No abstract

Background: Inhospital stroke (IHS) is defined as an acute ischemic infarction that occurs during hospitalization in a patient originally admitted for another diagnosis or procedure. Approximately 4 to 17 percent of all adult strokes are IHS, and most IHS occurs in cardiologic and cardiosurgical patients after catheterization or surgery. Time to brain imaging is longer in IHS vs community onset strokes (COS) due to delayed symptom recognition, and consequently, IHS patients have greater disability and increased mortality comparted to their COS counterparts. Purpose: The purpose of this project was to educate cardiac nurses to more rapidly and accurately recognize symptoms of acute ischemic stroke. We hypothesized that this education would shorten evaluation time for inpatient strokes and result in faster activation of the Code Stroke team. Methods: Two 4-hour “Heart to Brain Connection” seminars were offered. Course objectives targeted development of critical thinking regarding the relationship of cardiovascular and cerebrovascular disease. Content included cardiac and cerebral anatomy, recognition of ischemic stroke syndromes and NIH Stroke Scale review. All cardiac nurses completed NIH Stroke Scale Certification. Nurses were empowered to call a “Code Stroke” and educated on appropriate criteria. NIH Stroke Scale pocket cards and pencils with the code stroke number were distributed through the cardiac units. Results: We compared the median time from stroke symptom recognition to activation of “Code Stroke” before and after our interventions. Prior to the interventions, in 2014, the median time was 20 minutes; however, this time was decreased to 6.5 minutes in 2016 following our interventions. Further, in 2014, only 36 percent of “Code Strokes” were called by nurses. Following the interventions, “Code Strokes” were called by cardiac nurses in 75 percent of cases in 2016. Conclusions: Empowering cardiac nurses to call a “Code Stroke“ through targeted education and training increases the number of “Code Strokes” called by nurses and decreases the time from recognition to activation of the Code Stroke team thereby optimizing the patient’s potential outcome.

IntroductionPeripheral neutrophil (PMN) count is elevated within the first few hours of acute ischemic stroke (AIS), and neutrophilia is associated with greater AIS severity, larger infarct volume, and poor functional outcome. In animal models, PMN inhibition results in decreased infarct volume and improved functional outcome; however, this strategy has not been successfully translated in clinical trials. We hypothesize that PMNs are a heterogeneous population, consisting of both “beneficial” and “detrimental” subtypes, depending on their functional protein expression, and one PMN protein, arginase 1 (ARG1), may be a key contributor to detrimental PMN function post‐AIS. We have previously described a distinct temporal pattern of PMN expression following AIS between favorable and poor outcome AIS patients. Thus, the purpose of this study was to expand upon this examine the function relationship between ARG1, as well as other PMN proteins, and outcome following AIS.HypothesisWe hypothesized that PMNs isolated from AIS patients with poor outcome will have higher ARG1 expression compared to neutrophils in the favorable outcome group. Further, we hypothesize that PMNs isolated from AIS patients with poor outcome will have a distinct functional proteome, giving rise to altered or more aggressive function that leads to a poor outcome following AIS.MethodsWe quantified PMN ARG1 expression in a subset of 24 AIS patients – n=12 favorable and n=12 poor outcome. PMN ARG1 protein expression was determined by flow cytometry by co‐staining for the surface marker for PMNs, CD66b, and intracellular ARG1. Further, in a subset of these patients – n=3 favorable and n=3 poor outcome, we performed a proteomic analysis on isolated PMNs.ResultsARG1 protein expression was significantly higher in PMNs isolated from AIS patients with a poor outcome (mean ARG1 = 665 + 117) compared to AIS patients with a favorable outcome (mean ARG1 = 453+108) (p=0.008). Further, in the samples sent for proteomics, we observed several differences in the PMN proteome between the AIS outcome groups. Specifically, the PMN proteins ‐ ARG1, defensins 1 and 4, and protein s100a9 – were increased in the poor outcome compared to the favorable outcome group.ConclusionIn conclusion, targeting specific PMN proteins, such as ARG1, rather inhibiting PMNs as a whole, may represent a more targeted and successful approach to modulating PMNs post‐AIS to improve outcome.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

BACKGROUNDDifferential diagnosis of transient ischemic attack (TIA) versus acute ischemic stroke (AIS) is difficult, and neuroimaging with magnetic resonance imaging (MRI) is the only definitive method to confirm AIS. In a typical stoke page imaging protocol, patients initially receive a non‐contrast computed tomography (CT) scan to potentially confirm the presence of infarct, but more importantly, to rule out intracranial hemorrhage in order to administer tissue plasminogen activator (tPA). While this CT is rapid and appropriate for tPA decision‐making, approximately 60–70 percent of AIS cases, later confirmed with MRI, are initially CT‐negative. Further, it is even more difficult to differentiate mild AIS (National Institute of Health Stroke Scale < 5) from TIA, and the decision whether to treat mild AIS with tPA is currently controversial, making this differential diagnosis even more critical. Thus, the objective of this study was to determine if neutrophil count could assist in the accurate differential diagnosis of TIA versus mild AIS.METHODSWe performed a retrospective chart review of a random sample of 100 patients discharged from a local hospital with a discharge diagnosis of TIA. From the initial sample of 100 patients, 54 met inclusion criteria for this study. In addition, we matched a sample of 54 mild AIS patients and 54 control subjects for comparison. An independent samples T test was used to detect mean differences in neutrophil count, and logistic regression to determine the odds ratios for differential diagnosis.RESULTSUpon admission, neutrophil count is significantly higher in mild AIS (6.52 ±0.34 × 103 cells/uL) compared to TIA (5.35 ±0.26 × 103 cells/uL) (p =.042). Further, at a specificity of 82 percent, mild AIS patients are 3.1 times more likely to have a neutrophil count >6.52 compared to TIA (p=.021).CONCLUSIONSNeutrophil count is a simple, easy to interpret biomarker that can differentiate stroke from TIA with greater accuracy than CT scan. As such, neutrophil count may be used to assist in the decision to administer tPA to mild AIS.Support or Funding InformationNo funding was received for this project.This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

Introduction: The presence of white matter hyperintensities (WMH) is associated with stroke, dementia, depression and other medical problems. The presence of WMHs is an independent risk factor for stroke and is associated with worse outcomes after stroke. WMH is frequently seen on neuroimaging in above patients. Hypothesis: The pathophysiology behind the development of WMHs is poorly understood. It has been postulated that there is a link between the presence of carotid artery stenosis (CAS) and WMHs. The presence of carotid atherosclerotic disease could indicate the presence of atheromatous disease in smaller distal vessels leading to chronic small vessel disease and appearance of WMHs. Others have suggested chronic cerebral hypoperfusion resulting from CAS as the underlying mechanism behind the appearance of WMHs. Methods: We reviewed data for 99 stroke patients. We used CT angiogram to grade the degree of CAS. We developed a score of 0 to 3 based on the degree of stenosis. A score of 0 meant no stenosis while a score of 3 meant severe stenosis with > 70% stenosis. A score of 1 for mild stenosis (<50%) and score of two for moderate stenosis (50-69%). Score for right and left side were calculated and added, total range 0 to 6. Using the scoring system, we had 25 patients with no stenosis, 38 with mild, 11 with moderate and 25 with severe stenosis. Patients were matched according to age, NIHSS, CV risk factors. The degree of WMH was scored using Fazekas scoring system (0-3) using T2 FLAIR MRI. Results: Patients with any degree of CAS are 8.5 times more likely to have WMHs than patients without CAS (p>0.001). 74% of patients with CAS have WMHs compared to only 24% of patients without CAS. There is a significant correlation between increased CAS severity and increase WMHs (higher Fazekas score) (r=.324, p=.001). 39% of patients with CAS moderate to severe WMHs (Fazekas 2 or 3) compared to only 16% of patients without CAS. Conclusion: In our patient sample, there seems to be a strong correlation between the presence of carotid artery stenosis and white matter hyperintensities.