = 37) died. New microbleeds developed in 10.3% (n = 155) of participants with adequate follow-up MRIs and HT in 31.4% (n = 345). In the total sample of patients with adequate baseline and 26-week follow-up MRIs (n = 1507), new microbleeds occurred in 10.2% of patients assigned to any asundexian dose and 10.5% of patients assigned to placebo (OR, 0.96; 95% CI, 0.66-1.41). There were no interactions between microbleeds and treatment assignment for any of the outcomes (p for interaction > 0.05). The rates of new microbleeds, HT, and ICrH were numerically less in patients with microbleeds assigned to asundexian relative to placebo. The presence of microbleeds was associated with a higher risk of HT (aOR, 1.6; 95% CI, 1.2-2.1) and new microbleeds (aOR, 4.4; 95% CI, 3.0-6.3). Factor XIa inhibition with asundexian appears safe in patients with non-cardioembolic ischemic stroke and hemorrhage-prone cerebral small vessel disease marked by microbleeds on MRI. These preliminary findings will be confirmed in the ongoing OCEANIC-STROKE randomized trial. ClinicalTrials.gov Identifier: NCT04304508.

In-hospital mortality in patients with ischemic stroke and a large cerebral artery occlusion, who underwent mechanical thrombectomy

Occlusion of a large cerebral artery in ischemic stroke (IS) is associated with a high mortality rate. Despite the results of studies that have demonstrated the beneficial effect of endovascular therapy on functional outcome in IS, little research has been conducted on its impact on hospital mortality in IS, its timing and structure.Objective: to investigate hospital mortality in patients with IS and large cerebral artery occlusion, who underwent mechanical thrombectomy (MTE).Material and methods. The retrospective study included data from 233 patients with IS and confirmed occlusion of a large cerebral artery (internal carotid artery, M1 and M2 segments of the middle cerebral artery, basilar artery) treated at the regional vascular center V.V. Veresaev Hospital, Moscow, 2018 and 2022. A comparison of hospital mortality in the group of patients who underwent MTE and the group of patients who received basic therapy was performed.Results. MTE was performed in 107 patients (46%); 126 patients (54%) received only basic therapy. The mortality rate of all patients included in the study was 44.2%. Among all deaths, the proportion of patients with MTE was only 7.2%, while the proportion of patients on basic therapy was 36.9% (p&lt;0.001). Mortality in the MTE group was four times lower than in the basic therapy group – 15.8% compared to 68.2% (p&lt;0.001). We observed that certain manifestations were significantly more frequent in the basic therapy group: cerebral edema (42% vs. 18.6%), hemorrhagic transformation (19.9% vs. 12.9%), venous thromboembolism (6.3% vs. 3.7%) and infectious complications (42.8% vs. 14.3%). The mortality of patients in the basic therapy group was higher on the first day, on days 2–3 and also on days 4–7, while no differences in mortality were observed after the first week of the disease.Conclusion. Admission of a patient with IS within the “therapeutic window” creates the conditions for a significant reduction in hospital mortality and the incidence of stroke complications.

Pretreatment parameters associated with hemorrhagic transformation among successfully recanalized medium vessel occlusions.

Although pretreatment radiographic biomarkers are well established for hemorrhagic transformation (HT) following successful mechanical thrombectomy (MT) in large vessel occlusion (LVO) strokes, they are yet to be explored for medium vessel occlusion (MeVO) acute ischemic strokes. We aim to investigate pretreatment imaging biomarkers representative of collateral status, namely the hypoperfusion intensity ratio (HIR) and cerebral blood volume (CBV) index, and their association with HT in successfully recanalized MeVOs. A prospectively collected registry of acute ischemic stroke patients with MeVOs successfully recanalized with MT between 2019 and 2023 was retrospectively reviewed. A multivariate logistic regression for HT of any subtype was derived by combining significant univariate predictors into a forward stepwise regression with minimization of Akaike information criterion. Of 60 MeVO patients successfully recanalized with MT, HT occurred in 28.3% of patients. Independent factors for HT included: diabetes mellitus history (p = 0.0005), CBV index (p = 0.0071), and proximal versus distal occlusion location (p = 0.0062). A multivariate model with these factors had strong diagnostic performance for predicting HT (area under curve [AUC] 0.93, p < 0.001). Lower CBV indexes, distal occlusion location, and diabetes history are significantly associated with HT in MeVOs successfully recanalized with MT. Of note, HIR was not found to be significantly associated with HT.

A multitrait genetic study of hemostatic factors and hemorrhagic transformation after stroke treatment

BackgroundThrombolytic recombinant tissue plasminogen activator (r-tPA) treatment is the only pharmacologic intervention available in the ischemic stroke acute phase. This treatment is associated with an increased risk of intracerebral hemorrhages, known as hemorrhagic transformations (HTs), which worsen the patient’s prognosis. ObjectivesTo investigate the association between genetically determined natural hemostatic factors’ levels and increased risk of HT after r-tPA treatment. MethodsUsing data from genome-wide association studies on the risk of HT after r-tPA treatment and data on 7 hemostatic factors (factor [F]VII, FVIII, von Willebrand factor [VWF], FXI, fibrinogen, plasminogen activator inhibitor-1, and tissue plasminogen activator), we performed local and global genetic correlation estimation multitrait analyses and colocalization and 2-sample Mendelian randomization analyses between hemostatic factors and HT. ResultsLocal correlations identified a genomic region on chromosome 16 with shared covariance: fibrinogen-HT, P = 2.45 × 10−11. Multitrait analysis between fibrinogen-HT revealed 3 loci that simultaneously regulate circulating levels of fibrinogen and risk of HT: rs56026866 (PLXND1), P = 8.80 × 10−10; rs1421067 (CHD9), P = 1.81 × 10−14; and rs34780449, near ROBO1 gene, P = 1.64 × 10−8. Multitrait analysis between VWF-HT showed a novel common association regulating VWF and risk of HT after r-tPA at rs10942300 (ZNF366), P = 1.81 × 10−14. Mendelian randomization analysis did not find significant causal associations, although a nominal association was observed for FXI-HT (inverse-variance weighted estimate [SE], 0.07 [−0.29 to 0.00]; odds ratio, 0.87; 95% CI, 0.75-1.00; raw P = .05). ConclusionWe identified 4 shared loci between hemostatic factors and HT after r-tPA treatment, suggesting common regulatory mechanisms between fibrinogen and VWF levels and HT. Further research to determine a possible mediating effect of fibrinogen on HT risk is needed.

Association between infarct location and haemorrhagic transformation of acute ischaemic stroke after intravenous thrombolysis

To evaluate the association between computed tomography (CT)-based imaging variables at the time of admission and haemorrhagic transformation (HT) after intravenous thrombolysis (IVT). One hundred and eight patients who were treated with IVT for acute ischaemic stroke (AIS) during January 2021 to July 2023 were analysed retrospectively. The infarct location was classified as cortical or subcortical in accordance with the Alberta Stroke Program Early CT Score (ASPECTS) system. Logistic regression and receiver operating characteristic curve analyses were performed to determine the relationship between ischaemic variables and HT. Of the total, 18 (16.7%) patients had HT and seven (6.5%) had symptomatic intracerebral haemorrhage (sICH). Multivariate analysis revealed that cortical ASPECTS was independently associated with HT (odds ratio [OR], 0.197; 95% confidence interval [CI], 0.076-0.511; p=0.001) and cortical ASPECTS was independently associated with sICH (OR, 0.066; 95% CI, 0.009-0.510; p=0.009). To predict HT and sICH, cortical ASPECTS (HT area under the curve [AUC]=0.881, sICH AUC=0.971) provided a higher AUC compared with ASPECTS (HT AUC=0.850, sICH AUC=0.918). Cortical ASPECTS seen on CT at the time of admission is associated with HT and sICH after IVT.

Endovascular Embolization of Traumatic Vessel Injury Using N-butyl Cyanoacrylate: A Case Series.

There is limited evidence of N-butyl cyanoacrylate (n-BCA) use in endovascular embolization of traumatic face and neck vessel injuries. We investigated the safety and effectiveness of n-BCA for this purpose. We retrospectively analyzed consecutive patients presenting to a Level 1 trauma center between April 2021 and July 2022. We included patients aged ≥ 18years old with any vessel injury in the face and neck circulation requiring n-BCA embolization. The primary endpoint was n-BCA effectiveness defined as immediate control of active bleeding post-embolization. In total, 13 patients met the inclusion criteria. The median decade of life was 3 (IQR 3 - 5) with a male predominance (n = 11, 84.6%). Median Glasgow Coma Scale score on presentation was 15 (IQR 3-15). Eleven patients suffered gunshot wound injuries; two patients suffered blunt injuries. Injured vessels included facial artery (n = 6, 46.2%), buccal branch artery (n = 3, 23.1%), internal maxillary (n = 5, 38.5%), cervical internal carotid artery (n = 1, 7.7%), and vertebral artery (n = 1, 7.7%). All patients were treated with 1:2 n-BCA to ethiodol mixture with immediate extravasation control. No bleeding recurrence or need for retreatment occurred. One patient died in-hospital (7.7%). Patients were discharged to home (n = 8, 61.5%), day rehabilitation (n = 1, 7.7%), or acute rehabilitation (n = 3, 23.1%). One patient developed a right posterior cerebral artery infarct with hemorrhagic transformation. To our knowledge, this is the first study demonstrating the safety and effectiveness of n-BCA liquid embolism in traumatic vessel injuries, especially penetrating gunshot wounds.

Hemorrhagic transformation after IV-rTPA in COVID-19 patient with comorbidities of atrial fibrillation and hyperthyroid

Hemorrhagic transformation after IV-rTPA in COVID-19 patient with comorbidities of atrial fibrillation and hyperthyroid

GPR124 induces NLRP3 inflammasome-mediated pyroptosis in endothelial cells during ischemic injury

ObjectiveG protein-coupled receptor 124 (GPR124) regulates central nervous system angiogenesis and blood-brain barrier (BBB) integrity, and its deficiency aggravates BBB breakdown and hemorrhagic transformation in ischemic mice. However, excessive GPR124 expression promotes inflammation in atherosclerotic mice. In this study, we aimed to elucidate the role of GPR124 in hypoxia/ischemia-induced cerebrovascular endothelial cell injury. MethodsbEnd.3 cells were exposed to oxygen-glucose deprivation (OGD), and time-dependent changes in GPR124 mRNA and protein expression were evaluated using reverse transcription-polymerase chain reaction (RT-PCR) and Western blotting. The effects of GPR124 overexpression or knockdown on the expression of pyroptosis-related genes were assessed at the mRNA and protein levels. Tadehaginoside (TA) was screened as a potential small molecule targeting GPR124, and its effects on pyroptosis-related signaling pathways were investigated. Finally, the therapeutic efficacy of TA was evaluated using a rat model of transient middle cerebral artery occlusion/reperfusion (tMCAO/R). ResultsDuring OGD, the expression of GPR124 initially increased and then decreased over time, with the highest levels observed 1 h after OGD. The overexpression of GPR124 enhanced the OGD-induced expression of NLRP3, Caspase-1, and Gasdermin D (GSDMD) in bEnd.3 cells, whereas GPR124 knockdown reduced pyroptosis. Additionally, TA exhibited a high targeting ability to GPR124, significantly inhibiting its function and expression and suppressing the expression of pyroptosis-related proteins during OGD. Furthermore, TA treatment significantly reduced the cerebral infarct volume and pyroptotic signaling in tMCAO/R rats. ConclusionsOur findings suggest that GPR124 mediates pyroptotic signaling in endothelial cells during the early stages of hypoxia/ischemia, thereby exacerbating ischemic injury.

Why do some patients with acute ischemic stroke after intravenous thrombolytic therapy fail to improve? A case-control study

Introduction: thrombolytic therapy is the primary saving measure adopted in ischemic cerebrovascular accident (ICVA) victims, adequate for most of them. However, some patients do not show clinical progress, worsening the prognosis, which constitutes an essential scientific gap. Objective: to analyze the determinants of clinical non-improvement in stroke patients who used rt-PA thrombolytic agentes. Methods: retrospective observational case-control study, carried out from 2014 to 2017 through an active search of medical records of CVA patients undergoing thrombolytic therapy in a reference hospital in Ceará. Clinical failure was characterized as no reduction in the National Institutes of Health Stroke Scale-Score (NIHSS). Results: a total of 139 patients enrolled in the study in a single CVA unit. The mean age was 66.14 years (range 34 to 95). The 24-hour follow-up was completed in 100% of patients. A favorable result 24 hours post-thrombolysis was observed in 113 patients (81.29%), and there was no clinical improvement in 26 (18.7%). Post-thrombolysis hemorrhagic transformation was a strong predictor of no improvement (p=0.004), and diabetes was the main modifiable risk factor found (p=0.040). Conclusion: diabetes and hemorrhagic transformation after thrombolysis were identified as risk factors for clinical non-improvement in patients with acute stroke undergoing thrombolytic therapy.

Association of Early Longitudinal Changes in the Neutrophil-to-Lymphocyte Ratio With Adverse Clinical Outcomes in Acute Ischemic Stroke Patients After Endovascular Treatment

Background and PurposeWe aim to elucidate the contribution of early dynamic changes in the neutrophil-to-lymphocyte ratio (NLR) to poor clinical outcomes in acute ischemic stroke (AIS) patients after endovascular treatment (EVT). MethodsAIS patients who underwent EVT were consecutively recruited from January 2019 to July 2022. Blood cell counts were sampled at admission and at following 24 hours after EVT. Clinical outcome measures included 3-month functional dependence (modified Rankin scale of 3-6), symptomatic intracranial hemorrhage (sICH), and mortality at seven days and 30 days. Multinomial logistic regressions were used to evaluate the association of changes in NLR with unfavorable outcomes. Results590 patients were included in the final analysis. The multinomial logistic model indicated that the increasing changes in NLR after EVT was an independent factor for poor outcomes; the adjusted odds ratio (aOR) was 1.06 (95% CI 1.03-1.10; P<0.001) at poor 3-month functional outcomes, 1.07 (95% CI 1.04-1.10; P<0.001) at sICH, 1.08 (95% CI 1.05-1.12; P<0.001) at mortality at seven days, and 1.04 (95% CI 1.02-1.07; P=0.001) at mortality at 30 days. Areas under the curve (AUC) of changes in NLR to discriminate adverse outcomes were 0.725, 0.687, 0.664, and 0.659. The optimal cut-off values were 5.77 (56.6 % sensitivity, 81.0% specificity), 6.92 (60.0% sensitivity, 77.0% specificity), 8.64 (51.0% sensitivity, 82.0% specificity), and 8.64 (48.7% sensitivity, 83.0% specificity), respectively. ConclusionsNLR in AIS patients increased remarkably independent of successful reperfusion. Elevated changes in NLR might predict malignant hemorrhagic transformation, adverse functional outcomes, and short-term mortality.

Serum microRNA miR-491-5p and miR-206 as indicators for unfavorable outcomes and spontaneous hemorrhagic transformation after ischemic stroke

Serum microRNA miR-491-5p and miR-206 as indicators for unfavorable outcomes and spontaneous hemorrhagic transformation after ischemic stroke

Association of Atrial Fibrillation with Remote Intracerebral Hemorrhage After Intravenous Thrombolysis: Results from a Multicenter Study in China.

This study aimed to investigate the association between atrial fibrillation (AF), particularly newly diagnosed AF, and remote intracerebral hemorrhage (rICH) in patients with ischemic stroke who were treated with intravenous thrombolysis (IVT). This observational study was conducted on patients with ischemic stroke who received IVT with recombinant tissue-type plasminogen activator. The data were taken from a multicenter prospective registry of a Chinese population. rICH was defined as any extraischemic hemorrhage detected on computerized tomography (CT) 24h after intravenous thrombolysis. We collected and compared the demographic data and clinical characteristics of all the patients with rICH to those of patients without any type of hemorrhagic transformation. The association between AF and rICH was analyzed using univariate analysis and binary logistic regression. A total of 20,697 patients were included in the study, with 1566 (7.6%) experiencing intracerebral hemorrhage (ICH), 586 (2.8%) experiencing rICH, and 19,131 (92.4%) not experiencing any form of hemorrhagic transformation. Univariate analysis revealed significant differences in age, pre-thrombolysis systolic blood pressure, baseline National Institute of Health Stroke Scale score, previously known AF, newly diagnosed AF, coronary heart disease, congestive heart failure, hyperhomocysteinemia, and history of thrombolysis between the rICH and control groups (P < 0.05). Further multivariate logistic regression analysis indicated that total AF (OR 1.821, 95%CI 1.082-3.065, P < 0.05), previously known AF (OR 1.470, 95%CI 1.170-1.847), and newly diagnosed AF (OR 1.920, 95%CI 1.304-2.825) were independently associated with rICH. This study suggests that AF, regardless of whether it is newly diagnosed or previously known, may be associated with the occurrence of rICH following intravenous thrombolysis. Interestingly, our findings suggest that newly diagnosed AF may have a stronger impact on rICH than previously known AF, although confirmation from more studies is needed.