@article{FrantzFalcaoPiresBalligandetal.2018,
  author    = {Frantz, Stefan and Falcao-Pires, Ines and Balligand, Jean-Luc and Bauersachs, Johann and Brutsaert, Dirk and Ciccarelli, Michele and Dawson, Dana and de Windt, Leon J. and Giacca, Mauro and Hamdani, Nazha and Hilfiker-Kleiner, Denise and Hirsch, Emilio and Leite-Moreira, Adelino and Mayr, Manuel and Thum, Thomas and Tocchetti, Carlo G. and van der Velden, Jolanda and Varricchi, Gilda and Heymans, Stephane},
  title     = {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},
  series = {European Journal of Heart Failure},
  volume    = {20},
  journal   = {European Journal of Heart Failure},
  doi       = {10.1002/ejhf.1138},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-229091},
  pages     = {445-459},
  year      = {2018},
  abstract  = {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.},
  language  = {en}
}
@article{deBoerDeKeulenaerBauersachsetal.2019,
  author    = {de Boer, Rudolf A. and De Keulenaer, Gilles and Bauersachs, Johann and Brutsaert, Dirk and Cleland, John G. and Diez, Javier and Du, Xiao-Jun and Ford, Paul and Heinzel, Frank R. and Lipson, Kenneth E. and McDonagh, Theresa and Lopez-Andres, Natalia and Lunde, Ida G. and Lyon, Alexander R. and Pollesello, Piero and Prasad, Sanjay K. and Tocchetti, Carlo G. and Mayr, Manuel and Sluijter, Joost P. G. and Thum, Thomas and Tsch{\"o}pe, Carsten and Zannad, Faiez and Zimmermann, Wolfram-Hubertus and Ruschitzka, Frank and Filippatos, Gerasimos and Lindsey, Merry L. and Maack, Christoph and Heymans, Stephane},
  title     = {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},
  series = {European Journal of Heart Failure},
  volume    = {21},
  journal   = {European Journal of Heart Failure},
  doi       = {10.1002/ejhf.1406},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-223613},
  pages     = {272-285},
  year      = {2019},
  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.},
  language  = {en}
}