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      Classic and Novel Biomarkers as Potential Predictors of Ventricular Arrhythmias and Sudden Cardiac Death

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          Abstract

          Sudden cardiac death (SCD), most often induced by ventricular arrhythmias, is one of the main reasons for cardiovascular-related mortality. While coronary artery disease remains the leading cause of SCD, other pathologies like cardiomyopathies and, especially in the younger population, genetic disorders, are linked to arrhythmia-related mortality. Despite many efforts to enhance the efficiency of risk-stratification strategies, effective tools for risk assessment are still missing. Biomarkers have a major impact on clinical practice in various cardiac pathologies. While classic biomarkers like brain natriuretic peptide (BNP) and troponins are integrated into daily clinical practice, inflammatory biomarkers may also be helpful for risk assessment. Indeed, several trials investigated their application for the prediction of arrhythmic events indicating promising results. Furthermore, in recent years, active research efforts have brought forward an increasingly large number of “novel and alternative” candidate markers of various pathophysiological origins. Investigations of these promising biological compounds have revealed encouraging results when evaluating the prediction of arrhythmic events. To elucidate this issue, we review current literature dealing with this topic. We highlight the potential of “classic” but also “novel” biomarkers as promising tools for arrhythmia prediction, which in the future might be integrated into clinical practice.

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          Most cited references127

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          Galectin-3: an open-ended story.

          Galectins, an ancient lectin family, are characterized by specific binding of beta-galactosides through evolutionary conserved sequence elements of carbohydrate-recognition domain (CRD). A structurally unique member of the family is galectin-3; in addition to the CRD it contains a proline- and glycine-rich N-terminal domain (ND) through which is able to form oligomers. Galectin-3 is widely spread among different types of cells and tissues, found intracellularly in nucleus and cytoplasm or secreted via non-classical pathway outside of cell, thus being found on the cell surface or in the extracellular space. Through specific interactions with a variety of intra- and extracellular proteins galectin-3 affects numerous biological processes and seems to be involved in different physiological and pathophysiological conditions, such as development, immune reactions, and neoplastic transformation and metastasis. The review attempts to summarize the existing information on structural, biochemical and intriguing functional properties of galectin-3.
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            Osteopontin: role in immune regulation and stress responses.

            Recent research has led to a better but as yet incomplete understanding of the complex roles osteopontin plays in mammalian physiology. A soluble protein found in all body fluids, it stimulates signal transduction pathways (via integrins and CD44 variants) similar to those stimulated by components of the extracellular matrix. This appears to promote the survival of cells exposed to potentially lethal insults such as ischemia/reperfusion or physical/chemical trauma. OPN is chemotactic for many cell types including macrophages, dendritic cells, and T cells; it enhances B lymphocyte immunoglobulin production and proliferation. In inflammatory situations it stimulates both pro- and anti-inflammatory processes, which on balance can be either beneficial or harmful depending on what other inputs the cell is receiving. OPN influences cell-mediated immunity and has been shown to have Th1-cytokine functions. OPN deficiency is linked to a reduced Th1 immune response in infectious diseases, autoimmunity and delayed type hypersensitivity. OPN's role in the central nervous system and in stress responses has also emerged as an important aspect related to its cytoprotective and immune functions. Evidence suggests that either OPN or anti-OPN monoclonal antibodies (depending on the circumstances) might be clinically useful in modulating OPN function. Manipulation of plasma OPN levels may be useful in the treatment of autoimmune disease, cancer metastasis, osteoporosis and some forms of stress.
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              Measurement of the interleukin family member ST2 in patients with acute dyspnea: results from the PRIDE (Pro-Brain Natriuretic Peptide Investigation of Dyspnea in the Emergency Department) study.

              The aim of this study was to examine the value of measurement of the interleukin-1 receptor family member ST2 in patients with dyspnea. Concentrations of ST2 have been reported to be elevated in patients with heart failure (HF). Five hundred ninety-three dyspneic patients with and without acute destabilized HF presenting to an urban emergency department were evaluated with measurements of ST2 concentrations. Independent predictors of death at 1 year were identified. Concentrations of ST2 were higher among those with acute HF compared with those without (0.50 vs. 0.15 ng/ml; p or =0.20 ng/ml strongly predicted death at 1 year in dyspneic patients as a whole (HR = 5.6, 95% confidence interval [CI] 2.2 to 14.2; p < 0.001) as well as those with acute HF (hazard ratio [HR] = 9.3, 95% CI 1.3 to 17.8; p = 0.03). This risk associated with an elevated ST2 in dyspneic patients with and without HF appeared early and was sustained at 1 year after presentation (log-rank p value <0.001). A multi-marker approach with both ST2 and NT-proBNP levels identified subjects with the highest risk for death. Among dyspneic patients with and without acute HF, ST2 concentrations are strongly predictive of mortality at 1 year and might be useful for prognostication when used alone or together with NT-proBNP.
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                Author and article information

                Journal
                J Clin Med
                J Clin Med
                jcm
                Journal of Clinical Medicine
                MDPI
                2077-0383
                20 February 2020
                February 2020
                : 9
                : 2
                : 578
                Affiliations
                [1 ]Department of Cardiology I, Coronary and Peripheral Vascular Disease, Heart Failure, University Hospital Muenster, Albert Schweitzer Campus 1, A1, 48149 Muenster, Germany; zornitsa.shomanova@ 123456ukmuenster.de (Z.S.); christian.pogoda@ 123456ukmuenster.de (C.A.P.); holger.reinecke@ 123456ukmuenster.de (H.R.); rudin.pistulli@ 123456ukmuenster.de (R.P.)
                [2 ]Clinic II for Internal Medicine, Paracelsus Medical University, Muellner Hauptstrasse 48, 5020 Salzburg, Austria; b.ohnewein@ 123456salk.at (B.O.); c.schernthaner@ 123456salk.at (C.S.); k.hoefer@ 123456salk.at (K.H.); b.wernly@ 123456salk.at (B.W.); m.brandt@ 123456salk.at (M.C.B.); u.hoppe@ 123456salk.at (U.C.H.); b.strohmer@ 123456salk.at (B.S.)
                [3 ]Department of Cardiology II, Electrophysiology, University Hospital Muenster, Albert-Schweitzer-Campus 1, A1, D-48149 Muenster, Germany; gerrit.frommeyer@ 123456ukmuenster.de
                [4 ]Institute for Nursing and Practice, Paracelsus Medical University, Muellner Strubergasse 21, 5020 Salzburg, Austria; anna.dieplinger@ 123456pmu.ac.at
                Author notes
                [†]

                These authors contributed equally to this work.

                Author information
                https://orcid.org/0000-0003-2277-2880
                https://orcid.org/0000-0002-1431-9886
                https://orcid.org/0000-0003-4024-0220
                Article
                jcm-09-00578
                10.3390/jcm9020578
                7074455
                32093244
                e8e65fcf-17a6-4653-92ab-e39bbdb90dac
                © 2020 by the authors.

                Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ( http://creativecommons.org/licenses/by/4.0/).

                History
                : 31 January 2020
                : 14 February 2020
                Categories
                Review

                sudden cardiac death,ventricular arrhythmia,ventricular tachycardia,biomarkers,cardiac biomarkers,heart failure

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