Strain pattern and T-wave alterations are predictors of mortality and poor neurologic outcome following stroke.
应变模式和 T 波改变是卒中后死亡率和不良神经功能预后的预测因子。
- 作者列表："Braga GP","Gonçalves RS","Minicucci MF","Bazan R","Zornoff LAM
BACKGROUND:Stroke is associated with electrocardiogram (ECG) abnormalities. However, the role of strain pattern as predictor of poor neurologic outcome and mortality after stroke has not yet been demonstrated. HYPOTHESIS:ECG abnormalities, with a particular focus on ST-segment changes, are predictors of mortality and neurologic disability 90 days after stroke. METHODS:Patients with up to 24 hours of stroke were prospectively recruited. An ECG was taken at the time of admission. The patients' clinical evolution was evaluated during hospitalization and after discharge by means of a prescheduled return in 90 days. The degree of disability was measured by the modified Rankin scale (mRs). In relation to the mRs, patients were divided into those with scores from 0 to 2 and those with scores equal to or greater than 3 at the end of the observation period. RESULTS:Of the 112 patients studied, 29 (25.8%) died during the study period. Patients who died presented higher National Institute of Health Stroke Scale and mRs scores on admission, elevated biomarkers of myocardial necrosis, and abnormalities on the ECG. The prevalence of ECG abnormalities was 63%. A logistic regression model showed that strain pattern and T-wave alterations were predictors of mortality (odds ratio [OR]: 12.970, 95% confidence interval [CI]: 1.519-110.723, P = .019; OR: 3.873, 95% CI: 1.135-13.215, P = .031, respectively) and mRs at 90 days (OR: 12.557, 95% CI: 1.671-94.374, P = .014; OR: 15.970, 95% CI: 3.671-69.479, P < .001, respectively) after stroke, adjusted by sex, age, stroke subtype, entrance NIH, previous mRs score, and stroke thrombolysis. CONCLUSION:Strain pattern and T-wave alterations were predictors of mortality and poor neurologic outcome 90 days after stroke.
背景: 中风与心电图 (ECG) 异常有关。然而，应变模式作为卒中后神经功能预后不良和死亡率预测因子的作用尚未得到证实。 假设: 心电图异常，特别关注 ST 段改变，是卒中后 90 天死亡率和神经功能残疾的预测因子。 方法: 前瞻性招募卒中长达 24 小时的患者。入院时做心电图。在住院期间和出院后通过 90 天内预先安排的返回来评估患者的临床演变。采用改良 Rankin 量表 (mRs) 测量残疾程度。关于 mRs，在观察期结束时，将患者分为评分为 0 ~ 2 分的患者和评分等于或大于 3 分的患者。 结果: 在研究的 112 例患者中，29 例 (25.8%) 在研究期间死亡。死亡患者入院时出现较高的美国国立卫生研究院卒中量表和 mRs 评分，心肌坏死生物标志物升高，心电图异常。心电图异常患病率为 63%。Logistic 回归模型显示，应变模式和 T 波改变是死亡率的预测因子 (比值比 [OR]: 12.970，95% 置信区间 [CI]: 1.519-110.723，P =。 019; OR: 3.873，95% CI: 1.135-13.215，P =. 031，分别) 和 90 天的 mRs (OR: 12.557,95% CI: 1.671-94.374，P =.014; OR: 15.970，95% CI: 3.671-69.479，P
METHODS:BACKGROUND:People with stroke are not meeting recommended levels of physical activity. The modifiable factors associated with post-stroke physical activity levels need to be identified to develop targeted interventions. OBJECTIVE:The objective of this study was to investigate the factors at discharge from inpatient rehabilitation that are associated with physical activity levels at 3 months following discharge. DESIGN:This was a prospective cohort study. METHODS:Sixty-four people with stroke completed baseline assessments at discharge from inpatient rehabilitation and 55 completed the follow-up 3 months later. The candidate factors (i.e. gait speed, balance, strength, cognition, mood and motivation) were measured at discharge. The primary outcome measure at follow-up was walking related activity (measured by wrist-worn accelerometer). Secondary outcome measures were physical activity participation (Activity Card Sort) and intensity of physical activity (International Physical Activity Questionnaire - Short 7 days). Adjusted separate multivariable linear regression models or proportional odds regression models were used to evaluate the associations between candidate factors and physical activity. RESULTS:Gait speed and balance were associated with all aspects of physical activity. Higher level of intrinsic motivation was also associated with higher physical activity participation. Anxiety demonstrated a significant non-linear relationship with physical activity participation. LIMITATIONS:Inclusion of fatigue and individual muscle strength could have provided further insights into associations with steps per day. CONCLUSION:The results demonstrated that better physical function at discharge from inpatient rehabilitation was associated with future increased levels of physical activity. Additionally, higher levels of motivation impacted on increased physical activity participation. The influence of anxiety on physical activity participation requires further exploration. Mixed-method study designs can be utilized to further understand the factors associated with post-stroke physical activity.
METHODS:Cerebral ischemia-reperfusion (I/R) is characterized by initial transient cerebral ischemia followed by reperfusion. Various pathophysiological processes are involved in brain injury and functional recovery during cerebral I/R. There are few studies on dynamic metabolic process after cerebral I/R. The present study was to observe dynamic alteration of brain injury, functional recovery, and metabolites after cerebral I/R in rats and discover potential metabolic markers. The cerebral I/R model was established by middle cerebral artery occlusion (MCAO) for 90 min, following reperfusion in rats. The results of cerebral infarction area, cerebral edema, and behavior test showed that there were dynamic changes in brain injury and functional recovery at different periods after cerebral I/R. Further analysis showed that the brain injury was severe on the first day of cerebral I/R, and there was a significant functional recovery from the 7th day of cerebral I/R, followed by an aggravation trend of brain injury from the days 7 to 28. Furthermore, Matrix-assisted laser desorption ionization mass spectrometry imaging analysis showed that the expression of ATP, glucose, and citric acid on 7th day was the highest during cerebral I/R, which indicated that energy metabolism and oxidative phosphorylation played important roles during cerebral I/R. In addition, the untargeted metabolomic results showed that the level of isocitric acid, the ratio of oxyglutaric acid/glutamic acid, and the level of pyruvic acid associated with the TCA cycle were also the highest on the 7th day during cerebral I/R, which indicated that the transient spontaneous recovery of ischemic brain on the 7th day after ischemia-reperfusion might be related to oxidative phosphorylation and energy metabolism in the brain in this period. In conclusion, the results suggest that some small molecule metabolites participate in the brain injury and functional recovery during cerebral I/R, which is of great significance to the development of therapeutic drugs and diagnostic markers.
METHODS:The aims of this study were to study the effects of miR-2 on cerebral ischemia–reperfusion rats and to explore its further mechanism. Rats were assigned into sham, model, miR-22 control and miR-22 groups. Observation of neurological behaviors at 24 h after operation found that neurological functions were severely damaged in the model and miR-22 control groups and these damages were improved by miR-22. RT-PCR indicated that miR-22 mRNA level in the brain tissue was significantly decreased in the model and miR-22 control groups, but increased in the miR-22 group. TTC staining showed increased percentage of cerebral infarction volume in the model and miR-22 control groups and this increase was reduced by miR-22. Immunohistochemistry showed increased densities of CD34^+ and VEGF^+ microvessels in the cortex in the model and miR-22 control groups, which were further increased in the miR-22 group. ELISA showed increased serum VEGF and Ang-1 levels in the model and miR-22 control groups, which were also further increased in the miR-22 group. Western blot analysis showed increased phosphorylation level of PI3K and Akt in brain tissue in the model and miR-22 control groups, which were further increased in the miR-22 group. Administration of LY294002, a specific PI3K pathway inhibitor, significantly reversed all the effects of miR-22 on rats in the model group. miR-22 exerts its neuroprotective and angiogenic functions via the PI3K/Akt signaling pathway, at least partly, in rats under cerebral ischemia–reperfusion.