Rise in Low-Density Lipoprotein Cholesterol during Hospitalization is Related with Poor Outcome at Discharge in Patients with Acute Ischemic Stroke.

BACKGROUND: The statistical association between a short-term rise in low-density lipoprotein cholesterol (LDL-C) levels and the short-term outcome of acute ischemic stroke remains unknown. We aimed to evaluate the association in acute ischemic stroke patients during hospitalization. METHODS: Patients with acute ischemic stroke who received statin at discharge were enrolled in this multicenter registry study. LDL-C values were measured on the first day after admission and on the day before discharge to determine the rise in LDL-C levels. Poor outcome was defined as a modified Ranking Scale score ≥2 at discharge. The National Institutes of Health Stroke Scale increase from admission to discharge by 2 points was defined as clinical deterioration. Logistic regression analyses were used to analyze the relationship between LDL-C rise during hospitalization and poor outcome at discharge. Variables that were significantly different between the LDL-C rise and LDL-C fall groups were considered in adjustment for confounding variables in model 1. Age, sex, and those variables in model 1 were considered in adjustment for confounding variables in model 2. RESULTS: Among the 676 patients, 110 (16.3%) showed a rise in LDL-C levels during hospitalization. Multivariate analyses showed that LDL-C at admission <1.6 mmol/L was significantly correlated with LDL-C rise during hospitalization (p < 0.001). There were significantly more patients with a poor outcome in the "LDL-C rise" group than in the "LDL-fall" group (p = 0.002). Multiple models consistently showed that LDL-C rise increased the risk of a poor outcome at discharge in model 1 (OR [95% CI] 1.351 [1.059-1.723], p = 0.016) and model 2 (OR [95% CI] 1.370 [1.071-1.751], p = 0.012). LDL-C rise also increased the risk of clinical deterioration, although its p value only was 0.043 in model 1 and 0.048 in model 2. CONCLUSIONS: Rise in LDL-C during hospitalization from acute ischemic stroke is an independent predictor of poor outcome at discharge. In particular, patients with lower LDL-C values at admission are a higher at risk, and LDL-C in these patients should thus be monitored while in hospital.

Correlation of Stress Hyperglycemia after Ischemic Stroke with Early Vascular Cognitive Impairment.

Objective To investigate the influence and forecast value of stress hyperglycemia on the early vascular cognitive impairment (VCI) in stroke patients.Methods Totally 422 patients with acute non-diabetic stroke were divided into three groups according to the fasting plasma glucose level:the euglycemia group (<6.1 mmol/L),the mild stress hyperglycemia group (6.1-7.0 mmol/L),and the severe stress hyperglycemia group (≥7.0 mmol/L).Mini-mental state examination,Alzheimer's disease rating scale cognitive subscale,and clinical dementia rating scale were used to evaluate early cognition in post-stroke patients,and patients were divided into three groups accordingly:normal cognitive function group,mild VCI group,and vascular dementia group.Correlation analysis was carried out on the level of stress hyperglycemia and the degree of VCI.Results Of these 422 patients,stress hyperglycemia was identified in 62 cases (14.7%).The risk of stress hyperglycemia was higher in patients with a high degree of education [(8.39±3.85)years vs.(6.62±4.39)years,P=0.037)] or a history of cardiovascular disease (45.2% vs.18.3%,P=0.001).VCI was detected in 270 patients (64.0%).Age,sex,smoking,National Institute of Health Stroke Scale score,Hamilton Depression Rating Scale score,stress hyperglycemia,and history of cardiovascular disease were related with early VCI after non-diabetic ischemic stroke (P<0.05).Multivariate Logistic regression analysis showed that stress hyperglycemia was an independent risk factor for VCI in patients with non-diabetic ischemic stroke (OR=3.086,95% CI=1.065-8.929).The risks of cognitive impairment in the mild stress hyperglycemia group and the severe stress hyperglycemia group were higher than that of the euglycemia group,while it was also higher in the severe stress hyperglycemia group than in the mild stress hyperglycemia group (61.11% vs.75.00% vs.90.91%).Stress hyperglycemia was positively correlated with the high risk of early cognitive impairment in stroke patients (rs=0.185,P=0.007).Conclusion There is a significant correlation between stress hyperglycemia and early VCI after ischemic stroke.

Asymmetric distribution of pathogenic low wall shear stress of the bilateral subclavian arteries: two case reports.

The effects of increasing blood flow on the pathogenic wall shear stress (pWSS) of subclavian arteries (SAs) are currently unclear. Patient-specific models of the SA were constructed based on computed tomographic images from two patients. Using the Ansys Fluent 19.0 transient laminar flow solver, the finite volume method was chosen to solve the Navier-Stokes equation governing fluid behavior. The time-averaged wall shear stress, ratio of risk area, cumulative ratio of risk area (P¯), ratio of risk time, and ratio contour of risk time were calculated to describe the temporal and spatial distributions of pWSS. Virtually all pWSS occurred during the diastolic phase. The P¯ was 2.3 and 1.29 times higher on the left than on the right in Patients 1 (P1) and 2 (P2), respectively. Increasing the blood flow volume of the left SA by 20%, 40%, and 60% led to a 9.27%, 15.10%, and 20.99% decrease in P¯ for P1 and a 5.74%, 11.55%, and 17.14% decrease in P¯ for P2, respectively, compared with baseline values. In conclusion, the left SA showed greater diastolic pWSS than the right SA, and increasing the blood flow volume reduced the pWSS in the left SA.

Cilostazol plus clopidogrel in the prevention of in-stent stenosis after vertebral artery origin stenting in gout patients: three case reports.

It is unclear whether cilostazol instead of aspirin in combination with clopidogrel could prevent in-stent thrombosis in patients with a history of gout undergoing vertebral artery origin stenting. Three men (age range, 58-74 years) were diagnosed with acute ischaemic stroke or transient ischaemic attack. Vertebral artery origin stenosis was visible by computed tomographic angiography or digital subtraction angiography. Four bare metal stents were placed in the vertebral artery origin. The patients were administered 100 mg cilostazol orally twice a day and 75 mg clopidogrel orally once a day perioperatively and 100 mg cilostazol orally twice day was administered indefinitely after 3 months. No in-stent stenosis was observed in all of these patients during a follow-up period up to 19 months. Cilostazol plus clopidogrel has the potential to become an alternative to standard dual antiplatelet therapy in vertebral artery origin stenting. A high-quality clinical trial is needed to verify these preliminary findings.

A Grading Scale for Pial Collaterals in Middle Cerebral Artery Total Occlusion Based on Time-of-flight MR Angiography Source Images.

PURPOSE: To verify whether a new grading based on time-of-flight magnetic resonance angiography source images (TOF-MRAsi) can reflect the abundance of pial collaterals, in patients with total occlusion of M1 segment of middle cerebral artery in the chronic stage. METHODS: In this single-center retrospective study, consecutive patients with total occlusion of M1 segment of middle cerebral artery, with both magnetic resonances angiography and digital subtraction angiography image were included. Time-of-flight magnetic resonance angiography source images were evaluated in a blinded fashion for pial collaterals (PCs) that were graded on a four-point scale. Good and poor PCs were defined as TOF-MRAsis grade <2 and ≥2, respectively. Receiver operating characteristic curve analysis was done to calculate the area under curve, sensitivity, and specificity. RESULTS: A total of 26 patients were included. The inter-reader agreement for time TOF-MRAsi and digital subtraction angiography images were 0.930 and 0.843, respectively. Compared with digital subtraction angiography grading, the area under curve of pial collateral grading based on TOF-MRAsi was 0.830 (0.636-1.000; P = 0.006). The sensitivity and specificity were 0.700 and 0.933, respectively. The modified Rankin Scale at follow-up was lower in patients with good PCs than in those with poor PCs (0[0, 1] vs. 1[1, 3], P = 0.055), although statistical significance was not reached. CONCLUSION: The grading scale based on TOF-MRAsi could be a new empirical approach for pial collateral evaluation. The clinical use of the proposed approach for identifying patients with total occlusion of middle cerebral artery with a high risk of poor outcome requires evaluation in further studies.

Intensive Versus Moderate Statin Therapy Discontinuation in Patients With Acute Ischemic Stroke or Transient Ischemic Attack.

PURPOSE: The differences of discontinuation risk between intensive and mild-to-moderate statin therapy in patients with acute ischemic stroke is not clear. This study aimed to clarify whether intensive statin therapy resulted in a significant increase in discontinuation early after discharge. METHODS: This multicenter registry study enrolled consecutive hospitalized patients with ischemic stroke or transient ischemic attack. All the patients were prescribed statin therapy at discharge. Intensity of statin therapy was defined according to the 2013 American College of Cardiology/American Heart Association guideline on the treatment of blood cholesterol. A logistic regression model was used to analyze the association between statin therapy intensity and discontinuation. FINDINGS: This study included 505 patients, of whom 64 and 441 received intensive and moderate statin therapy, respectively (mean follow-up, approximately 6 months). The rates of discontinuation of intensive and moderate statin therapy were 31.3% and 10.7% (P < 0.001), respectively. Variables with significant differences between the intensive and moderate statin therapy groups were included in the adjusted logistic regression model. Intensive statin therapy significantly increased discontinuation risk by 273.0% (odds ratio = 3.730; 95% CI, 2.013-6.911; P < .001) compared with moderate statin therapy. The result was consistent in most subgroups, except for patients with National Institutes of Health Stroke Scale scores ≥4. IMPLICATIONS: In stroke secondary prevention, intensive statin therapy may significantly increase the risk of early discontinuation compared with moderate statin therapy. Future clinical trials that involve a comparison between intensive and moderate statin therapy for stroke secondary prevention should address the differences in discontinuation between these 2 groups.

Age and composite end-point events in medium follow-up of patients with carotid artery total occlusion using drug therapy.

BACKGROUND AND AIMS: The outcome of carotid artery total occlusion (CATO) is unclear. The aim of this study is to report the medium incidence of composite end-point events and risk factors (especially age), in patients with CATO, treated medically. METHODS: This was a single center retrospective study. Composite end-point events included death, ischemic stroke, transient ischemic attack, hemorrhagic stroke, myocardial infarction, or angina. Logistic regression analysis was used to analyze risk factors of composite end-point events. RESULTS: A total of 94 patients with CATO were included in the study. The mean follow-up duration was 30 ± 16 months. There were 16 cases who experienced composite end-point events (17.0%); among them, there were 15 cases of death (16.0%), 8 cases of ischemic stroke (7 cases of fatal stroke and 1 case of non-fatal stroke) (8.5%), and 1 case of angina pectoris (1%) (the patient later developed ischemic stroke). With increased age, the incidence of composite end-point events was significantly increased (p = 0.002). Multivariate logistic regression analysis showed that only age was a risk factor (OR = 3.051 (1.351-6.890), p = 0.007). CONCLUSIONS: The incidence of composite end-point events in patients with CATO was as high as 17.0% at approximately 3 years after drug therapy alone. For every 10 years of age increase, the risk increase of composite end-point events doubles.