OBJECTIVE:Patients with internal carotid artery occlusion (ICAO) present with a heavy thrombosis burden and bad lateral circulation, which are associated with unfavorable outcomes following endovascular therapy (EVT). In this study, authors explored the risk factors associated with poor outcomes in patients with ICAO undergoing EVT and developed and validated a dynamic nomogram for predicting poor outcomes. METHODS:Five hundred seventy-seven patients from the multicenter, randomized, double-blind, placebo-controlled MARVEL (Methylprednisolone as Adjunctive to Endovascular Treatment for Acute Large Vessel Occlusion) trial were included in the current retrospective study. The patients, all of whom had ICAO and received EVT between February 2022 and June 2023, were split into training (60%) and internal validation (40%) cohorts. Additionally, 281 patients from the Endovascular Treatment for Acute Anterior Circulation Ischemic Stroke registry (ACTUAL registry) served as the external validation cohort. Least absolute shrinkage and selection operator (LASSO) and multivariate logistic regression analyses were applied to identify risk factors to establish a dynamic nomogram prediction model. RESULTS:Five risk factors were independently associated with poor outcome, including age (OR 0.951, 95% CI 0.935-0.968, p < 0.001), baseline Alberta Stroke Programme Early CT Score (OR 1.176, 95% CI 1.075-1.286, p < 0.001), baseline National Institutes of Health Stroke Scale score (OR 0.850, 95% CI 0.801-0.901, p < 0.001), baseline American Society of Interventional and Therapeutic Neuroradiology and Society of Interventional Radiology grade (OR 1.646, 95% CI 1.388-1.951, p < 0.001), and baseline glucose levels (OR 0.891, 95% CI 0.827-0.959, p = 0.002). The prediction model, based on these five factors, showed moderate performance with an area under the curve of 0.786 (95% CI 0.728-0.844) in the internal validation and 0.795 (95% CI 0.743-0.847) in the external validation, with the calibration curve closely aligning with the ideal diagonal line. CONCLUSIONS:This predictive model can accurately forecast poor outcomes for patients with ICAO undergoing EVT, serving as a useful adjunct in operative decision-making for both physicians and patient families.

BACKGROUND:Acupuncture is an effective adjunctive therapy for stroke and has been suggested for the treatment for acute cerebral infarction (ACI). However, there is a lack of high-quality data from randomized clinical trials. Thus, this study aims to reach a consensus to guide the clinical research and practice. METHODS:The initial project list was based on a systematic review of research evidence and a clinical problem survey conducted by a multidisciplinary team. After discussion with experts and a two-round Delphi consensus survey, the final list was optimized. Then, Likert scale of 9 points was used to measure the degree of expert consensus (1 = strongly disagree, 9 = strongly agree) and 80% of scores between 7 and 9 were defined as "agreement." RESULTS:A total of 30 professionals (response rate: 100%) confirmed their participation in the voting group. After two rounds of Delphi voting, a consensus was achieved including 34 items that can be broadly categorized into six aspects. According to expert consensus, acupuncture should be initiated within 6 h and the main acupoints are Shuigou (GV26), Neiguan (PC6), Hegu (LI4), and Taichong (LR3), while the auxiliary acupoints include Quchi (LI11), Waiguan (SJ5), Huantiao (GB30), Weizhong (BL40), etc. Furthermore, the adverse events of acupuncture are generally considered to be few, only subcutaneous hematoma is commonly reported. CONCLUSION:This expert consensus provides recommendations for clinical research and practice in treating ACI with acupuncture. However, due to the limited clinical evidence, further exploration is needed through rigorous clinical trials.

The molecular mechanisms of brain-body interactions in the progression of brain diseases remain unknown. Through integrative analysis of multi-organ proteomic, metabolomic, and transcriptomic data following ischemic stroke, we identified dynamic molecular signatures across organs. The heart exhibited the highest number of differentially expressed proteins (DEPs), followed by spleen and intestine. Ten DEPs were shared among three organs post-stroke, with eight in heart, six in spleen, and five in intestine. Notably, organs displayed accelerated biological aging, particularly the intestine, ‌which is implicated in neurobehavioral regulation. Conjoint analysis further confirmed that DEPs originated from both intrinsic and immune cells that systemically infiltrated multiple organs. Finally, plasma DEPs showed high correlations with corresponding protein levels in distinct organs, potentially resulting in the systemic circulation of stroke. Our findings provide a comprehensive atlas of stroke-induced multi-organ molecular remodeling and establish a foundational framework for developing systemic therapeutic strategies targeting brain-body interactions in brain injury.

This study aimed to analyze the association between baseline National Institutes of Health Stroke Scale (NIHSS) scores and clinical outcomes in patients with large core infarctions undergoing endovascular treatment (EVT), a relationship that remains unclear. Data were obtained from the MAGIC study, a prospective multicenter cohort study focusing on patients with acute large core ischemic stroke. This analysis evaluated the impact of NIHSS scores on EVT outcomes in patients with large core infarctions. Primary outcome metrics included favorable outcomes (modified Rankin Scale [mRS] of 0–3 at 90 days), while secondary outcomes encompassed shifts in mRS scores, functional independence (mRS score of 0–2), mRS score of 0–4, and successful recanalization rates. Adverse events considered were symptomatic intracranial hemorrhage (sICH) and mortality. A total of 490 patients were enrolled in this study. Higher baseline NIHSS scores were inversely correlated with favorable outcomes (adjusted odds ratio [OR] in model 3, 0.848 [0.797–0.903], P < 0.001), particularly in patients with NIHSS scores above 20 (adjusted OR in model 3, 0.518 [0.306–0.878] vs. 0.290 [0.161–0.523]). Regarding adverse events, higher baseline NIHSS scores significantly correlated with increased 90-day mortality rates (adjusted OR in model 3, 1.129 [1.072–1.189], P < 0.001). This correlation became insignificant when baseline NIHSS scores exceeded 22. Additionally, baseline NIHSS scores partially mediated the association between age (indirect effect = − 0.0005, 19.39

Aim: Although lactate supplementation at the reperfusion stage of ischemic stroke has been shown to offer neuroprotection, whether the role of accumulated lactate at the ischemia phase is neuroprotection or not remains largely unknown. Thus, in this study, we aimed to investigate the roles and mechanisms of accumulated brain lactate at the ischemia stage in regulating brain injury of ischemic stroke. Methods and Results: Pharmacological inhibition of lactate production by either inhibiting LDHA or glycolysis markedly attenuated the mouse brain injury of ischemic stroke. In contrast, additional lactate supplement further aggravates brain injury, which may be closely related to the induction of neuronal death and A1 astrocytes. The contributing roles of increased lactate at the ischemic stage may be related to the promotive formation of protein lysine lactylation (Kla), while the post-treatment of lactate at the reperfusion stage did not influence the brain protein Kla levels with neuroprotection. Increased protein Kla levels were found mainly in neurons by the HPLC-MS/MS analysis and immunofluorescent staining. Then, pharmacological inhibition of lactate production or blocking the lactate shuttle to neurons showed markedly decreased protein Kla levels in the ischemic brains. Additionally, Ldha specific knockout in astrocytes (Aldh1l1 CreERT2; Ldha fl/fl mice, cKO) mice with MCAO were constructed and the results showed that the protein Kla level was decreased accompanied by a decrease in the volume of cerebral infarction in cKO mice compared to the control groups. Furthermore, blocking the protein Kla formation by inhibiting the writer p300 with its antagonist A-485 significantly alleviates neuronal death and glial activation of cerebral ischemia with a reduction in the protein Kla level, resulting in extending reperfusion window and improving functional recovery for ischemic stroke. Conclusion: Collectively, increased brain lactate derived from astrocytes aggravates ischemic brain injury by promoting the protein Kla formation, suggesting that inhibiting lactate production or the formation of protein Kla at the ischemia stage presents new therapeutic targets for the treatment of ischemic stroke.

The effectiveness and safety of human urinary kallidinogenase (HUK) in acute ischemic stroke (AIS) patients undergoing endovascular therapy (EVT) due to large vessel occlusion (LVO) was unclear. A pooled analysis was performed using individual data from the DEVT and RESCUE BT trials. Patients were divided into two groups based on HUK treatment. The primary outcome was the 90-day modified Rankin Scale (mRS) score. Safety outcomes included 90-day mortality and symptomatic intracranial hemorrhage (sICH) within 48 hours. A total of 1174 patients were included in the study. Of these, 150 (12.8%) patients received HUK. The adjusted common odds ratio (OR) of the mRS score was 1.458 (95% confidence interval [CI] = 1.072–1.983; p = 0.016) favoring HUK. The incidence of sICH (2.0% vs. 8.6%; adjusted OR: 0.198; 95% CI: 0.061–0.638; p = 0.007) and mortality (11.3% vs.18.5%; adjusted OR: 0.496; 95% CI: 0.286–0.862; p = 0.013) was lower in HUK group than non-HUK group. This association was consistent with propensity score-matching and the inverse probability of treatment weighting analysis. In conclusion, HUK was safe and associated with a preferable prognosis in AIS patients due to LVO in the anterior circulation.

Background The presence of sudden onset to maximal deficit (SOTMD) in patients with acute basilar artery occlusion often results in more severe outcomes. However, the effect of endovascular therapy on SOTMD and whether the outcome is affected by onset‐to‐puncture time remain unclear. Methods and Results This retrospective analysis was conducted using data from the prospective BASILAR (Endovascular Treatment for Acute Basilar Artery Occlusion Study Registry). Consecutive patients with basilar artery occlusion receiving endovascular therapy were dichotomized into SOTMD and non‐SOTMD cohorts. The primary outcomes included a favorable outcome (modified Rankin scale 0–3), recanalization, and mortality at 90 days. The outcomes of patients with SOTMD were analyzed using multivariable logistic regression. In the multivariate analysis, a favorable outcome was similar between the two cohorts (odds ratio [OR], 0.88 [95% CI, 0.58–1.34]; P=0.5), although the mortality of patients with SOTMD was higher than that of patients with non‐SOTMD (OR, 1.67 [95% CI, 1.14–2.44]; P=0.008). The probability of mortality increased from 40.0% at 1 hour to 70.0% at 6 hours in the SOTMD cohort, and favorable outcomes of patients with non‐SOTMD declined from 38.0% at 1 hour to 18.0% at 8 hours. Conclusions No significant difference was observed in favorable outcomes between the SOTMD and non‐SOTMD groups, although mortality was higher in the SOTMD cohort. The patients with SOTMD had a stronger time dependence for endovascular therapy in terms of mortality, while the time dependency regarding favorable outcome in the NSOTMD group was even higher. Registration URL: https://www.chictr.org.cn; Unique identifier: ChiCTR1800014759.

Prior studies on anterior circulation stroke have demonstrated that the benefits of endovascular treatment (EVT) may be absent in patients with poor collaterals. Our study focused on patients with basilar artery occlusion (BAO) to investigate time-dependent EVT effects according to the posterior circulation collateral score (PC-CS). The BASILAR study was a nationwide prospective Chinese registry of consecutive BAO patients. Patients were divided into groups receiving standard medical therapy alone (SMT group) or SMT plus EVT (EVT group). Restricted cubic spline analyses (RCSA) were performed to explore the nonlinear and linear relationships between EVT time and outcomes for different PC-CS. We included 828 patients with acute BAO. Compared with the poor collateral (PC-CS 0–3), the adjusted odds ratio of favorable outcome was 1.311 in patients with moderate (PC-CS 4–5) (95% CI, 0.781–2.201) and 1.899 with good (PC-CS 6–10) collateral (1.125–3.207) for EVT. RCSA revealed that in patients with PC-CS 0–3, the favorable outcome probability after EVT significantly decreased to 10% within 6 h and stabilized thereafter ( P nonlinearity = 0.035), while in patients with moderate and good collateral, the probability was maintained at approximately 30% and 40% respectively, even beyond 6 h (all P nonlinearity > 0.05). Among patients with BAO, good collateral circulation was independently associated with improved outcomes along with the usage of thrombectomy. Patients with poor collaterals should receive EVT as early as possible, especially within 6 h of symptom onset, while the time window may be extended in patients with moderate and good collaterals. Unique identifier: ChiCTR1800014759.

Bankground: Basilar artery occlusion (BAO) is related to a high risk of morbidity and mortality. Our aim was to investigate the values of posterior circulation collateral score (PC-CS) on treatment decision-making and individualizing time window of patients with acute BAO in endovascular treatment. Methods: The BASILAR study was a nationwide prospective registry of consecutive patients presenting with symptomatic, radiologically confirmed within 24 hours of symptoms onset. Patients were divided into two groups according to the treatment they received: standard medical therapy alone and medical therapy plus endovascular therapy (EVT). We used a 10-points grading system based on computed tomography angiography to quantify the potential for collateral flow in the posterior circulation. We defined modified Rankin Scale score &It;3 within 3 months as favorable outcome, as well as mortality within 90 days were included as primary outcomes. Results: A total of 828 eligible consecutive patients with acute BAO were enrolled in our study with trichotomized PC-CS. EVT was associated with higher rate of favorable outcomes (adjusted odds radio with 95% CI, 7.02 [1.48-33.29]; 4.84[1.82-12.87] and 6.16 [2.69-14.08]; respectively) and lower mortality (57.4% versus 84.8%, P =0.001; 47.4% versus 75% , P &It ; 0.001 and 34.9% versus 58.8%, P &It;0.001) than standard medical therapy group in the trichotomized PC-CS. And higher PC-CS is associated with favorable outcomes in EVT group. More importantly, the patients received endovascular treatment with poor collateral circulation (PC-CS 0-3) could benefit only within 6 hours of symptom onset, while the time window will be extended to 24 hours in the patients with good collateral circulation (PC-CS 4-10). Conclusions: The PC-CS is a vital marker for predict favorable outcomes and treatment decision-making and individualizing time window in patients with acute BAO in endovascular treatment.

Abstract Background Patients with acute non-lacunar single subcortical infarct (SSI) associated with mild intracranial atherosclerosis (ICAS) have a relatively high incidence of early neurological deterioration (END), resulting in unfavorable functional outcomes. Whether the early administration of argatroban and aspirin or clopidogrel within 6–12 h after symptom onset is effective and safe in these patients is unknown. Methods A review of the stroke database of Weihai Municipal Hospital, Cheeloo College of Medicine, Shandong University and Qingdao Center Hospital, Qingdao University Medical College in China was undertaken from May 2017 to January 2020 to identify all patients with non-lacunar SSI caused by ICAS within 6–12 h of symptom onset based on MRI screening. Patients were divided into two groups, one comprising those who received argatroban and mono antiplatelet therapy with aspirin or clopidogrel on admission (argatroban group), and the other those who received dual antiplatelet therapy (DAPT) with aspirin and clopidogrel during hospitalization (DAPT group). The primary outcome was recovery by 90 days after stroke based on a modified Rankin scale (mRS) score (0 to 1). The secondary outcome was END incidence within 120 h of admission. Safety outcomes were intracranial hemorrhage (ICH) and major extracranial bleeding. The probability of clinical benefit (mRS score 0–1 at 90 days) was estimated using multivariable logistic regression analysis. Results A total of 304 acute non-lacunar SSI associated with mild ICAS patients were analyzed. At 90 days, 101 (74.2%) patients in the argatroban group and 80 (47.6%) in the DAPT group had an mRS score that improved from 0 to 1 (P < 0.001). The relative risk (95% credible interval) for an mRS score improving from 0 to 1 in the argatroban group was 1.50 (1.05–2.70). END occurred in 10 (7.3%) patients in the argatroban group compared with 37 (22.0%) in the DAPT group (P < 0.001). No patients experienced symptomatic hemorrhagic transformation. Conclusions Early combined administration of argatroban and an antiplatelet agent (aspirin or clopidogrel) may be beneficial for patients with non-lacunar SSI associated with mild ICAS identified by MRI screening and may attenuate progressive neurological deficits. Trial registration Our study is a retrospectively registered trial.

Abstract Objective: Toll-like receptor (TLR) activation plays an important role in cerebral ischemia-reperfusion injury. In addition, increasing evidence suggests that TLRs may affect cognitive behavior through TLR-mediated signaling. Here, we explored the protective effects of TLR3 on cognitive dysfunction after ischemia in the context of poly(I:C) preconditioning.Materials and Methods : Mice (n=84) were randomly divided into the sham group, AAV (vector) group, middle cerebral artery occlusion (MCAO) model group, poly(I:C) (pre) + MCAO model group, and AAV (TRAF6) + poly(I:C) (pre) + MCAO model group. The mice were injected i.p. with poly(I:C) (1.25 mg/g) 24 h prior to cerebral ischemia. Then, neurological scores were assessed, and the infarct volume was measured after cerebral ischemia-reperfusion. We evaluated the poly(I:C) preconditioning-induced attenuation of neuronal damage using Nissl and TUNEL staining. We assessed the poly(I:C) preconditioning-mediated inhibition of I/R-induced glial activation, inflammatory factor levels and TRAF6 expression. We also assessed whether TRAF6 affects poly(I:C) preconditioning to improve cognitive dysfunction and neuroprotection.Results: The results showed that compared with those of the sham group and AAV (vector) group, the functional neurological scores and focal infarct volume of the MCAO group and poly(I:C) preconditioning group were significantly increased. The results also showed that compared with those of the MCAO group, the functional neurological scores and focal infarct volume of the poly(I:C) preconditioning group were significantly reduced. Our results indicated that poly(I:C) preconditioning significantly attenuated neuronal apoptosis and cell loss. Poly(I:C) preconditioning also inhibited I/R-induced glial cell activation and reduced NF-κB, TNF-α and IL-β levels. Our findings showed that poly(I:C) preconditioning affected cognitive dysfunction following cerebral I/R. Here, we observed that poly(I:C) preconditioning affected the expression and distribution of TRAF6 following cerebral I/R. TRAF6 overexpression abolished poly(I:C)-induced neuroprotection and worsened cognitive dysfunction in cerebral I/R injury.Significance: Our findings suggested that poly(I:C) preconditioning ameliorates cognitive dysfunction after cerebral I/R injury by inhibiting TRAF6 signaling, which is a potential therapeutic target for the treatment of cognitive dysfunction after stroke.

Objective: Toll-like receptor (TLR) activation plays an important role in cerebral ischemia-reperfusion injury. In addition, increasing evidence suggests that TLRs may affect cognitive behavior through TLR-mediated signaling. Here, we explored the protective effects of TLR3 on cognitive dysfunction after ischemia in the context of poly(I:C) preconditioning.Materials and Methods : Mice (n=84) were randomly divided into the sham group, AAV (vector) group, middle cerebral artery occlusion (MCAO) model group, poly(I:C) (pre) + MCAO model group, and AAV (TRAF6) + poly(I:C) (pre) + MCAO model group. The mice were injected i.p. with poly(I:C) (1.25 mg/g) 24 h prior to cerebral ischemia. Then, neurological scores were assessed, and the infarct volume was measured after cerebral ischemia-reperfusion. We evaluated the poly(I:C) preconditioning-induced attenuation of neuronal damage using Nissl and TUNEL staining. We assessed the poly(I:C) preconditioning-mediated inhibition of I/R-induced glial activation, inflammatory factor levels and TRAF6 expression. We also assessed whether TRAF6 affects poly(I:C) preconditioning to improve cognitive dysfunction and neuroprotection.Results: The results showed that compared with those of the sham group and AAV (vector) group, the functional neurological scores and focal infarct volume of the MCAO group and poly(I:C) preconditioning group were significantly increased. The results also showed that compared with those of the MCAO group, the functional neurological scores and focal infarct volume of the poly(I:C) preconditioning group were significantly reduced. Our results indicated that poly(I:C) preconditioning significantly attenuated neuronal apoptosis and cell loss. Poly(I:C) preconditioning also inhibited I/R-induced glial cell activation and reduced NF-κB, TNF-α and IL-β levels. Our findings showed that poly(I:C) preconditioning affected cognitive dysfunction following cerebral I/R. Here, we observed that poly(I:C) preconditioning affected the expression and distribution of TRAF6 following cerebral I/R. TRAF6 overexpression abolished poly(I:C)-induced neuroprotection and worsened cognitive dysfunction in cerebral I/R injury.Significance: Our findings suggested that poly(I:C) preconditioning ameliorates cognitive dysfunction after cerebral I/R injury by inhibiting TRAF6 signaling, which is a potential therapeutic target for the treatment of cognitive dysfunction after stroke.

NLRP6 inflammasome, one of the important intracellular innate immune sensors, has been shown to regulate immune responses. However, its roles in the intracerebral hemorrhage (ICH) are completely not clear. In the present study, we investigated the expression profile and biological roles of NLRP6 inflammasome in perihematomal brain tissues of mice subjected to ICH. In this study, we investigated the expression profile of NLRP6 inflammasome in the perihematomal brain tissues and explored the biological role of NLRP6 inflammasome upon acute brain injury in mice subjected to ICH. Increased expression of NLRP6 inflammasome was found in perihematomal brain tissues ranging from 6 h to 3 days, with a peak level at 1 day after ICH. Immunohistochemistry staining also showed that NLRP6 inflammasome was significantly increased in the perihematomal brain tissues at 1 day after ICH. Moreover, immunofluorescence staining showed that NLRP6 inflammasome was mainly colocalized in glial fibrillary acidic protein (GFAP)-positive astrocytes, while with little colocalized expression in NeuN-positive neurons and without expression in CD11b-positive microglia and CD31-positive endothelial cell in the perihematomal brain tissue of mice after ICH. Furthermore, NLRP6−/− ICH mice exhibited significantly higher brain water contents (BMCs), proinflammatory cytokines, NF-κB activity and neurological deficit scores when compared with the wild type (WT) ICH mice. In addition, we found that Toll-like receptor 4 (TLR4)−/− mice, as well as the TAK242 treated mice, had markedly lower expression of NLRP6 inflammasome expression in the perihematomal brain tissue at 1 day after ICH. Our data suggest that the upregulated NLRP6 inflammasome in perihematomal brain tissues attenuates ICH-induced brain injury.

BACKGROUND:Phospholipids and their metabolisms are closely allied to nosogenesis and aggravation of Type 2 diabetes mellitus and cognitive impairment. The aim of this study is to characterize the plasma levels of phospholipids in type 2 diabetes patients and type 2 diabetes patients with mild cognitive impairment (MCI), and to identify potential biomarkers of type 2 diabetes patients with MCI.METHODS:In this cross-sectional study, a total of 374 type 2 diabetes patients were prospectively enrolled. There were 103 patients with MCI and 271 patients without MCI. Plasma levels of lysophosphatidic acid (LPA) and phospholipids with solubility similar to that of LPA (PSS-LPA) were assayed.RESULTS:Plasma LPA and PSS-LPA levels were significantly higher in patients with MCI than those without MCI (P = 0.007, P ＜ 0.001). A logistic regression analysis indicates that elevated plasma PSSLPA was associated with increased risk of MCI in type 2 diabetic patients, with an OR of 1.87 (1.04- 3.47) after additional adjustment for hyperlipidemia, hypertension, High-sensitivity C-reactive protein, hemoglobin A1c, Intima-media thickness, ankle brachial index, and brachial-ankle pulse wave velocity. In type 2 diabetic patients with MCI, there were negative correlations between plasma LPA, PSS-LPA and the MoCA scores (r =﹣0.322, P < 0.01; r =﹣0.349, P < 0.001). Furthermore, plasma PSS-LPA exhibited a fair diagnostic value for MCI, with an area under the curve of 0.86.CONCLUSION:The level of plasma PSS-LPA may be an important biomarker for diagnosis of MCI.

Sleep disorder is a common complication after ischemic stroke. If it is not timely diagnosed and treated, it may affect the rehabilitation of stroke and recurrence. The manifestations of sleep disorders have various forms according to the different locations of infarction. For the treatment of sleep disorder after stroke, the method of the combination of drugs and physical therapy is used in clinical practice at present. In recent years, with the widely use of the polysomnography, poststroke sleep disorders can be diagnosed clearly and carefully. The treatment for sleep disorders after stroke may significantly improve the prognosis of patients. Key words: Stroke; Brain Ischemia; Sleep Wake Disorders; Continuous Positive Airway Pressure

Platelet activation and aggregation, as well as thrombosis, play an important role in the pathological and physiological processes of recurrent ischemic vascular events in stroke patients. The purpose of this study is to investigate the correlation of platelet function and recurrent ischemic vascular events in the secondary prevention of stroke. A total of 350 stroke patients within 72 h of onset from September 2014 to April 2015 were included in this study. The patients were administered aspirin starting from the day of admission. After 7-10 days, the platelet aggregation ratio was detected using method with continuous platelet counting, and the baseline data were recorded. The patients underwent a 6-month follow-up period, and the recurrent ischemic vascular events were observed. Logistic regression analysis was performed to obtain the risk factors for recurrent ischemic vascular events and the receiver operating characteristic (ROC) curve. The predictive value of the platelet aggregation ratio by method with continuous platelet counting detection for ischemic vascular events was analyzed. Among the 350 stroke patients, 52 patients had recurrent ischemic vascular events during the follow-up period. The proportion of the patients with recurrent ischemic events who also had diabetes (48.01% vs. 23.15%, P<0.001), low-density lipoprotein (LDL) cholesterol (3.02+/-0.74 vs. 2.74+/-0.72, P=0.016), an arachidonic acid-induced maximum platelet aggregation ratio (MAR-AA) (27.31+/-9.49 vs. 18.85+/-6.60, P<0.001), and an epinephrine-induced maximum platelet aggregation ratio (MAR-EPI) (61.26+/-13.02 vs. 51.41+/- 14.81, P<0.001) was significantly higher than that of the patients in the no ischemic vascular event group. These increased parameters were determined to be the independent risk factors for the occurrence of ischemic vascular events in stroke patients. MAR-AA was most closely related to the occurrence of ischemic vascular events (OR=1.133, 95% CI: 1.080+/-1.188, P<0.001) and showed a good predictive value for ischemic events with an area under the ROC curve (AUC) of 0.803. The increase in MAR-AA was also an independent risk factor for stroke recurrence (OR=1.090, 95% CI: 1.037+/-1.145, P=0.001). In the secondary prevention of stroke, platelet function measured with the continuous platelet counting method is closely related to recurrent ischemic vascular events; thus, this parameter has a good predictive value for recurrent ischemic vascular events.

To investigate the changes of plasma lysophosphatidic acid(LPA) or acidic phospholipids (AP) levels in patients with nonvalvular atrial fibrillation (NVAF) or NVAF-associated ischemic stroke and to provide biochemistry evidence to antithrombotic therapy. The present study examined plasma LPA/AP

Acute stroke and transient ischemic attack (TIA) is a great burden not only during hospitalization but also after hospital discharge. The objective of this meta-analysis was to evaluate the hospital readmissions, causes and risk factors after survival of acute stroke and TIA. Pubmed, Web of Science, Cochrane Library, OVID and EMBASE databases were searched to identify studies reporting hospital readmissions after acute stroke and TIA. The primary outcomes were hospital readmission rates during 30 days and 1 year after discharge. The primary causes and risk factors of hospital readmissions were also identified. Ten studies with 253,680 patients were eligible for inclusion. The pooled 30-day and 1-year hospital readmission rates were 17.4 % (95 % CI, 12.7–23.5 %) and 42.5 % (95 % CI, 34.1–51.3 %), respectively. The three major causes of 30-day hospital readmissions were infection (19.9 %), coronary artery disease (CAD) (17.8 %) and recurrent stroke (16.0 %) successively, while the three major causes were recurrent stroke (19.4 %), infection (19.3 %) and CAD (16.3 %) during 1 year’s follow-up. There were more patients with CAD in readmits group than that in control group (p = 0.030). The length of index admission, defined as any eligible admission to an acute care hospital assessed in the measure for the outcome, was longer (p = 0.000) and admission National Institutes of Health Stroke Score (NIHSS) was higher (p = 0.002) in readmits group than these in control group. In conclusion, there is high risk of early and long-term hospital readmissions after survival of acute stroke and TIA. These patients with coronary artery disease, longer length of index admission and higher NIHSS deserve deep attention after hospital discharge.

Background: To investigate the effect of creatine and coenzyme Q10 (CoQ10) combination therapy on mild cognitive impairment (MCI) in Parkinson's disease (PD; PD-MCI) and its influences on plasma phospholipid (PL) levels in PD-MCI. Methods: The demographic data of 75 PD-MCI patients who enrolled in this collaborative PD study were collected. These patients were evaluated using the Unified Parkinson's Disease Rating Scale (UPDRS) III and the Montreal Cognitive Assessment (MoCA). These 75 PD-MCI patients were randomly treated with creatine monohydrate 5 g b.i.d. and CoQ10 100 mg t.i.d. orally or placebo. MoCA evaluation and PL level measurements were performed after 12 and 18 months of treatment. Results: After 12 and 18 months of treatment, the differences in the MoCA scores of the combination therapy and control groups were statistically significant (p < 0.05 at 12 months and p < 0.01 at 18 months), and the plasma PL levels of the combination therapy group were significantly lower than those of the control group (p < 0.01 at 12 months and p < 0.001 at 18 months). Conclusions: Combination therapy with creatine and CoQ10 could delay the decline of cognitive function in PD-MCI patients and could lower their plasma PL levels; therefore, this combination therapy may have a neuroprotective function.