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Common mechanistic pathways in cancer and heart failure. A scientific roadmap on behalf of the Translational Research Committee of the Heart Failure Association (HFA) of the European Society of Cardiology (ESC).

Authors :
de Boer, Rudolf
de Boer, Rudolf
Hulot, Jean-Sébastien
Tocchetti, Carlo
Aboumsallem, Joseph
Ameri, Pietro
Anker, Stefan
Bauersachs, Johann
Bertero, Edoardo
Coats, Andrew
Čelutkienė, Jelena
Chioncel, Ovidiu
Dodion, Pierre
Eschenhagen, Thomas
Farmakis, Dimitrios
Bayes-Genis, Antoni
Jäger, Dirk
Jankowska, Ewa
Kitsis, Richard
Konety, Suma
Larkin, James
Lehmann, Lorenz
Lenihan, Daniel
Maack, Christoph
Moslehi, Javid
Müller, Oliver
Nowak-Sliwinska, Patrycja
Piepoli, Massimo
Ponikowski, Piotr
Pudil, Radek
Rainer, Peter
Ruschitzka, Frank
Sawyer, Douglas
Seferovic, Petar
Suter, Thomas
Thum, Thomas
van der Meer, Peter
Van Laake, Linda
von Haehling, Stephan
Heymans, Stephane
Lyon, Alexander
Backs, Johannes
de Boer, Rudolf
de Boer, Rudolf
Hulot, Jean-Sébastien
Tocchetti, Carlo
Aboumsallem, Joseph
Ameri, Pietro
Anker, Stefan
Bauersachs, Johann
Bertero, Edoardo
Coats, Andrew
Čelutkienė, Jelena
Chioncel, Ovidiu
Dodion, Pierre
Eschenhagen, Thomas
Farmakis, Dimitrios
Bayes-Genis, Antoni
Jäger, Dirk
Jankowska, Ewa
Kitsis, Richard
Konety, Suma
Larkin, James
Lehmann, Lorenz
Lenihan, Daniel
Maack, Christoph
Moslehi, Javid
Müller, Oliver
Nowak-Sliwinska, Patrycja
Piepoli, Massimo
Ponikowski, Piotr
Pudil, Radek
Rainer, Peter
Ruschitzka, Frank
Sawyer, Douglas
Seferovic, Petar
Suter, Thomas
Thum, Thomas
van der Meer, Peter
Van Laake, Linda
von Haehling, Stephan
Heymans, Stephane
Lyon, Alexander
Backs, Johannes
Source :
European Journal of Heart Failure; vol 22, iss 12
Publication Year :
2020

Abstract

The co-occurrence of cancer and heart failure (HF) represents a significant clinical drawback as each disease interferes with the treatment of the other. In addition to shared risk factors, a growing body of experimental and clinical evidence reveals numerous commonalities in the biology underlying both pathologies. Inflammation emerges as a common hallmark for both diseases as it contributes to the initiation and progression of both HF and cancer. Under stress, malignant and cardiac cells change their metabolic preferences to survive, which makes these metabolic derangements a great basis to develop intersection strategies and therapies to combat both diseases. Furthermore, genetic predisposition and clonal haematopoiesis are common drivers for both conditions and they hold great clinical relevance in the context of personalized medicine. Additionally, altered angiogenesis is a common hallmark for failing hearts and tumours and represents a promising substrate to target in both diseases. Cardiac cells and malignant cells interact with their surrounding environment called stroma. This interaction mediates the progression of the two pathologies and understanding the structure and function of each stromal component may pave the way for innovative therapeutic strategies and improved outcomes in patients. The interdisciplinary collaboration between cardiologists and oncologists is essential to establish unified guidelines. To this aim, pre-clinical models that mimic the human situation, where both pathologies coexist, are needed to understand all the aspects of the bidirectional relationship between cancer and HF. Finally, adequately powered clinical studies, including patients from all ages, and men and women, with proper adjudication of both cancer and cardiovascular endpoints, are essential to accurately study these two pathologies at the same time.

Details

Database :
OAIster
Journal :
European Journal of Heart Failure; vol 22, iss 12
Notes :
application/pdf, European Journal of Heart Failure vol 22, iss 12
Publication Type :
Electronic Resource
Accession number :
edsoai.on1452695993
Document Type :
Electronic Resource