Towards better definition, quantification and treatment of fibrosis in heart failure. A scientific roadmap by the Committee of Translational Research of the Heart Failure Association (HFA) of the European Society of Cardiology

de Boer, R. A. et al. (2019) Towards better definition, quantification and treatment of fibrosis in heart failure. A scientific roadmap by the Committee of Translational Research of the Heart Failure Association (HFA) of the European Society of Cardiology. European Journal of Heart Failure, 21(3), pp. 272-285. (doi:10.1002/ejhf.1406) (PMID:30714667) (PMCID:PMC6607480)

de Boer, R. A. et al. (2019) Towards better definition, quantification and treatment of fibrosis in heart failure. A scientific roadmap by the Committee of Translational Research of the Heart Failure Association (HFA) of the European Society of Cardiology. European Journal of Heart Failure, 21(3), pp. 272-285. (doi:10.1002/ejhf.1406) (PMID:30714667) (PMCID:PMC6607480)

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Abstract

Fibrosis is a pivotal player in heart failure development and progression. Measurements of (markers of) fibrosis in tissue and blood may help to diagnose and risk stratify patients with heart failure, and its treatment may be effective in preventing heart failure and its progression. A lack of pathophysiological insights and uniform definitions has hampered the research in fibrosis and heart failure. The Translational Research Committee of the Heart Failure Association discussed several aspects of fibrosis in their workshop. Early insidious perturbations such as subclinical hypertension or inflammation may trigger first fibrotic events, while more dramatic triggers such as myocardial infarction and myocarditis give rise to full blown scar formation and ongoing fibrosis in diseased hearts. Aging itself is also associated with a cardiac phenotype that includes fibrosis. Fibrosis is an extremely heterogeneous phenomenon, as several stages of the fibrotic process exist, each with different fibrosis subtypes and a different composition of various cells and proteins — resulting in a very complex pathophysiology. As a result, detection of fibrosis, e.g. using current cardiac imaging modalities or plasma biomarkers, will detect only specific subforms of fibrosis, but cannot capture all aspects of the complex fibrotic process. Furthermore, several anti‐fibrotic therapies are under investigation, but such therapies generally target aspecific aspects of the fibrotic process and suffer from a lack of precision. This review discusses the mechanisms and the caveats and proposes a roadmap for future research.

Item Type:Articles
Status:Published
Refereed:Yes
Glasgow Author(s) Enlighten ID:Cleland, Professor John
Authors: de Boer, R. A., De Keulenaer, G., Bauersachs, J., Brutsaert, D., Cleland, J. G., Diez, J., Du, X.-J., Ford, P., Heinzel, F. R., Lipson, K., McDonagh, T., Lopez-Andres, N., Lunde, I. G., Lyon, A. R., Pollesello, P., Prasad, S. K., Tocchetti, C. G., Mayr, M., Sluijter, J. P.G., Thum, T., Tschöpe, C., Zannad, F., Zimmermann, W.-H., Ruschitzka, F., Filippatos, G., Lindsey, M. L., Maack, C., and Heymans, S.
College/School:College of Medical Veterinary and Life Sciences > Institute of Health and Wellbeing > Robertson Centre
Journal Name:European Journal of Heart Failure
Publisher:Wiley
ISSN:1388-9842
ISSN (Online):1879-0844
Published Online:04 February 2019
Copyright Holders:Copyright © 2019 The Authors
First Published:First published in European Journal of Heart Failure 21(3):272-285
Publisher Policy:Reproduced under a Creative Commons License

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