Cardiac remodelling – Part 1: From cells and tissues to circulating biomarkers. A review from the Study Group on Biomarkers of the Heart Failure Association of the European Society of Cardiology. (21st April 2022)

• Record Type: Journal Article
• Authors: González, Arantxa; Richards, A. Mark; de Boer, Rudolf A.; Thum, Thomas; Arfsten, Henrike; Hülsmann, Martin; Falcao‐Pires, Inês; Díez, Javier; Foo, Roger S.Y.; Chan, Mark Y.; Aimo, Alberto; Anene‐Nzelu, Chukwuemeka G.; Abdelhamid, Magdy; Adamopoulos, Stamatis; Anker, Stefan D.; Belenkov, Yuri; Gal, Tuvia B.; Cohen‐Solal, Alain; Böhm, Michael; Chioncel, Ovidiu; Delgado, Victoria; Emdin, Michele; Jankowska, Ewa A.; Gustafsson, Finn; Hill, Loreena; Jaarsma, Tiny; Januzzi, James L.; Jhund, Pardeep S.; Lopatin, Yuri; Lund, Lars H.; Metra, Marco; Milicic, Davor; Moura, Brenda; Mueller, Christian; Mullens, Wilfried; Núñez, Julio; Piepoli, Massimo F.; Rakisheva, Amina; Ristić, Arsen D.; Rossignol, Patrick; Savarese, Gianluigi; Tocchetti, Carlo G.; Van Linthout, Sophie; Volterrani, Maurizio; Seferovic, Petar; Rosano, Giuseppe; Coats, Andrew J.S.; Bayés‐Genís, Antoni;
• Is Part Of: European journal of heart failure. Volume 24:Number 6(2022)
• Page Start: 927
• Page End: 943
• Publication Date: 2022-04-21
• Subjects: Biomarkers -- Remodeling -- Cells -- Tissue; Heart failure -- Periodicals; Heart Failure -- Periodicals; Insuffisance cardiaque -- Périodiques; Heart failure; Periodicals; 616.129005
• DOI: 10.1002/ejhf.2493
• Languages: English
• ISSNs: 1388-9842

Abstract

Abstract : Cardiac remodelling refers to changes in left ventricular structure and function over time, with a progressive deterioration that may lead to heart failure (HF) development (adverse remodelling) or vice versa a recovery (reverse remodelling) in response to HF treatment. Adverse remodelling predicts a worse outcome, whilst reverse remodelling predicts a better prognosis. The geometry, systolic and diastolic function and electric activity of the left ventricle are affected, as well as the left atrium and on the long term even right heart chambers. At a cellular and molecular level, remodelling involves all components of cardiac tissue: cardiomyocytes, fibroblasts, endothelial cells and leucocytes. The molecular, cellular and histological signatures of remodelling may differ according to the cause and severity of cardiac damage, and clearly to the global trend toward worsening or recovery. These processes cannot be routinely evaluated through endomyocardial biopsies, but may be reflected by circulating levels of several biomarkers. Different classes of biomarkers (e.g. proteins, non‐coding RNAs, metabolites and/or epigenetic modifications) and several biomarkers of each class might inform on some aspects on HF development, progression and long‐term outcomes, but most have failed to enter clinical practice. This may be due to the biological complexity of remodelling, so that no single biomarker could provide great insight on remodelling when assessed alone. Another possible reason is a still incomplete understanding of the role of biomarkers in the pathophysiology of cardiac remodelling. Such role will be investigated in the first part of this review paper on biomarkers of cardiac remodelling. Abstract : Integrated view of different cell types, derived‐biomarkers and their pathophysiological impact in cardiac remodelling. At the histocellular level, cardiac remodelling is the result of alterations in all cell types present in the myocardium, which also interact closely with each other in response to cardiac damage, injury, neurohormonal activation and stress. A number of molecules are potential circulating biomarkers of the different features of cardiac remodelling. A combination of such biomarkers will provide incremental information of the major histocellular alterations present in heart failure patients. ADM, adrenomedullin; BNP, B‐type natriuretic peptide; CITP, collagen type I carboxy‐terminal telopeptide; CNP, C‐type natriuretic peptide; ECM, extracellular matrix; EV, extracellular vesicle; GDF‐15, growth differentiation factor‐15; MMP‐1, matrix metalloproteinase‐1; MRpro‐ANP, mid‐regional pro‐atrial natriuretic peptide; ncRNA, non‐coding RNA; NT‐proBNP, amino‐terminal fragment of pro‐B‐type natriuretic peptide; PICP, procollagen type I carboxy‐terminal propeptide; PIIINP, procollagen type III amino‐terminal propeptide; sST2, soluble ST2; TGF‐β, transforming growth factor‐β; TNF‐α, tumour necrosis factor‐α; VCAM‐1, vascular cell adhesion molecule‐1; vW, von Willebrand.