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      Impact of Hemoglobin Levels and Anemia on Mortality in Acute Stroke: Analysis of UK Regional Registry Data, Systematic Review, and Meta‐Analysis

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          Abstract

          Background

          The impact of hemoglobin levels and anemia on stroke mortality remains controversial. We aimed to systematically assess this association and quantify the evidence.

          Methods and Results

          We analyzed data from a cohort of 8013 stroke patients (mean± SD, 77.81±11.83 years) consecutively admitted over 11 years (January 2003 to May 2015) using a UK Regional Stroke Register. The impact of hemoglobin levels and anemia on mortality was assessed by sex‐specific values at different time points (7 and 14 days; 1, 3, and 6 months; 1 year) using multiple regression models controlling for confounders. Anemia was present in 24.5% of the cohort on admission and was associated with increased odds of mortality at most of the time points examined up to 1 year following stroke. The association was less consistent for men with hemorrhagic stroke. Elevated hemoglobin was also associated with increased mortality, mainly within the first month. We then conducted a systematic review using the Embase and Medline databases. Twenty studies met the inclusion criteria. When combined with the cohort from the current study, the pooled population had 29 943 patients with stroke. The evidence base was quantified in a meta‐analysis. Anemia on admission was found to be associated with an increased risk of mortality in both ischemic stroke (8 studies; odds ratio 1.97 [95% CI 1.57–2.47]) and hemorrhagic stroke (4 studies; odds ratio 1.46 [95% CI 1.23–1.74]).

          Conclusions

          Strong evidence suggests that patients with anemia have increased mortality with stroke. Targeted interventions in this patient population may improve outcomes and require further evaluation.

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          Most cited references37

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          Association of hemoglobin levels with clinical outcomes in acute coronary syndromes.

          In the setting of an acute coronary syndrome (ACS), anemia has the potential to worsen myocardial ischemia; however, data relating anemia to clinical outcomes in ACS remain limited. We examined the association between baseline hemoglobin values and major adverse cardiovascular events through 30 days in 39,922 patients enrolled in clinical trials of ACS. After adjustment for differences in baseline characteristics and index hospitalization treatments, a reverse J-shaped relationship between baseline hemoglobin values and major adverse cardiovascular events was observed. In patients with ST-elevation myocardial infarction, when those with hemoglobin values between 14 and 15 g/dL were used as the reference, cardiovascular mortality increased as hemoglobin levels fell below 14 g/dL, with an adjusted OR of 1.21 (95% CI 1.12 to 1.30, P 17 g/dL also had excess mortality (OR 1.79, 95% CI 1.18 to 2.71, P=0.007). In patients with non-ST-elevation ACS, with those with hemoglobin 15 to 16 g/dL used as the reference, the likelihood of cardiovascular death, myocardial infarction, or recurrent ischemia increased as the hemoglobin fell below 11 g/dL, with an adjusted OR of 1.45 (95% CI 1.33 to 1.58, P 16 g/dL also had an increased rate of death or ischemic events (OR 1.31, 95% CI 1.03 to 1.66, P=0.027). Anemia is a powerful and independent predictor of major adverse cardiovascular events in patients across the spectrum of ACS.
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            Blood transfusion in elderly patients with acute myocardial infarction.

            Anemia may have adverse effects in patients with coronary artery disease. However, the benefit of blood transfusion in elderly patients with acute myocardial infarction and various degrees of anemia is uncertain. We conducted a retrospective study of data on 78,974 Medicare beneficiaries 65 years old or older who were hospitalized with acute myocardial infarction. Patients were categorized according to the hematocrit on admission (5.0 to 24.0 percent, 24.1 to 27.0 percent, 27.1 to 30.0 percent, 30.1 to 33.0 percent, 33.1 to 36.0 percent, 36.1 to 39.0 percent, or 39.1 to 48.0 percent), and data were evaluated to determine whether there was an association between the use of transfusion and 30-day mortality. Patients with lower hematocrit values on admission had higher 30-day mortality rates. Blood transfusion was associated with a reduction in 30-day mortality among patients whose hematocrit on admission fell into the categories ranging from 5.0 to 24.0 percent (adjusted odds ratio, 0.22; 95 percent confidence interval, 0.11 to 0.45) to 30.1 to 33.0 percent (adjusted odds ratio, 0.69; 95 percent confidence interval, 0.53 to 0.89). It was not associated with a reduction in 30-day mortality among those whose hematocrit values fell in the higher ranges. In one of seven subgroup analyses (among patients who survived at least two days), transfusion was not associated with a reduction in mortality for patients with hematocrit values of 30.1 percent or higher. Blood transfusion is associated with a lower short-term mortality rate among elderly patients with acute myocardial infarction if the hematocrit on admission is 30.0 percent or lower and may be effective in patients with a hematocrit as high as 33.0 percent on admission.
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              Shear stress selectively upregulates intercellular adhesion molecule-1 expression in cultured human vascular endothelial cells.

              Hemodynamic forces induce various functional changes in vascular endothelium, many of which reflect alterations in gene expression. We have recently identified a cis-acting transcriptional regulatory element, the shear stress response element (SSRE), present in the promoters of several genes, that may represent a common pathway by which biomechanical forces influence gene expression. In this study, we have examined the effect of shear stress on endothelial expression of three adhesion molecules: intercellular adhesion molecule-1 (ICAM-1), which contains the SSRE in its promoter, and E-selectin (ELAM-1) and vascular cell adhesion molecule-1 (VCAM-1), both of which lack the SSRE. Cultured human umbilical vein endothelial cells, subjected to a physiologically relevant range of laminar shear stresses (2.5-46 dyn/cm2) in a cone and plate apparatus for up to 48 h, showed time-dependent but force-independent increases in surface immunoreactive ICAM-1. Upregulated ICAM-1 expression was correlated with increased adhesion of the JY lymphocytic cell line. Northern blot analysis revealed increased ICAM-1 transcript as early as 2 h after the onset of shear stress. In contrast, E-selectin and vascular cell adhesion molecule-1 transcript and cell-surface protein were not upregulated at any time point examined. This selective regulation of adhesion molecule expression in vascular endothelium suggests that biomechanical forces, in addition to humoral stimuli, may contribute to differential endothelial gene expression and thus represent pathophysiologically relevant stimuli in inflammation and atherosclerosis.
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                Author and article information

                Journal
                J Am Heart Assoc
                J Am Heart Assoc
                10.1002/(ISSN)2047-9980
                JAH3
                ahaoa
                Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease
                John Wiley and Sons Inc. (Hoboken )
                2047-9980
                17 August 2016
                August 2016
                : 5
                : 8 ( doiID: 10.1002/jah3.2016.5.issue-8 )
                : e003019
                Affiliations
                [ 1 ] Epidemiology GroupInstitute of Applied Health Sciences AberdeenUK
                [ 2 ] Stroke Research GroupNorfolk and Norwich University Hospital NorwichUK
                [ 3 ] Norwich Medical SchoolUniversity of East Anglia NorwichUK
                [ 4 ] Nuffield Department of Population HealthUniversity of Oxford UK
                [ 5 ] Keele Cardiovascular Research Group Institutes of Science and Technology in Medicine and Primary Care and Health SciencesKeele University Stoke‐on‐TrentUK
                Author notes
                [*] [* ] Correspondence to: Phyo K. Myint, MD, School of Medicine, Sciences and Nutrition, University of Aberdeen, Room 4:013, Polwarth Building, Foresterhill, AB25 2ZD Aberdeen, Scotland, UK. E‐mail: phyo.myint@ 123456abdn.ac.uk
                Article
                JAH31650
                10.1161/JAHA.115.003019
                5015269
                27534421
                a8721599-0325-4782-abfe-b211730ddbc2
                © 2016 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley Blackwell.

                This is an open access article under the terms of the Creative Commons Attribution‐NonCommercial‐NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made.

                History
                : 10 March 2016
                : 17 June 2016
                Page count
                Pages: 16
                Funding
                Funded by: Norfolk and Norwich University Hospital National Health Service Foundation Trust Stroke Services
                Funded by: Norfolk and Norwich University Hospital Research and Development Department through Research Capability Funds
                Categories
                Original Research
                Original Research
                Stroke
                Custom metadata
                2.0
                jah31650
                August 2016
                Converter:WILEY_ML3GV2_TO_NLMPMC version:4.9.4 mode:remove_FC converted:24.08.2016

                Cardiovascular Medicine
                hemoglobin,mortality,prognosis,stroke,cerebrovascular disease/stroke,epidemiology,intracranial hemorrhage,ischemic stroke

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