{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,19]],"date-time":"2026-05-19T14:15:16Z","timestamp":1779200116959,"version":"3.51.4"},"reference-count":181,"publisher":"MDPI AG","issue":"6","license":[{"start":{"date-parts":[[2021,3,14]],"date-time":"2021-03-14T00:00:00Z","timestamp":1615680000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"name":"Ubbo Emmius Fund (UEF)","award":["661779"],"award-info":[{"award-number":["661779"]}]},{"name":"PLN foundation","award":["n.a."],"award-info":[{"award-number":["n.a."]}]},{"name":"CVON DOSIS","award":["2014-40"],"award-info":[{"award-number":["2014-40"]}]},{"name":"CVON e-DETECT","award":["2015-12"],"award-info":[{"award-number":["2015-12"]}]},{"name":"CVON DOUBLE DOSE","award":["2020B005"],"award-info":[{"award-number":["2020B005"]}]},{"name":"CVON SHE-PREDICTS-HF","award":["2017-21"],"award-info":[{"award-number":["2017-21"]}]},{"name":"CVON RED-CVD","award":["2017-11"],"award-info":[{"award-number":["2017-11"]}]},{"name":"CVON PREDICT2","award":["2018-30"],"award-info":[{"award-number":["2018-30"]}]},{"DOI":"10.13039\/501100000781","name":"European Research Council","doi-asserted-by":"publisher","award":["CoG 818715"],"award-info":[{"award-number":["CoG 818715"]}],"id":[{"id":"10.13039\/501100000781","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001674","name":"Fondation Leducq","doi-asserted-by":"publisher","award":["CURE-PLaN"],"award-info":[{"award-number":["CURE-PLaN"]}],"id":[{"id":"10.13039\/501100001674","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["IJMS"],"abstract":"<jats:p>For patients with hypertrophic cardiomyopathy (HCM), dilated cardiomyopathy (DCM) or arrhythmogenic cardiomyopathy (ACM), screening for pathogenic variants has become standard clinical practice. Genetic cascade screening also allows the identification of relatives that carry the same mutation as the proband, but disease onset and severity in mutation carriers often remains uncertain. Early detection of disease onset may allow timely treatment before irreversible changes are present. Although plasma biomarkers may aid in the prediction of disease onset, monitoring relies predominantly on identifying early clinical symptoms, on imaging techniques like echocardiography (Echo) and cardiac magnetic resonance imaging (CMR), and on (ambulatory) electrocardiography (electrocardiograms (ECGs)). In contrast to most other cardiac diseases, which are explained by a combination of risk factors and comorbidities, genetic cardiomyopathies have a clear primary genetically defined cardiac background. Cardiomyopathy cohorts could therefore have excellent value in biomarker studies and in distinguishing biomarkers related to the primary cardiac disease from those related to extracardiac, secondary organ dysfunction. Despite this advantage, biomarker investigations in cardiomyopathies are still limited, most likely due to the limited number of carriers in the past. Here, we discuss not only the potential use of established plasma biomarkers, including natriuretic peptides and troponins, but also the use of novel biomarkers, such as cardiac autoantibodies in genetic cardiomyopathy, and discuss how we can gauge biomarker studies in cardiomyopathy cohorts for heart failure at large.<\/jats:p>","DOI":"10.3390\/ijms22062955","type":"journal-article","created":{"date-parts":[[2021,3,14]],"date-time":"2021-03-14T22:13:10Z","timestamp":1615759990000},"page":"2955","update-policy":"https:\/\/doi.org\/10.3390\/mdpi_crossmark_policy","source":"Crossref","is-referenced-by-count":17,"title":["The Time Has Come to Explore Plasma Biomarkers in Genetic Cardiomyopathies"],"prefix":"10.3390","volume":"22","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-7658-9291","authenticated-orcid":false,"given":"Nienke M.","family":"Stege","sequence":"first","affiliation":[{"name":"Department of Cardiology, University Medical Center Groningen, University of Groningen, Hanzeplein 1, AB43, 9713 GZ Groningen, The Netherlands"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Rudolf A.","family":"de Boer","sequence":"additional","affiliation":[{"name":"Department of Cardiology, University Medical Center Groningen, University of Groningen, Hanzeplein 1, AB43, 9713 GZ Groningen, The Netherlands"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Maarten P.","family":"van den Berg","sequence":"additional","affiliation":[{"name":"Department of Cardiology, University Medical Center Groningen, University of Groningen, Hanzeplein 1, AB43, 9713 GZ Groningen, The Netherlands"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Herman H. W.","family":"Sillj\u00e9","sequence":"additional","affiliation":[{"name":"Department of Cardiology, University Medical Center Groningen, University of Groningen, Hanzeplein 1, AB43, 9713 GZ Groningen, The Netherlands"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"1968","published-online":{"date-parts":[[2021,3,14]]},"reference":[{"key":"ref_1","doi-asserted-by":"crossref","first-page":"999","DOI":"10.1016\/0092-8674(90)90274-I","article-title":"A molecular basis for familial hypertrophic cardiomyopathy: A \u03b2 cardiac myosin heavy chain gene missense mutation","volume":"62","author":"Kass","year":"1990","journal-title":"Cell"},{"key":"ref_2","doi-asserted-by":"crossref","first-page":"722","DOI":"10.1161\/CIRCRESAHA.117.309711","article-title":"Classification, Epidemiology, and Global Burden of Cardiomyopathies","volume":"121","author":"McKenna","year":"2017","journal-title":"Circ. 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