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      Unlocking the Value of White Blood Cells for Heart Failure Diagnosis

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          Abstract

          Cardiovascular disease (CVD) is the single greatest cause of mortality and morbidity worldwide. Inciting 85% of CVD fatalities is heart failure, often resulting in or from a myocardial infarction. Early detection along with pharmacological treatment and lifestyle adaptation can result in better prognosis. Biomarkers are molecular or physiological measures that indicate disease presence, status, and severity. However, not all forms of heart failure are created equal. Current mainstay biomarkers for heart failure, including NT-pro-BNP and ejection fraction, lack sensitivity for many patients. Circulating white blood cells and peripheral blood mononuclear cells (PBMCs) are emerging as surrogate biopsies, reflecting molecular changes in the heart. We discuss the advantages of PBMCs over other sources, as well as limitations and considerations. We urge medical center biobanks to collect, isolate and store circulating white blood cells as a rich source of biomarkers to catalyze the discovery of novel diagnostic tools for heart failure.

          Electronic supplementary material

          The online version of this article (10.1007/s12265-020-10007-6) contains supplementary material, which is available to authorized users.

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          Most cited references39

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          Global Public Health Burden of Heart Failure.

          Heart failure (HF) is a global pandemic affecting at least 26 million people worldwide and is increasing in prevalence. HF health expenditures are considerable and will increase dramatically with an ageing population. Despite the significant advances in therapies and prevention, mortality and morbidity are still high and quality of life poor. The prevalence, incidence, mortality and morbidity rates reported show geographic variations, depending on the different aetiologies and clinical characteristics observed among patients with HF. In this review we focus on the global epidemiology of HF, providing data about prevalence, incidence, mortality and morbidity worldwide.
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            Dilated cardiomyopathy: the complexity of a diverse genetic architecture.

            Remarkable progress has been made in understanding the genetic basis of dilated cardiomyopathy (DCM). Rare variants in >30 genes, some also involved in other cardiomyopathies, muscular dystrophy, or syndromic disease, perturb a diverse set of important myocardial proteins to produce a final DCM phenotype. Large, publicly available datasets have provided the opportunity to evaluate previously identified DCM-causing mutations, and to examine the population frequency of sequence variants similar to those that have been observed to cause DCM. The frequency of these variants, whether associated with dilated or hypertrophic cardiomyopathy, is greater than estimates of disease prevalence. This mismatch might be explained by one or more of the following possibilities: that the penetrance of DCM-causing mutations is lower than previously thought, that some variants are noncausal, that DCM prevalence is higher than previously estimated, or that other more-complex genomics underlie DCM. Reassessment of our assumptions about the complexity of the genomic and phenomic architecture of DCM is warranted. Much about the genomic basis of DCM remains to be investigated, which will require comprehensive genomic studies in much larger cohorts of rigorously phenotyped probands and family members than previously examined.
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              Current Diagnostic and Treatment Strategies for Specific Dilated Cardiomyopathies: A Scientific Statement From the American Heart Association.

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                Author and article information

                Contributors
                emma.l.robinson7@googlemail.com
                Journal
                J Cardiovasc Transl Res
                J Cardiovasc Transl Res
                Journal of Cardiovascular Translational Research
                Springer US (New York )
                1937-5387
                1937-5395
                4 May 2020
                4 May 2020
                2021
                : 14
                : 1
                : 53-62
                Affiliations
                [1 ]GRID grid.5012.6, ISNI 0000 0001 0481 6099, Faculty of Science and Engineering, , Maastricht University, ; 6211 KR Maastricht, The Netherlands
                [2 ]GRID grid.5012.6, ISNI 0000 0001 0481 6099, Department of Cardiology, Cardiovascular Research Institute Maastricht, , Maastricht University, ; 6229 ER Maastricht, The Netherlands
                [3 ]GRID grid.412966.e, ISNI 0000 0004 0480 1382, Department of Cardiology, , Maastricht University Medical Centre, ; 6229 HX Maastricht, The Netherlands
                [4 ]Centre for Molecular and Vascular Biology (CMVB), Department of Cardiovascular Sciences, KU Leuven, B3000 Leuven, Belgium
                Author notes

                Associate Editor Saskia de Jager oversaw the review of this article

                Article
                10007
                10.1007/s12265-020-10007-6
                7892730
                32367341
                15c33e66-f6d9-48c5-a513-664a371c3410
                © The Author(s) 2020

                Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.

                History
                : 11 March 2020
                : 15 April 2020
                Funding
                Funded by: FundRef http://dx.doi.org/10.13039/501100002996, Hartstichting;
                Award ID: EARLY-HFPEF-2015
                Award Recipient :
                Categories
                Review Article
                Custom metadata
                © Springer Science+Business Media, LLC, part of Springer Nature 2021

                Cardiovascular Medicine
                heart failure,biomarker,diagnosis,endomyocardial biopsy,white blood cells,pbmcs,buffy coat

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