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

Rudolf A. de Boer, Gilles De Keulenaer, Johann Bauersachs, Dirk Brutsaert, John G. Cleland, Javier Diez, Xiao Jun Du, Paul Ford, Frank R. Heinzel, Kenneth E. Lipson, Theresa McDonagh, Natalia Lopez-Andres, Ida G. Lunde, Alexander R. Lyon, Piero Pollesello, Sanjay K. Prasad, Carlo G. Tocchetti, Manuel Mayr, Joost P.G. Sluijter, Thomas ThumCarsten Tschöpe, Faiez Zannad, Wolfram Hubertus Zimmermann, Frank Ruschitzka, Gerasimos Filippatos, Merry L. Lindsey, Christoph Maack, Stephane Heymans

Research output: Contribution to journalReview article

18 Scopus citations

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.

Original languageEnglish (US)
Pages (from-to)272-285
Number of pages14
JournalEuropean Journal of Heart Failure
Volume21
Issue number3
DOIs
StatePublished - Mar 2019

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Keywords

  • Biomarkers
  • Fibroblast
  • Fibrosis
  • Heart failure
  • Imaging
  • Matrix
  • Prognosis

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

Cite this

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. E., 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., ... Heymans, S. (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), 272-285. https://doi.org/10.1002/ejhf.1406