Browsing by keyword "Ischemic stroke"
Now showing items 1-4 of 4
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Clinical impact of leukoaraiosis burden and chronological age on neurological deficit recovery and 90-day outcome after minor ischemic strokeBACKGROUND AND AIMS: Ischemic stroke remains a leading cause of disability, particularly among the elderly, but this association has not been consistently noted among patients with minor stroke. We sought to determine the association of chronological age and leukoaraiosis, which is considered a marker of biological age, with the degree of neurological deficit recovery and 90-day disability after minor ischemic stroke. METHODS: We retrospectively analyzed 185 patients with a minor ischemic stroke (National Institutes of Health Stroke Scale [NIHSS] score < /=5). Leukoaraiosis severity was graded according to the van Swieten scale. NIHSS was assessed at baseline, discharge, and 90-days. Multivariable linear and ordinal logistic regression analyses were constructed to identify independent predictors of the degree of NIHSS-improvement (DeltaNIHSS) and 90-day outcome as assessed by the modified Rankin Scale (mRS). RESULTS: Patients with severe leukoaraiosis had attenuated DeltaNIHSS at 90days as compared to patients with none-to-mild leukoaraiosis (p=0.028). After adjustment, leukoaraiosis severity (p < 0.001) but not chronological age (p=0.771) was independently associated with the DeltaNIHSS by day 90. Severe leukoaraiosis (p=0.003, OR 3.1, 95%-CI 1.5-6.4), older age (p=0.001, OR 1.0 95%-CI 1.0-1.1), and admission NIHSS (p < 0.001, OR 1.5, 95%-CI 1.2-1.8) were independent predictors of the 90-day mRS. CONCLUSION: Leukoaraiosis is a more sensitive predictor for neurological deficit recovery after ischemic stroke than chronological age. Further study is required to establish the specific contribution of leukoaraiosis to functional outcome after minor ischemic stroke beyond its impact on recovery mechanisms.
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Estimated stroke risk, yield, and number needed to screen for atrial fibrillation detected through single time screening: a multicountry patient-level meta-analysis of 141,220 screened individualsBACKGROUND: The precise age distribution and calculated stroke risk of screen-detected atrial fibrillation (AF) is not known. Therefore, it is not possible to determine the number needed to screen (NNS) to identify one treatable new AF case (NNS-Rx) (i.e., Class-1 oral anticoagulation [OAC] treatment recommendation) in each age stratum. If the NNS-Rx is known for each age stratum, precise cost-effectiveness and sensitivity simulations can be performed based on the age distribution of the population/region to be screened. Such calculations are required by national authorities and organisations responsible for health system budgets to determine the best age cutoffs for screening programs and decide whether programs of screening should be funded. Therefore, we aimed to determine the exact yield and calculated stroke-risk profile of screen-detected AF and NNS-Rx in 5-year age strata. METHODS AND FINDINGS: A systematic review of Medline, Pubmed, and Embase was performed (January 2007 to February 2018), and AF-SCREEN international collaboration members were contacted to identify additional studies. Twenty-four eligible studies were identified that performed a single time point screen for AF in a general ambulant population, including people > /=65 years. Authors from eligible studies were invited to collaborate and share patient-level data. Statistical analysis was performed using random effects logistic regression for AF detection rate, and Poisson regression modelling for CHA2DS2-VASc scores. Nineteen studies (14 countries from a mix of low- to middle- and high-income countries) collaborated, with 141,220 participants screened and 1,539 new AF cases. Pooled yield of screening was greater in males across all age strata. The age/sex-adjusted detection rate for screen-detected AF in > /=65-year-olds was 1.44% (95% CI, 1.13%-1.82%) and 0.41% (95% CI, 0.31%-0.53%) for < 65-year-olds. New AF detection rate increased progressively with age from 0.34% ( < 60 years) to 2.73% ( > /=85 years). Neither the choice of screening methodology or device, the geographical region, nor the screening setting influenced the detection rate of AF. Mean CHA2DS2-VASc scores (n = 1,369) increased with age from 1.1 ( < 60 years) to 3.9 ( > /=85 years); 72% of > /=65 years had > /=1 additional stroke risk factor other than age/sex. All new AF > /=75 years and 66% between 65 and 74 years had a Class-1 OAC recommendation. The NNS-Rx is 83 for > /=65 years, 926 for 60-64 years; and 1,089 for < 60 years. The main limitation of this study is there are insufficient data on sociodemographic variables of the populations and possible ascertainment biases to explain the variance in the samples. CONCLUSIONS: People with screen-detected AF are at elevated calculated stroke risk: above age 65, the majority have a Class-1 OAC recommendation for stroke prevention, and > 70% have > /=1 additional stroke risk factor other than age/sex. Our data, based on the largest number of screen-detected AF collected to date, show the precise relationship between yield and estimated stroke risk profile with age, and strong dependence for NNS-RX on the age distribution of the population to be screened: essential information for precise cost-effectiveness calculations.
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Modelling the impact of clot fragmentation on the microcirculation after thrombectomyMany ischaemic stroke patients who have a mechanical removal of their clot (thrombectomy) do not get reperfusion of tissue despite the thrombus being removed. One hypothesis for this 'no-reperfusion' phenomenon is micro-emboli fragmenting off the large clot during thrombectomy and occluding smaller blood vessels downstream of the clot location. This is impossible to observe in-vivo and so we here develop an in-silico model based on in-vitro experiments to model the effect of micro-emboli on brain tissue. Through in-vitro experiments we obtain, under a variety of clot consistencies and thrombectomy techniques, micro-emboli distributions post-thrombectomy. Blood flow through the microcirculation is modelled for statistically accurate voxels of brain microvasculature including penetrating arterioles and capillary beds. A novel micro-emboli algorithm, informed by the experimental data, is used to simulate the impact of micro-emboli successively entering the penetrating arterioles and the capillary bed. Scaled-up blood flow parameters-permeability and coupling coefficients-are calculated under various conditions. We find that capillary beds are more susceptible to occlusions than the penetrating arterioles with a 4x greater drop in permeability per volume of vessel occluded. Individual microvascular geometries determine robustness to micro-emboli. Hard clot fragmentation leads to larger micro-emboli and larger drops in blood flow for a given number of micro-emboli. Thrombectomy technique has a large impact on clot fragmentation and hence occlusions in the microvasculature. As such, in-silico modelling of mechanical thrombectomy predicts that clot specific factors, interventional technique, and microvascular geometry strongly influence reperfusion of the brain. Micro-emboli are likely contributory to the phenomenon of no-reperfusion following successful removal of a major clot.
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Whole blood microRNA expression associated with stroke: Results from the Framingham Heart StudyEmerging evidence suggests microRNAs (miRNAs) may play an important role in explaining variation in stroke risk and recovery in humans, yet there are still few longitudinal studies examining the association between whole blood miRNAs and stroke. Accounting for multiple testing and adjusting for potentially confounding technical and clinical variables, here we show that whole blood miR-574-3p expression was significantly lower in participants with chronic stroke compared to non-cases. To explore the functional relevance of our findings, we analyzed miRNA-mRNA whole blood co-expression, pathway enrichment, and brain tissue gene expression. Results suggest miR-574-3p is involved in neurometabolic and chronic neuronal injury response pathways, including brain gene expression of DBNDD2 and ELOVL1. These results suggest miR-574-3p plays a role in regulating chronic brain and systemic cellular response to stroke and thus may implicate miR-574-3p as a partial mediator of long-term stroke outcomes.
