TY  - JOUR
A1  - de Boer, Rudolf A.
A1  - De Keulenaer, Gilles
A1  - Bauersachs, Johann
A1  - Brutsaert, Dirk
A1  - Cleland, John G.
A1  - Diez, Javier
A1  - Du, Xiao-Jun
A1  - Ford, Paul
A1  - Heinzel, Frank R.
A1  - Lipson, Kenneth E.
A1  - McDonagh, Theresa
A1  - Lopez-Andres, Natalia
A1  - Lunde, Ida G.
A1  - Lyon, Alexander R.
A1  - Pollesello, Piero
A1  - Prasad, Sanjay K.
A1  - Tocchetti, Carlo G.
A1  - Mayr, Manuel
A1  - Sluijter, Joost P. G.
A1  - Thum, Thomas
A1  - Tschöpe, Carsten
A1  - Zannad, Faiez
A1  - Zimmermann, Wolfram-Hubertus
A1  - Ruschitzka, Frank
A1  - Filippatos, Gerasimos
A1  - Lindsey, Merry L.
A1  - Maack, Christoph
A1  - Heymans, Stephane
T1  - 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
JF  - European Journal of Heart Failure
N2  - 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.
KW  - fibrosis
KW  - heart failure
KW  - biomarkers
KW  - fibroblast
KW  - matrix
KW  - prognosis
KW  - imaging
Y1  - 2019
U6  - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-223613
VL  - 21
ER  - 
TY  - JOUR
A1  - Frantz, Stefan
A1  - Falcao-Pires, Ines
A1  - Balligand, Jean-Luc
A1  - Bauersachs, Johann
A1  - Brutsaert, Dirk
A1  - Ciccarelli, Michele
A1  - Dawson, Dana
A1  - de Windt, Leon J.
A1  - Giacca, Mauro
A1  - Hamdani, Nazha
A1  - Hilfiker-Kleiner, Denise
A1  - Hirsch, Emilio
A1  - Leite-Moreira, Adelino
A1  - Mayr, Manuel
A1  - Thum, Thomas
A1  - Tocchetti, Carlo G.
A1  - van der Velden, Jolanda
A1  - Varricchi, Gilda
A1  - Heymans, Stephane
T1  - The innate immune system in chronic cardiomyopathy: a European Society of Cardiology (ESC) scientific statement from the Working Group on Myocardial Function of the ESC
JF  - European Journal of Heart Failure
N2  - Activation of the immune system in heart failure (HF) has been recognized for over 20 years. Initially, experimental studies demonstrated a maladaptive role of the immune system. However, several phase III trials failed to show beneficial effects in HF with therapies directed against an immune activation. Preclinical studies today describe positive and negative effects of immune activation in HF. These different effects depend on timing and aetiology of HF. Therefore, herein we give a detailed review on immune mechanisms and their importance for the development of HF with a special focus on commonalities and differences between different forms of cardiomyopathies. The role of the immune system in ischaemic, hypertensive, diabetic, toxic, viral, genetic, peripartum, and autoimmune cardiomyopathy is discussed in depth. Overall, initial damage to the heart leads to disease specific activation of the immune system whereas in the chronic phase of HF overlapping mechanisms occur in different aetiologies.
KW  - immune system
KW  - macrophage
KW  - T-cell
KW  - ischaemic cardiomyopathy
KW  - hypertensive cardiomyopathy
KW  - diabetic cardiomyopathy
KW  - toxic cardiomyopathy
KW  - viral cardiomyopathy
KW  - genetic cardiomyopathy
KW  - peripartum cardiomyopathy
KW  - autoimmune cardiomyopathy
Y1  - 2018
U6  - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-229091
VL  - 20
ER  -