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      Red blood cell distribution width: A marker of anisocytosis potentially associated with atrial fibrillation

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          Abstract

          The incorporation of biomarkers in the actually used risk scores seem to be helpful for early identifying atrial fibrillation (AF) patients at higher risk. The aim of this critical review of the scientific literature is to investigate the potential clinical significance of red blood cell distribution width (RDW) in AF. A systematic electronic search was carried out to identify all articles describing an epidemiological association between RDW and AF in adult human populations. Data abstraction was conducted on a final number of 35 articles (13 cross-sectional, 12 prospective and 10 retrospective studies). The results of these epidemiological investigations were all virtually concordant to emphasize that an enhanced RDW value is not only a predictive factor and a marker of AF but its measurement may also be helpful for predicting the risk of developing many adverse complications in patients with AF, such as recurrence and duration of AF, hospitalization for heart failure, bleeding, left atrial thrombosis and stasis, thromboembolic events and mortality. AF patients with RDW values exceeding the local reference range may be more aggressively investigated and managed, in order to identify and attenuate the impact of possible underlying disorders causing both anisocytosis and AF.

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          Inflammation and the pathogenesis of atrial fibrillation.

          Atrial fibrillation (AF) is the most common cardiac arrhythmia. However, the development of preventative therapies for AF has been disappointing. The infiltration of immune cells and proteins that mediate the inflammatory response in cardiac tissue and circulatory processes is associated with AF. Furthermore, the presence of inflammation in the heart or systemic circulation can predict the onset of AF and recurrence in the general population, as well as in patients after cardiac surgery, cardioversion, and catheter ablation. Mediators of the inflammatory response can alter atrial electrophysiology and structural substrates, thereby leading to increased vulnerability to AF. Inflammation also modulates calcium homeostasis and connexins, which are associated with triggers of AF and heterogeneous atrial conduction. Myolysis, cardiomyocyte apoptosis, and the activation of fibrotic pathways via fibroblasts, transforming growth factor-β and matrix metalloproteases are also mediated by inflammatory pathways, which can all contribute to structural remodelling of the atria. The development of thromboembolism, a detrimental complication of AF, is also associated with inflammatory activity. Understanding the complex pathophysiological processes and dynamic changes of AF-associated inflammation might help to identify specific anti-inflammatory strategies for the prevention of AF.
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            Hematopoiesis.

            Hematopoiesis - the process by which blood cells are formed - has been studied intensely for over a century using a variety of model systems. There is conservation of the overall hematopoietic process between vertebrates, although some differences do exist. Over the last decade, the zebrafish has come to the forefront as a new model in hematopoiesis research, as it allows the use of large-scale genetics, chemical screens and transgenics. This comparative approach to understanding hematopoiesis has led to fundamental knowledge about the process and to the development of new therapies for disease. Here, we provide a broad overview of vertebrate hematopoiesis. We also highlight the benefits of using zebrafish as a model.
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              A biomarker-based risk score to predict death in patients with atrial fibrillation: the ABC (age, biomarkers, clinical history) death risk score

              Abstract Aims In atrial fibrillation (AF), mortality remains high despite effective anticoagulation. A model predicting the risk of death in these patients is currently not available. We developed and validated a risk score for death in anticoagulated patients with AF including both clinical information and biomarkers. Methods and results The new risk score was developed and internally validated in 14 611 patients with AF randomized to apixaban vs. warfarin for a median of 1.9 years. External validation was performed in 8548 patients with AF randomized to dabigatran vs. warfarin for 2.0 years. Biomarker samples were obtained at study entry. Variables significantly contributing to the prediction of all-cause mortality were assessed by Cox-regression. Each variable obtained a weight proportional to the model coefficients. There were 1047 all-cause deaths in the derivation and 594 in the validation cohort. The most important predictors of death were N-terminal pro B-type natriuretic peptide, troponin-T, growth differentiation factor-15, age, and heart failure, and these were included in the ABC (Age, Biomarkers, Clinical history)-death risk score. The score was well-calibrated and yielded higher c-indices than a model based on all clinical variables in both the derivation (0.74 vs. 0.68) and validation cohorts (0.74 vs. 0.67). The reduction in mortality with apixaban was most pronounced in patients with a high ABC-death score. Conclusion A new biomarker-based score for predicting risk of death in anticoagulated AF patients was developed, internally and externally validated, and well-calibrated in two large cohorts. The ABC-death risk score performed well and may contribute to overall risk assessment in AF. ClinicalTrials.gov identifier NCT00412984 and NCT00262600
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                Author and article information

                Contributors
                Journal
                World J Cardiol
                WJC
                World Journal of Cardiology
                Baishideng Publishing Group Inc
                1949-8462
                26 December 2019
                26 December 2019
                : 11
                : 12
                : 292-304
                Affiliations
                Section of Clinical Biochemistry, University of Verona, Verona 37134, Italy
                Emergency Department, University Hospital of Parma, Parma 43126, Italy
                Department of Physiology, Faculty of Medicine, University of Valencia and INCLIVA Biomedical Research Institute, Valencia 46010, Spain. fabian.sanchis@ 123456uv.es
                Author notes

                Author contributions: Lippi G and Cervellin G contributed equally to this work; Lippi G and Sanchis-Gomar F generated the tables and figures; Lippi G, Cervellin G and Sanchis-Gomar F reviewed wrote the paper contributed to editing, reviewing, and final approval of the article.

                Corresponding author: Fabian Sanchis-Gomar, MD, Research Scientist, Department of Physiology, Faculty of Medicine, University of Valencia and INCLIVA Biomedical Research Institute, Av. Blasco Ibañez 15, Valencia 46010, Spain. fabian.sanchis@ 123456uv.es

                Telephone: +34-96-5813115 Fax: +34-96-3864642

                Article
                jWJC.v11.i12.pg292
                10.4330/wjc.v11.i12.292
                6937412
                31908729
                aa798306-3b63-4a25-bc0d-c14eb4b173c7
                ©The Author(s) 2019. Published by Baishideng Publishing Group Inc. All rights reserved.

                This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial.

                History
                : 14 March 2019
                : 21 August 2019
                : 18 October 2019
                Categories
                Review

                atrial fibrillation,arrhythmia,erythrocytes,red blood cell distribution width

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