Developing a nomogram model for 3-month prognosis in patients who had an acute ischaemic stroke after intravenous thrombolysis: a multifactor logistic regression model approach.

OBJECTIVES: This study is to establish a nomination graph model for individualised early prediction of the 3-month prognosis of patients who had an acute ischaemic stroke (AIS) receiving intravenous thrombolysis with recombinant tissue plasminogen activator. DESIGN: For the period from January 2016 through August 2022, 991 patients who had an acute stroke eligible for intravenous thrombolysis were included in the retrospective analysis study. The study was based on multifactor logistic regression. PARTICIPANTS: Patients who received treatment from January 2016 to February 2021 were included in the training cohort, and those who received treatment from March 2021 to August 2022 were included in the testing cohort. INTERVENTIONS: Each patient received intravenous thrombolysis within 4.5 hours of onset, with treatment doses divided into standard doses (0.9 mg/kg). PRIMARY AND SECONDARY OUTCOME MEASURES: The primary outcome measure was a 3-month adverse outcome (modified Rankin Scale 3-6). RESULTS: The National Institutes of Health Stroke Scale Score after thrombolysis (OR=1.18; 95% CI: 1.04 to 1.36; p = 0.015), door-to-needle time (OR=1.01; 95% CI: 1.00 to 1.02; p = 0.003), baseline blood glucose (OR=1.08; 95% CI: 1.00 to 1.16; p=0.042), blood homocysteine (OR=7.14; 95% CI: 4.12 to 12.71; p<0.001), monocytes (OR=0.05; 95% CI: 0.01 to 0.043; p=0.005) and monocytes/high-density lipoprotein (OR=62.93; 95% CI: 16.51 to 283.08; p<0.001) were independent predictors of adverse outcomes 3 months after intravenous thrombolysis, and the above six factors were included in the nominated DGHM2N nomogram. The area under the receiver operating characteristic curve value of the training cohort was 0.870 (95% CI: 0.841 to 0.899) and in the testing cohort was 0.822 (95% CI: 0.769 to 0.875). CONCLUSIONS: A reliable nomogram model (DGHM2N model) was developed and validated in this study. This nomogram could individually predict the adverse outcome of patients who had an AIS receiving intravenous thrombolysis with alteplase for 3 months.

[The effects of salidroside on the apoptosis pathway of myocardial cells in acute exhausted rats].

OBJECTIVE: To investigate whether salidroside (Sal) plays a part in protecting myocardial cell through reducing the myocardial ischemia and the apoptosis pathway of both death receptors and mitochondria in acute exhausted rats. METHODS: Male SD rats were randomly divided into 4 groups (n=6): control group(Con), acute exhaustive swimming group (EE), low-dose and high-dose Sal pre-treatment exhaustive swimming group (SLE, SHE). Rats were treated with Sal solution (15 or 30 mg/(kg·d)) or 0.9%NaCl (3 ml/(kg·d)) by intraperitoneal injection for 15 d, respectively. The Con group did not carry out swimming training. The next day after the end of intraperitoneal administration, the rats in EE, SLE and SHE group were forced to swim until they were exhausted followed the standard of Thomas. After the end of exhaustive exercise, the rats were anesthetized and the blood samples and hearts were collected immediately. The myocardial ischemia and hypoxia area and myocardial apoptosis index (AI) were also observed. Serum ischemia modified albumin (IMA), cardiac troponin I (cTnI), brain natriuretic peptide(BNP) and myocardial cell Bcl-2-associated X protein (Bax), B-cell lymphoma-2 (Bcl-2) were determined. The expressions of myocardial TNF receptor superfamily member 6 (Fas), cytochrome C (Cyto-c), aspartate proteolytic enzyme-3(Caspase-3), aspartate proteolytic enzyme-8(Caspase-8), and aspartate proteolytic enzyme-9(Caspase-9) were detected. RESULTS: Compared with the Con group, the myocardial ischemia and hypoxia area in EE group was increased significantly. The serum levels of IMA, cTnI and BNP, AI and Bax levels and cardiac Fas, Cyto-C, Caspase-3, Caspase-8 and Caspase-9 protein expressions of EE group were also increased significantly (P＜0.01), while the protein expression of Bcl-2 in cardiac tissues was decreased significantly (P＜0.01). Compared with the EE group, the myocardial ischemia and hypoxia area, serum levels of IMA, cTnI and BNP, AI and Bax levels, and the protein expressions of cardiac Fas, Cyto-C, Caspase-3, Caspase-8 and Caspase-9 in Sal group were all decreased significantly(P＜0.01). while the protein expression of cardiac Bcl-2 in Sal group were increased significantly (P＜0.01). CONCLUSION: Sal plays a role in protecting myocardial cell through reducing the myocardial ischemia and inhibiting myocardial cell apoptosis in exhaustive exercise rats. The mechanism of reducing myocardial cell apoptosis may be related to inhibiting the expressions of Fas, Cyto-C, Caspase-3, Caspase-8, Caspase-9 and increasing the expression of Bcl-2.