No abstract

BackgroundWe aimed to develop and validate a new nomogram for predicting the risk of intracranial hemorrhage (ICH) in patients with acute ischemic stroke (AIS) after intravenous thrombolysis (IVT).MethodsA retrospective study enrolled 553 patients with AIS treated with IVT. The patients were randomly divided into two cohorts: the training set (70%, n = 387) and the testing set (30%, n = 166). The factors in the predictive nomogram were filtered using multivariable logistic regression analysis. The performance of the nomogram was assessed based on the area under the receiver operating characteristic curve (AUC-ROC), calibration plots, and decision curve analysis (DCA).ResultsAfter multivariable logistic regression analysis, certain factors, such as smoking, National Institutes of Health of Stroke Scale (NIHSS) score, blood urea nitrogen-to-creatinine ratio (BUN/Cr), and neutrophil-to-lymphocyte ratio (NLR), were found to be independent predictors of ICH and were used to construct a nomogram. The AUC-ROC values of the nomogram were 0.887 (95% CI: 0.842–0.933) and 0.776 (95% CI: 0.681–0.872) in the training and testing sets, respectively. The AUC-ROC of the nomogram was higher than that of the Multicenter Stroke Survey (MSS), Glucose, Race, Age, Sex, Systolic blood Pressure, and Severity of stroke (GRASPS), and stroke prognostication using age and NIH Stroke Scale-100 positive index (SPAN-100) scores for predicting ICH in both the training and testing sets (p < 0.05). The calibration plot demonstrated good agreement in both the training and testing sets. DCA indicated that the nomogram was clinically useful.ConclusionsThe new nomogram, which included smoking, NIHSS, BUN/Cr, and NLR as variables, had the potential for predicting the risk of ICH in patients with AIS after IVT.

Background/Aims: Kallikrein, a serine proteinase, has been reported to have many functions, such as selectively dilating arterioles in the ischemic area and enhancing angiogenesis and neurogenesis. Therefore, it may promote cerebral poststroke reorganization. We observed the effect of human tissue kallikrein on the brain motor activation of acute ischemic stroke patients and evaluated patient condition severity and prognosis. Methods: Forty-four cases suffering from cerebral infarction between 6 and 72 h of onset were randomly assigned into the kallikrein group (n = 24) and the control group (n = 20). The control group was given conventional treatment, whereas the kallikrein group was given both conventional treatment and human tissue kallikrein over the course of 12–14 days. The activation of the sensorimotor cortex (SMC) and cerebellum, the affected forefinger strength and the NIHSS scores were evaluated before and after treatment. The MBI and MRS scores were assessed at 30 and 90 days after stroke onset. Results: There were no differences between the two groups in activation volume, patient condition and scores before treatment. After treatment, the ipsilesional SMC activation volume was significantly larger and the increase in the volume was significantly greater in the kallikrein group than in the control group (p < 0.05 for both). The NIHSS score was significantly smaller and the improvement in the score was significantly greater in the kallikrein group after treatment (p < 0.05 for both). Moreover, the MBI scores at 30 days were significantly higher, whereas the MRS scores at 30 days were significantly lower in the kallikrein group than in the control group (p < 0.05 for both). Conclusions: Kallikrein improved neural function effectively and quickly after stroke, and promoting cerebral reorganization might be an important mechanism for kallikrein in the treatment of acute cerebral infarction.

No abstract