Prevalence and Predictors of Cerebral Microangiopathy Determined by Pulsatility Index in an Asymptomatic Population From the ILERVAS Project

Background: Little is known about the prevalence of cerebral microangiopathy (CM), which is related to cognitive impairment, in an asymptomatic population. Pulsatility index (PI) is an easily measurable parameter of cerebral vascular resistance in transcranial duplex of the middle cerebral artery (MCA) study. We aimed to determine the prevalence of CM measured by PI of MCA in low to moderate vascular risk subjects. Methods: We included 3,721 subjects between 45 and 70 years without previous history of vascular disease or diabetes mellitus and with at least one other vascular risk factor from the cross-sectional study ILERVAS (Lleida, Spain). Patients underwent transcranial duplex to determine MCA-PI. Possible CM was defined by MCA-PI >1.1. Carotid and femoral arteries ultrasound registration was done to determine the presence, the number, and the area of atheromatous plaques. Body mass index (BMI), pulse pressure (PP) and laboratory data were also recorded. Results: 439 (11.8%) subjects were excluded due to the low quality of transcranial duplex images. Median age was 57 [IQR 52, 62] years. Possible CM was found in 424 (12.9%) subjects. CM patients had higher prevalence of plaques than non-CM (77.4 vs. 66.4%, p < 0.001). PI showed a positive linear correlation with the number of territories with plaques (r = 0.130, p < 0.001), and the total plaque area (r = 0.082, p < 0.001). The predictors of possible CM were the age, male gender, and PP. Conclusions: In low-to-moderate vascular risk asymptomatic population, the proportion of abnormal brain microvascular bed determined by MCA-PI is not negligible. The planned 10-year follow-up will describe the clinical relevance of these findings.This work was supported by grants from the Diputacio de Lleida, Instituto de Salud Carlos III (RETIC RD16/0009/0011) and Ministerio de Ciencia, Inovación y Universidades (IJC2018-037792-I). FP was supported by the Catalan Autonomous Government’s Agència de Gestió d’Ajuts Universitaris i de Recerca (2017 suport a les activitats dels grups de recerca 1628). RP was supported by the Spanish Ministry of Science, Innovation, and Universities (grant RTI2018-099200-B-I00), and the Generalitat of Catalonia: Agency for Management of University and Research Grants (2017SGR696). This study was co-financed by FEDER funds from the European Union (A way to build Europe). IRBLleida is a CERCA Programme/Generalitat of Catalonia

Inflammatory Response of Ischemic Tolerance in Circulating Plasma : Preconditioning-Induced by Transient Ischemic Attack (TIA) Phenomena in Acute Ischemia Patients (AIS)

Ischemic tolerance (IT) refers to a state where cells are resistant to the damaging effects caused by periods of ischemia. In a clinical scenario, the IT phenomenon would be activated by a recent transient ischemic attack (TIA) before an ischemic stroke (IS). The characterization of inflammatory protein expression patterns will contribute to improved understanding of IT. A total of 477 IS patients from nine hospitals, recruited between January 2011 and January 2016, were included in the current study and divided in three groups: 438 (91.9%) patients without previous TIA (group 1), 22 (4.6%) patients who suffered TIA 24 h before IS (group 2), and 17 (3.5%) patients who suffered TIA between 24 h and 7 days prior to IS (group 3). An inflammatory biomarker panel (IL-6, NT-proBNP, hsCRP, hs-Troponin, NSE, and S-100b) on plasma and a cytokine antibody array was performed to achieve the preconditioning signature potentially induced by TIA phenomena. Primary outcome was modified rankin scale (mRs) score at 90 days. Recent previous TIA was associated with better clinical outcome at 90 days (median mRS of group 1: 2.0 [1.0-4.0]; group 2: 2.0 [0.0-3.0]; group 3: 1.0 [0-2.5]; p = 0.086) and smaller brain lesion (group 1: 3.7 [0.7-18.3]; group 2: 0.8 [0.3-8.9]; group 3: 0.6 [0.1-5.5] mL; p = 0.006). All inflammation biomarkers were down regulated in the groups of recent TIA prior to IS compared to those who did not suffer a TIA events. Moreover, a cytokine antibody array revealed 30 differentially expressed proteins between the three groups. Among them, HRG1-alpha (Fold change 74.4 between group 1 and 2; 74.2 between group 1 and 3) and MAC-1 (Fold change 0.05 between group 1 and 2; 0.06 between group 1 and 3) expression levels would better stratify patients with TIA 7 days before IS. These two proteins showed an earlier inflammation profile that was not detectable by the biomarker panel. Inflammatory pathways were activated by transient ischemic attack, however the period of time between this event and a further ischemic stroke could be determined by a protein signature that would contribute to define the role of ischemic tolerance induced by TIA

Erratum to: 36th International Symposium on Intensive Care and Emergency Medicine

[This corrects the article DOI: 10.1186/s13054-016-1208-6.]

Evidence for the decay BS0→K‾∗0μ+μ− {B}_S^0\to {\overline{K}}^{\ast 0}{\mu}^{+}{\mu}^{-}

International audienceA search for the decay ${B}_S^0\to {\overline{K}}^{\ast 0}{\mu}^{+}{\mu}^{-}$ is presented using data sets corresponding to 1.0, 2.0 and 1.6 fb$^{−1}$ of integrated luminosity collected during pp collisions with the LHCb experiment at centre-of-mass energies of 7, 8 and 13 TeV, respectively. An excess is found over the background-only hypothesis with a significance of 3.4 standard deviations. The branching fraction of the ${B}_S^0\to {\overline{K}}^{\ast 0}{\mu}^{+}{\mu}^{-}$ decay is determined to be $\mathrm{\mathcal{B}}\left({B}_s^0\to {\overline{K}}^{\ast 0}{\mu}^{+}{\mu}^{-}\right)=\left[2.9\pm 1.0\left(\mathrm{stat}\right)\pm 0.2\left(\mathrm{syst}\right)\pm 0.3\left(\mathrm{norm}\right)\right]\times {10}^{-8}$ , where the first and second uncertainties are statistical and systematic, respectively. The third uncertainty is due to limited knowledge of external parameters used to normalise the branching fraction measurement

Lipidomic signature of stroke recurrence after transient ischemic attack

Abstract Objective To find new biomarkers of early stroke recurrence (SR) by using lipidomic strategies on patients who suffered a transient ischemic attack. Methods Untargeted lipidomic analysis was performed in plasma samples of 460 consecutive TIA patients. Recruited &lt; 24 hours after the onset of symptoms. Results SR at 90 days follow-up was showed by 37 (8%) patients. In Cox proportional hazards models previous ischemic stroke (95%CI, 1.07–5.75), motor weakness (95%CI, 1.14–4.98), large-artery atherosclerosis (95%CI, 1.20–5.23) and female sex (95%CI, 1.31–5.46) were predictors of SR. Lipidomic profiling disclosed specific SR biomarkers: 7 lipid species differentially expressed between groups. Interestingly, 6 of these 7 lipid species belonged to the glycerolipid family and the other one is a plasmalogen, pointing to bioenergetics pathways, as well as oxidative stress response. Indeed, the detected lipid set express a condition of impaired response to energy supply and stress in SR patients compared to TIA non-SR patients. In this context, it is proposed the PE(P-18:0/18:2) as potential biomarker of SR condition. Conclusion the lipidomic profiles of TIA subjects with non-SR and SR were different, with minor but significant changes. The observed changes in lipid patternssuggest pathophysiological mechanisms associated with the different formation of lipid droplets that is translated to plasma level as consequence of a more intensive or high-risk ischemic condition related to early SR.</jats:p

Lipidomic signature of stroke recurrence after transient ischemic attack

Abstract While TIA patients have transient symptoms, they should not be underestimated, as they could have an underlying pathology that may lead to a subsequent stroke: stroke recurrence (SR). Previously, it has been described the involvement of lipids in different vascular diseases. The aim of the current study was to perform a lipidomic analysis to identify differences in the lipidomic profile between patients with SR and patients without. Untargeted lipidomic analysis was performed in plasma samples of 460 consecutive TIA patients recruited < 24 h after the onset of symptoms. 37 (8%) patients suffered SR at 90 days. Lipidomic profiling disclosed 7 lipid species differentially expressed between groups: 5 triacylglycerides (TG), 1 diacylglyceride (DG), and 1 alkenyl-PE (plasmalogen) [specifically, TG(56:1), TG(63:0), TG(58:2), TG(50:5), TG(53:7, DG(38:5)) and PE(P-18:0/18:2)]. 6 of these 7 lipid species belonged to the glycerolipid family and a plasmalogen, pointing to bioenergetics pathways, as well as oxidative stress response. In this context, it was proposed the PE(P-18:0/18:2) as potential biomarker of SR condition. The observed changes in lipid patterns suggest pathophysiological mechanisms associated with lipid droplets metabolism and antioxidant protection that is translated to plasma level as consequence of a more intensive or high-risk ischemic condition related to SR