Ischemic Lesion Size Research Articles

The Effect of Extremely Low-Frequency Magnetic Field on Stroke Patients: A Systematic Review.

The aim of this study was to review the current state of scientific evidence on the effect of extremely low-frequency magnetic fields stimulation (ELF-MFs) on stroke patients. A systematic review of PubMed, ScienceDirect, PeDro and Embase databases was conducted. Only articles published in English, involving adult participants and focusing on individuals who had experienced a stroke, specifically examining the impact of ELF-MFs on post-stroke patients and had well-defined criteria for inclusion and exclusion of participants, were included. The methodological quality of the included studies was assessed using the Quality Assessment Tool for Quantitative Studies (QATQS). A total of 71 studies were identified through database and reference lists' search, from which 9 were included in the final synthesis. All included studies showed a beneficial effect of ELF-MFs on stroke patients, however seven of the included studies were carried by the same research group. Improvements were observed in domains such as oxidative stress, inflammation, ischemic lesion size, functional status, depressive symptoms and cognitive abilities. The available literature suggests a beneficial effect of ELF-MFs on post-stroke patients; however, the current data are too limited to broadly recommend the use of this method. Further research with improved methodological quality is necessary.

Targeting SRSF3 restores immune mRNA translation in microglia/macrophages following cerebral ischemia

We recently described a novel ribosome-based regulatory mechanism/checkpoint that controls innate immune gene translation and microglial activation in non-sterile inflammation orchestrated by RNA binding protein SRSF3. Here we describe a role of SRSF3 in the regulation of microglia/macrophage activation phenotypes after experimental stroke. Using a model-system for analysis of the dynamic translational state of microglial ribosomes we show that 24h after stroke highly upregulated immune mRNAs are not translated resulting in a marked dissociation of mRNA and protein networks in activated microglia/macrophages. Next, microglial activation after stroke was characterized by a robust increase in pSRSF3/SRSF3 expression levels. Targeted knockdown of SRSF3 using intranasal delivery of siRNA 24h after stroke caused a marked knockdown of endogenous protein. Further analyses revealed that treatment with SRSF3-siRNA alleviated translational arrest of selected genes and induced a transient but significant increase in innate immune signaling and IBA1+ immunoreactivity peaking 5days after initial injury. Importantly, delayed SRSF3-mediated increase in immune signaling markedly reduced the size of ischemic lesion measured 7days after stroke. Together, our findings suggest that targeting SRSF3 and immune mRNA translation may open new avenues formolecular/therapeutic reprogramming of innate immune response after ischemic injury.

Diagnostic test accuracy study of a commercially available deep learning algorithm for ischemic lesion detection on brain MRIs in suspected stroke patients from a non-comprehensive stroke center

PurposeTo estimate the ability of a commercially available artificial intelligence (AI) tool to detect acute brain ischemia on Magnetic Resonance Imaging (MRI), compared to an experienced neuroradiologist. MethodsWe retrospectively included 1030 patients with brain MRI, suspected of stroke from January 6th, 2020 to 1st of April 2022, based on these criteria: Age ≥ 18 years, symptoms within four weeks before the scan. The neuroradiologist reinterpreted the MRI scans and subclassified ischemic lesions for reference. We excluded scans with interpretation difficulties due to artifacts or missing sequences. Four MRI scanner models from the same vendor were used. The first 800 patients were included consecutively, remaining enriched for less frequent lesions. The index test was a CE-approved AI tool (Apollo version 2.1.1 by Cerebriu). ResultsThe final analysis cohort comprised 995 patients (mean age 69 years, 53 % female). A case-based analysis for detecting acute ischemic lesions showed a sensitivity of 89 % (95 % CI: 85 %–91 %) and specificity of 90 % (95 % CI: 87 %–92 %). We found no significant difference in sensitivity or specificity based on sex, age, or comorbidities. Specificity was reduced in cases with DWI artifacts. Multivariate analysis showed that increasing ischemic lesion size and fragmented lesions were independently associated with higher sensitivity, while non-acute lesion ages lowered sensitivity. ConclusionsThe AI tool exhibits high sensitivity and specificity in detecting acute ischemic lesions on MRI compared to an experienced neuroradiologist. While sensitivity depends on the ischemic lesions' characteristics, specificity depends on the image quality.

P21.01.A EPIDEMIOLOGY OF ISCHEMIC LESIONS AFTER RESECTION OF LOW-GRADE GLIOMAS

Abstract BACKGROUND Diffuse low-grade gliomas are slow-growing malignant brain tumors that mainly affect people in their 30s and 40s, usually resulting in death within a decade. The standard treatment is surgery, which has a moderate risk of neurological sequelae. Clinical experience indicates that not all sequels are directly related to the resected area but rather caused by collateral damage, such as tissue- and vascular damages at the surgical site, causing ischemic lesions in the surrounding tissue. In this study, the epidemiology of these lesions is investigated, in terms of how common they are and how they are related to the size, type and location of the tumor. MATERIAL AND METHODS One hundred and sixty-six patients who underwent resection for grade II glioma (WHO 2007 or 2016) between 2012 and 2017 at any of nine hospitals in Sweden and Norway and had a postoperative MRI scan including diffusion-weighted imaging within three days after surgery, were included in this study. Lesions were segmented on the b1000 image, using the ADC and T1 image to exclude hyperintense areas caused by other factors than ischemia. Statistical analyses were performed using IBM SPSS Statistics version 27.0 (IBM Corp., Armonk, NY, USA). Analyses were carried out with ischemic lesion size as a continuous variable, and since the volumes were not normally distributed, non-parametric tests were used. RESULTS Ischemic lesions were found in 146 out of 166 (88%) cases, the median volume of the segmented lesions was 1.9 ml, with an interquartile range (IQR) of 0.95-4.5 ml. Patients with new or worsened deficits did have significantly larger ischemic volumes than does who did not (1.7 vs 2.8 ml, p=0.03). Ischemic volume was significantly correlated to both pre- and post-operative tumor volume (Spearmans rho = 0.370 and 0.304, p<0.001). No difference in ischemic volume was found between astrocytoma and oligodendroglioma, based on reported histopathologic diagnosis (p=0.43) or molecular status (p=0.44), neither between main tumor local (frontal (60%) vs temporal (19%), parietal (8%) or insular (12%), p>0.37). CONCLUSION Ischemic lesions after glioma resection are very common, but mostly small and restricted to a region close to the resection cavity. Large ischemic regions were associated with new or worsened neurological deficits and were mostly found in association with large tumors. More fine-tuned measures might be needed to find potential associations between tumor local and ischemic lesions.

#2648 IMPACT OF ACUTE AND CHRONIC KIDNEY FUNCTION ON THE SIZE AND PROGNOSIS OF ISCHEMIC STROKE AFTER THROMBECTOMY

Abstract Background and Aims Patients with Chronic Kidney Disease (CKD) have an increased risk of ischemic and haemorrhagic stroke and CKD seem associated with worse outcome after a stroke. Few studies specifically investigated the impact of mechanical thrombectomy on outcomes after an ischemic stroke. The main objectives of our study RISOTTO were to evaluate the influence of CKD (eGFR < 60 mL/min/1.73m²) and Acute Kidney Injury (AKI) on the size of cerebral ischemic lesions and their outcome. Method Multicenter cohort study. Patients with at the acute phase of ischemic stroke following a large artery occlusion managed with mechanical thrombectomy were included. CKD was defined as eGFR < 60 mL/min/1.73m² for more than 3 months, AKI by 2012 KDIGO score, infarcted volume by ASPECTS and functional prognosis at 3 month by modified Rankin Scale (mRS). Results 296 patients were included. Sixty-three patients (22.8%) had CKD. In univariate analysis, patients with CKD had more white matter vascular lesions (Fazekas 1.7±0.8 vs. 1.0±0.8, p<0.0001), had lower initial infarcted volume (ASPECTS 7.6±1.7 vs. 6.7±1.8, p = 0.003), for equivalent severity (NIHSS: 9.2±7.0 vs. 10.1±7.7, p = 0.404), had more thrombectomy failure (12.7% vs. 3.8%, p = 0.008) compared to non-CKD patients. At 3 months, CKD was associated with equivalent functional prognosis (mRS 3–6: 51.6% vs. 42.2%, p = 0.193) but higher mortality: 24.2% vs. 9.5%, p = 0.004. Forty-eight patients (19.6%) developed an AKI. AKI was associated with increased initial gravity (NIHSS 18.8±5.2 vs. 16.7±5.7, p = 0.014, equivalent stroke volume (ASPECTS 7.3±1.9 vs. 6.8±1.8, p = 0.254. At 3 months, CKD was associated with poorer functional prognosis (mRS 3–6: 64.6% vs. 39.4%, p = 0,002) and mortality: 25.0% vs. 8.4%, p = 0.003. In multivariate analysis, AKI appeared as a independent risk factor of poor neurological outcome (OR 2.16 [1.05-4.46], p = 0,036 and mortality: OR 2.47 [0.96-6.35], p = 0.059 at 3 month, as CKD was not. Conclusion CKD was associated with smaller initial ischemic lesions for equivalent neurological severity, and more recanalization failures. CKD was not an independent risk factor for mortality or poor functional prognosis at 3 months. CKD patients seem to benefit from thrombectomy and should not be contraindicated to this technique. AKI is associated with greater initial neurological severity, poorer functional prognosis and increased mortality at 3 months and is an independent risk factor for poor prognosis.

Carbon dioxide flooding to reduce postoperative neurological injury following surgery for acute type A aortic dissection: a prospective, randomised, blinded, controlled clinical trial, CARTA study protocol - objectives and design

IntroductionNeurological complications after surgery for acute type A aortic dissection (ATAAD) increase patient morbidity and mortality. Carbon dioxide flooding is commonly used in open-heart surgery to reduce the risk of...

The impact of anesthetic drugs on hemodynamic parameters and neurological outcomes following temporal middle cerebral artery occlusion in rats.

The induction of ischemic stroke in the experimental model requires general anesthesia. One of the factors that can be effective in the size of ischemic brain lesions and neurological outcomes is the type of anesthesia. So, the current study was designed to compare the impacts of the most important and widely used anesthetics including halothane, isoflurane, and chloral hydrate on the transient middle cerebral artery occlusion (MCAO) outcomes. Adult Male Sprague-Dawley rats were randomly divided into three groups as follows: (1) MCAO + halothane group, (2) MCAO + isoflurane group, and (3) MCAO + chloral hydrate group. After 24 h, the mortality rate, infarct size, tissue swelling, neurological function, hemodynamic, and arterial blood gas parameters were assessed. Our finding showed that 60 min MCAO rats anesthetized with chloral hydrate significantly increased mortality rate, infarct size, tissue swelling, and neurological deficits compared with halothane and isoflurane anesthetics after 24 h of MCAO. Also, chloral hydrate caused a significant decrease in mean arterial pressure and arterial pO2 compared to halothane and isoflurane anesthetics. On the basis of the current data, we concluded that chloral hydrate increased cerebral infarct volume and neurological outcomes and reduced hemodynamic and metabolic parameters compared with halothane and isoflurane-anesthetized rats temporal MCAO.

Regional Anesthesia for Carotid Endarterectomy in Patients with Acute Ischemic Stroke (Pilot Study)

Objective. The aim of this study is to assess the safety of the use of regional anesthesia for performing carotid endarterectomy (CEA) in patients in the acute phase of ischemic stroke.Material and methods. The study included 66 patients in the acute phase of ischemic stroke (atherothrom-botic subtype according to the TOAST classification) who underwent carotid endarterectomy. The inclusion criteria for the study were as follows: acute phase of atherothrombotic ischemic stroke (first 28 days), ipsilateral symptomatic ≥ 50% stenosis of the internal carotid artery, 1-4 points neurological deficit according to the modified Rankin Scale (mRS), 1-13 points neurological deficit according to the National Institutes of Health Stroke Scale (NIHSS), size of the cerebral ischemic lesion ≤ 4 cm. This single-center prospective cohort study compared two anesthetic approaches, regional anesthesia (RA, 46 patients) and general anesthesia (GA, 20 patients). The RA techniques included ultrasound-guided superficial and deep cervical plexus blocks on the side of the surgery.Results. The study found no significant differences in the baseline patient characteristics, surgery techniques and clinical outcomes between the groups. There were no neurological or cardiovascular toxic reactions to the local anesthetics. Conversions from RA to GA were not performed. In the RA group, recurrent ipsilateral ischemic strokes, myocardial infarctions, wound hemorrhagic complications and lethal outcomes did not occur.Conclusion. This pilot study has demonstrated the safety of RA for performing CEA in patients in the acute phase of ischemic stroke. RA provides adequate neuromonitoring and timely intraoperative recognition of «new» ischemic complications. To compare the efficacy of RA and GA for performing CEA in patients with acute ischemic stroke, large randomized controlled trials are needed.

The association between the serum vitamin D levels and the stroke lesion size, functional ability, and cognition in elderly Korean ischemic stroke patients

The purpose of this study was to confirm the association between the serum vitamin D levels and ischemic stroke lesion size, functional ability, and cognitive function in elderly ischemic stroke patients. This study included Korean ischemic stroke patients aged 65 to 85 years. The size of the lesion was measured in brain images taken within 24 hours of hospitalization. The level of 25-(OH) Vitamin D (ng/mL), a metabolite of vitamin D, in the serum collected within 48 hours of hospitalization, and the modified Barthel index (MBI), gait performance, the muscle power of hip and knee extensors on the hemiplegic side, and mini-mental status examination (MMSE) were recorded within 1 week of the onset of the disease. Each factor was compared through correlation analysis, and the significance was confirmed using the Spearman correlation coefficient method. The association between the serum vitamin D levels and the size of the ischemic stroke lesion, the MBI, gait performance, the muscle power of hip and knee extensors on the hemiplegic side, and the MMSE were analyzed. It was confirmed that there was a significant correlation between all the factors (P < .005). In patients with serum vitamin D levels of ≥ 30 ng/mL, both the functional ability and cognitive functions were better than in patients lower than 30 ng/mL. We confirmed the lower the level of serum vitamin D levels, the larger the size of the ischemic stroke lesion when it occurred in elderly Koreans. And we confirmed that serum vitamin D levels affected the functional ability and cognitive function. And we recommend that elderly Koreans should maintain their blood vitamin D level above 30 ng/mL. We believe that this will help preserve the functional ability and cognitive function when ischemic stroke occurred.

Tenascin-C restricts reactive astrogliosis in the ischemic brain

Cellular responses in glia play a key role in regulating brain remodeling post-stroke. However, excessive glial reactivity impedes post-ischemic neuroplasticity and hampers neurological recovery. While damage-associated molecular patterns and activated microglia were shown to induce astrogliosis, the molecules that restrain astrogliosis are largely unknown. We explored the role of tenascin-C (TnC), an extracellular matrix component involved in wound healing and remodeling of injured tissues, in mice exposed to ischemic stroke induced by transient intraluminal middle cerebral artery occlusion. In the healthy adult brain, TnC expression is restricted to neurogenic stem cell niches. We previously reported that TnC is upregulated in ischemic brain lesions. We herein show that the de novo expression of TnC post-stroke is closely associated with reactive astrocytes, and that astrocyte reactivity at 14 days post-ischemia is increased in TnC-deficient mice (TnC−/−). By analyzing the three-dimensional morphology of astrocytes in previously ischemic brain tissue, we revealed that TnC−/− reduces astrocytic territorial volume, branching point number, and branch length, which are presumably hallmarks of the homeostatic regulatory astrocyte state, in the post-acute stroke phase after 42 days. Interestingly, TnC−/− moderately increased aggrecan, a neuroplasticity-inhibiting proteoglycan, in the ischemic brain tissue at 42 days post-ischemia. In vitro in astrocyte-microglia cocultures, we showed that TnC−/− reduces the microglial migration speed on astrocytes and elevates intercellular adhesion molecule 1 (ICAM1) expression. Post-stroke, TnC−/− did not alter the ischemic lesion size or neurological recovery, however microglia-associated ICAM1 was upregulated in TnC−/− mice during the first week post stroke. Our data suggest that TnC plays a central role in restraining post-ischemic astrogliosis and regulating astrocyte-microglial interactions.

Early Brain Volume Changes After Stroke: Subgroup Analysis From the AXIS-2 Trial.

Background and PurposeThe evolution of total brain volume early after stroke is not well understood. We investigated the associations between age and imaging features and brain volume change in the first month after stroke.MethodsWe retrospectively studied patients with acute ischemic stroke enrolled in the AXIS-2 trial. Total brain volume change from hyperacute MRI data to the first month after stroke was assessed using unified segmentation in SPM12. We hypothesized that age, ischemic brain lesion size, and white matter (WM) changes were associated with larger brain volume change. Enlarged perivascular spaces (EPVSs) and white matter hyperintensities (WMHs) were rated visually and the presence of lacunes was assessed.ResultsWe enrolled 173 patients with a mean age of 67 ± 11 years, 44% were women. There was a median 6 ml decrease in volume (25th percentile −1 ml to 75th percentile 21 ml) over time, equivalent to a median 0.5% (interquartile range [IQR], −0.07%−1.4%), decrease in brain volume. Age was associated with larger brain volume loss (per 10 years of age, 5 ml 95% CI 2–8 ml). Baseline diffusion weighted imaging (DWI) lesion volume was not associated with greater volume loss per 10 ml of lesion volume, change by 0 ml (95% CI −0.1 to 0.1 ml). Increasing Fazekas scores of deep WMH were associated with greater tissue loss (5 ml, 95% CI 1–10 ml).ConclusionsTotal brain volume changes in a heterogenous fashion after stroke. Volume loss occurs over 1 month after stroke and is associated with age and deep WM disease. We did not find evidence that more severe strokes lead to increased early tissue loss.

Effect of nicorandil on the spatial arrangement of primary motor cortical neurons in the sub-acute phase of stroke in a rat model

IntroductionIschemic stroke remains a major cause of disability and death worldwide. The density and the spatial distribution of the primary motor (M1) cortical neurons are important in signal transmission and control the movement-related functions. Recently, the neuroprotective effect of nicorandil in cerebral ischemia was described through its anti-apoptosis, antioxidant and anti-inflammatory properties. This study aimed to determine the effects of nicorandil on the neurobehavioral outcome, infarct size, and density, and spatial distribution of M1 cortical neurons after cerebral ischemia. MethodsThirty Sprague-Dawley rats were randomly divided into three groups. Sham underwent surgery without middle cerebral artery occlusion (MCAO) and drug. The MCAO and treatment groups after MCAO received saline or nicorandil 2, 24, 48, and 72 h after the induction of brain ischemia. Neurobehavioral tests were performed, brains removed, sectioned, and stained by 2,3,5-triphenyltetrazolium chloride (TTC) to estimate the size of the infarction and Nissl staining to evaluate the numerical density, mean area, and the distribution pattern of M1 cortical neurons, using Voronoi spatial tessellation. ResultsAlthough nicorandil treatment significantly decreased the neurological deficits and density of neuronal neighbors, it could not preserve the normal regular spatial distributions of M1 cortical neurons after MCAO. It also could not significantly improve motor function or reduce ischemic lesion size. ConclusionsTreatment using the present dose of nicorandil during sub-acute ischemic stroke could not increase neuronal density or preserve the normal regular spatial distributions after MCAO. However, it had beneficial effects on neurobehavioral and motor function and somewhat reduced ischemic lesion size.

PI3KC2β inactivation stabilizes VE-cadherin junctions and preserves vascular integrity.

Endothelium protection is critical, because of the impact of vascular leakage and edema on pathological conditions such as brain ischemia. Whereas deficiency of class II phosphoinositide 3-kinase alpha (PI3KC2α) results in an increase in vascular permeability, we uncover a crucial role of the beta isoform (PI3KC2β) in the loss of endothelial barrier integrity following injury. Here, we studied the role of PI3KC2β in endothelial permeability and endosomal trafficking in vitro and in vivo in ischemic stroke. Mice with inactive PI3KC2β showed protection against vascular permeability, edema, cerebral infarction, and deleterious inflammatory response. Loss of PI3KC2β in human cerebral microvascular endothelial cells stabilized homotypic cell-cell junctions by increasing Rab11-dependent VE-cadherin recycling. These results identify PI3KC2β as a potential new therapeutic target to prevent aggravating lesions following ischemic stroke.

Abstract P370: Early Brain Volume Change After Stroke: Subgroup Analysis From the Axis-2 Trial

Objective: The timing of brain atrophy after stroke is not well understood. We investigated the associations between age and imaging features and brain volume change in the first month after stroke. Methods: We retrospectively studied patients with acute ischemic stroke enrolled in the AXIS-2 trial. Total brain volume change from hyperacute MRI data to the first month after stroke was assessed using unified segmentation in SPM12. We hypothesized that age, ischemic brain lesion size and white matter changes were associated with larger brain volume change. Enlarged perivascular spaces (EPVS) and white matter hyperintensities (WMH) were rated visually and the presence of lacunes was assessed. Results: We enrolled 173 patients with a mean age of 67±11 years, 44 % were female. There was a median 6 mL decrease in volume (25th percentile -1mL-75th percentile 21mL) over time, equivalent to a median 0.5% (IQR-0.07% - 1.4%), decrease in brain volume. Age was associated with larger brain volume loss (per 10 years of age, 5 mL 95% CI 2 mL-8 mL). Baseline DWI lesion volume was not associated with greater volume loss (per 10 mL of lesion volume, change by 0 mL (95% CI -0.1 mL-0.1mL). Increasing Fazekas scores of deep white matter hyperintensity were associated with greater tissue loss (5 mL, 95% CI 1 mL-10 mL). Brain volume change was associated with ordinal change on the modified Rankin scale at 90 days (per 10 ml, OR 1.085, 95% CI 1.031-1.141) but the association was not present when adjusting for age, baseline diffusion lesion volume and NIHSS score (OR 1.044, 95% CI 0.990-1.010).Interpretation-Global brain volume loss occurs over 1 month after stroke and is associated with age and deep white matter disease. We did not find evidence that more severe strokes lead to increased early tissue loss.

Unfavorable Changes of Platelet Reactivity on Clopidogrel Therapy Assessed by Impedance Aggregometry Affect a Larger Volume of Acute Ischemic Lesions in Stroke.

Background: High on-treatment platelet reactivity or its equivalent—resistance to the antiplatelet agent—significantly reduces the efficacy of the therapy, contributing to a negative impact on stroke course. Previous studies demonstrated that aspirin resistance is associated with a larger size of acute ischemic infarct. Due to the increasing use of clopidogrel in the secondary prevention of stroke, we aimed to assess the impact of clopidogrel resistance on the size and extent of ischemic lesions, both acute and chronic. Methods: This prospective, single-center and observational study involved 74 ischemic stroke subjects, treated with 75 mg of clopidogrel. We used impedance aggregometry to determine platelet reactivity 6–12 h after a dose of clopidogrel as a first assessment and 48 h later as the second measurement. A favorable dynamics of platelet reactivity over time was the decrease in the minimum value equal to the median in the entire study. The volume of acute ischemic infarct was estimated within 48 h after onset in diffusion-weighted imaging and fluid-attenuated inversion recovery sequences of magnetic resonance and the severity of chronic vascular lesions by Fazekas scale. Results: Subjects with mild severity of chronic vascular lesions (Fazekas 1) exhibited a significant decrease of platelet reactivity over time (p = 0.035). Dynamics of platelet reactivity over time differed between subjects with large, moderate, mild and insignificant size of acute ischemic lesion (Kruskall-Wallis H = 3.2576; p = 0.048). In multivariate regression models, we reported unfavorable dynamics of platelet reactivity alone and combined with a high initial value of platelet reactivity as independent predictors of higher risk of a significant ischemic infarct volume (OR 7.16 95%CI 1.69–30.31, p = 0.008 and 26.49 95%CI 1.88–372.4, p = 0.015, respectively). Conclusions: We emphasized that unfavorable dynamics of platelet reactivity over time during clopidogrel therapy in acute phase of stroke affect the volume of acute infarct and the severity of chronic vascular lesions.

D-dimer Level is Correlated with Prognosis, Infarct Size, and NIHSS in Acute Ischemic Stroke Patients.

Stroke ranks the fourth leading disease causing adult mortality and disability. D-dimer (D-D) is the ultimate product of plasmin-mediated degradation of fibrin-rich thrombi. D-D is a simple readily accessible biomarker employed within the diagnostic algorithms for the exclusion of venous thromboembolism. The correlation between D-D infarct size in MRI brain, APACHE II score, and the National Institute of Health Stroke Scale (NIHSS) score in critically ill acute stroke patients has not been fully investigated before.ObjectiveWe aimed to investigate the diagnostic and prognostic value of elevated plasma D-D in critically ill patients admitted with acute cerebrovascular accidents. As far as we know, we are the first to investigate the correlation between plasma D-D levels and the ischemic lesion size in MRI brain and also APACHE II score and NIHSS in critically ill acute ischemic cerebrovascular patients.Setting and participantsA prospective, observational cohort study inside the Critical Care Medicine Department. Thirty patients with AIS were enrolled additionally to 1 healthy age- and sex-matched controls.InterventionsWe employed particle-enhanced, immunoturbidimetric assay to detect plasma D-D concentrations. D-D levels D0 and D1 were measured upon admission and 24 hours later, respectively. We reviewed the patient' s health records; additionally, demographic, clinical, laboratory, and neuroimaging information was abstracted.ResultsD-D concentrations were significantly higher in acute stroke patients compared to healthy controls. ROC curve analysis showed that elevated D-D level more than 310 ng/mL can predict infarct lesion size >1.5 cm in diffusion-weighted MRI brain with sensitivity and specificity (100 and 83%, respectively) and also admission D-D (D0) at cutoff concentration 350 ng/mL and D1 at cutoff value 370 ng/mL are predictors of complicated course with sensitivity and specificity (100 and 84.6%, respectively). There was no significant difference between D0 and D1 D-D levels (p-value >0.05).ConclusionThe plasma D-D biomarker can be a simple readily available test reliable predictor of infarct lesion size >1.5 cm in DW-MRI and outcome in union with the common practice instrumental tests.How to cite this articleAbbas NI, Sayed O, Samir S, Abeed N. D-dimer Level is Correlated with Prognosis, Infarct Size, and NIHSS in Acute Ischemic Stroke Patients. Indian J Crit Care Med 2021;25(2):193–198.

The correlation between the cardiovascular instability and the size of the developed ischaemic lesions in patients who underwent carotid stenting.

In this study we investigated the relationship between cardiovascular instability and the size of the developed ischaemic lesions during carotid stent implantation by diffusion-weighted (DWI) magnetic resonance (MR) examination. We retrospectively analyzed anaesthesia reports and follow-up MR examinations after stent implantation of 192 patients in a 3-year period. Nineteen aspects of cardiovascular status were analyzed. We registered the duration of the intervention, low and high blood pressure (BP) values during anaesthesia and heart rates. The fluctuations of BP and heart rate and the time of their compensations after the stent expansion were also recorded. Values were compared with the number and the size of ischaemic lesions on DWI scans. We used Spearman and Kendall rank correlations and Welch's tests for statistical analysis. Values of p ≤ 0.05 were considered as statistically significant. Decreased heart rate significantly correlated with the number (p = 0.0123) and size (p = 0.00323) of ischaemic lesions during stent expansion. Other cardiovascular parameters did not show any significant correlations. Our results indicate that only heart rate attenuation affects the size of ischaemic lesions; thus the prevention of bradycardia is highly important.

Diagnostic benefit of high b-value computed diffusion-weighted imaging in acute brainstem infarction

Background and purposeDiffusion-weighted imaging (DWI) is a cornerstone in diagnostic of ischemic stroke. The aim of this study was to investigate the usefulness of high-b-value computed DWI (c-DWI) in comparison to standard DWI in patients with acute brainstem infarction. Materials and methods56 patients with acute brainstem infarction were retrospectively analysed by two readers. DWI was obtained with the b-values 0, 500 and 1000 s/mm² on either a 1.5 or 3 T magnetic resonance imaging (MRI) scanner. c-DWI was calculated with a monoexponential model with high b-values 2000, 3000, 4000 and 5000 s/mm². All c-DWI series with high-b-values were compared to the standard DWI sequence at b-value of 1000 s/mm² in terms of image artifacts, lesion extent and contrast. ResultsThere was no statistically significant difference between 1.5 and 3 T MRI regarding the measured ischemic lesion size. There were no statistically significant differences between the ischemic lesion sizes on DWI at b-values of 1000 s/mm² and on c-DWI at higher b-values. Overall, the contrast between the lesion and the surrounding normal areas improved with increasing b-value on the isotropic DWIs: maximum at b = 5000, followed by that at b 2000 and b 1000 s/mm², in order. The best relation between artifacts and lesion contrast was identified for b 2000 s/mm². ConclusionHigh b-value DWI derived from c-DWI has a higher visibility for ischemic brainstem lesions compared to standard DWI without additional time cost. The b-2000 image is recommended to use in clinical routine, higher b-value images lead to more imaging artifacts, which might result in misdiagnosis.

Vascular PDGFR-alpha protects against BBB dysfunction after stroke in mice.

Blood-brain barrier (BBB) dysfunction underlies the pathogenesis of many neurological diseases. Platelet-derived growth factor receptor-alpha (PDGFRα) induces hemorrhagic transformation (HT) downstream of tissue plasminogen activator in thrombolytic therapy of acute stroke. Thus, PDGFs are attractive therapeutic targets for BBB dysfunction. In the present study, we examined the role of PDGF signaling in the process of tissue remodeling after middle cerebral arterial occlusion (MCAO) in mice. Firstly, we found that imatinib increased lesion size after permanent MCAO in wild-type mice. Moreover, imatinib-induced HT only when administrated in the subacute phase of MCAO, but not in the acute phase. Secondly, we generated genetically mutated mice (C-KO mice) that showed decreased expression of perivascular PDGFRα. Additionally, transient MCAO experiments were performed in these mice. We found that the ischemic lesion size was not affected; however, the recruitment of PDGFRα/type I collagen-expressing perivascular cells was significantly downregulated, and HT and IgG leakage was augmented only in the subacute phase of stroke in C-KO mice. In both experiments, we found that the expression of tight junction proteins and PDGFRβ-expressing pericyte coverage was not significantly affected in imatinib-treated mice and in C-KO mice. The specific implication of PDGFRα signaling was suggestive of protective effects against BBB dysfunction during the subacute phase of stroke. Vascular TGF-β1 expression was downregulated in both imatinib-treated and C-KO mice, along with sustained levels of MMP9. Therefore, PDGFRα effects may be mediated by TGF-β1 which exerts potent protective effects in the BBB.

Casper vs. Closed-Cell Stent : Carotid Artery Stenting Randomized Trial.

The aim of this trial was to compare the efficacy of closed-cell stents with Casper stents during carotid angioplasty stenting (CAS). This was arandomized superiority trial in which 88patients were enrolled. The primary end points were the incidence, number, and size of new ischemic brain lesions after CAS under distal embolic protection devices (EPD). The secondary end points included stroke, transient ischemic attack (TIA) and myocardial infarction (MI). Ischemic brain lesions were assessed by adiffusion-weighted magnetic resonance image (DW-MRI). Neurological outcomes were evaluated by means of the National Institutes of Health scale score (NIHSS) and the modified Rankin scale (mRS). Compared with closed-cell stents (n = 47), Casper stents (n = 41), resulted in no significant reduction in the incidence (44.7% versus 39%, P = 0.592), number (1.3 ± 1.8 versus 0.9 ± 1.5, p = 0.444), and size (3.9 ± 5.8 mm versus 2.8 ± 4.1 mm, p = 0.353) of new ischemic brain lesions. The global rate of stroke/TIA/MI was (2/88, 2.3%). Two TIA occurred during the hospitalization period, one in each group (1/41, 2.4% vs 1/47, 2.1%). One patient of the Casper group had an asymptomatic in-stent thrombosis. One patient of the control group had aMI (1/47, 2.1%) after discharge. The Casper stents did not show superiority in the rate of incidence, number and size of new silent ischemic brain lesions detect by DW-MRI when compared to close cell stents during CAS under distal EPD.