Heinzel, F.R. (Frank R.)

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2018 - 20192

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    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
    (Wiley, 2019) McDonagh, T. (Theresa); Heinzel, F.R. (Frank R.); Lindsey, M.L. (Merry L.); Ruschitzka, F. (Frank); Lyon, A.R. (Alexander R.); Thum, T. (Thomas); Maack, C. (Christoph); Sluijter, J.P.G. (Joost P. G.); Brutsaert, D. (Dirk); Bauersachs, J. (Johann); Boer, R.A. (Rudolf A.) de; Keulenaer, G. (Gilles) de; Ford, P. (Paul); Lunde, I.G. (Ida G.); Tschöpe, C. (Carsten); Heymans, S. (Stephane); Zannad, F. (Faiez); Pollesello, P. (Piero); Tocchetti, C.G. (Carlo G.); Zimmermann, W.H. (Wolfram Hubertus); Filippatos, G. (Gerasimos); Lopez-Andres, N. (Natalia); Lipson, K.E. (Kenneth E.); Du, X.J. (Xiao Jun); Mayr, M. (Manuel); Prasad, S.K. (Sanjay K.); Diez, J. (Javier); Cleland, J.G. (John G.)
    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.
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    Heart failure and diabetes: metabolic alterations and therapeutic interventions: a state-of-the-art review from the Translational Research Committee of the Heart Failure Association-European Society of Cardiology
    (European Society of Cardiology, 2018) Staels, B. (Bart); Heinzel, F.R. (Frank R.); Rosano, G. (Giuseppe); Huelsmann, M. (Martin); Hulot, J.S. (Jean-Sebastien); Ruschitzka, F. (Frank); Lyon, A.R. (Alexander R.); Laake, L.W. (Linda W.) van; Maack, C. (Christoph); Cosentino, F. (Francesco); Brutsaert, D. (Dirk); Rena, G. (Graham); Bauersachs, J. (Johann); Farmakis, D. (Dimitrios); Boer, R.A. (Rudolf A.) de; Keulenaer, G. (Gilles) de; Taegtmeyer, H. (Heinrich); Lunde, I.G. (Ida G.); Iaccarino, G. (Guido); Dei-Cas, A. (Alessandra); Clarke, K. (Kieran); Heymans, S. (Stephane); Pollesello, P. (Piero); Gonzalez, A. (Arantxa); Seferovic, P. (Petar); Paulus, W.J. (Walter J.); Wanner, C. (Christoph); Backs, J. (Johannes); Bugger, H. (Heiko); Riksen, N.P. (Niels P.); Lehrke, M. (Michael); Filippatos, G. (Gerasimos); Marx, N. (Nikolaus); Rossignol, P.(Patrick); Bayes-Genis, A. (Antoni)
    Heart failure (HF) is growing to a modern epidemic and despite advances in therapy, it still carries an ominous prognosis and a significant socioeconomic burden. Many novel agents that emerged as promising HF drugs failed to improve residual morbidity and mortality.2,3 Since developing and testing new agents has become increasingly costly,4 the concept of repurposing existing drugs for new indications has gained considerable importance. Conceptually, comorbidities such as type 2 diabetes mellitus (T2DM), obesity or chronic kidney disease, all highly prevalent in HF populations, have shifted from being innocent bystanders to drivers of HF. This applies especially to HF with preserved ejection fraction (HFpEF), a phenotype that accounts for more than 50% of HF patients and for which no effective therapy exists thus far.5,6 In particular, the prevalence of T2DM, thereby its combination with HF is rapidly increasing, mainly due to the obesity epidemic. Cardiovascular (CV) outcomes are addressed by an increasing number of clinical studies in T2DM, mainly as safety endpoints for anti-diabetic agents. Some of those drugs have beneficial CV effects independent of their glucose-lowering action. Consequently, antidiabetic agents have gained interest for their potential repurposing in HF treatment. In this context, the Translational Research Committee of the Heart Failure Association (HFA) of the European Society of Cardiology (ESC) organized a workshop on HF and T2DM, focusing on the pathophysiological and therapeutic aspects of this relationship. Here, we summarize the main points raised during this workshop, providing an overview of current evidence and open issues.