TY - JOUR
T1 - 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)
AU - de Boer, Rudolf A..
AU - Hulot, Jean-Sébastien
AU - Tocchetti, Carlo Gabriele
AU - Aboumsallem, Joseph Pierre
AU - Ameri, Pietro
AU - Anker, Stefan D.
AU - Bauersachs, Johann
AU - Bertero, Edoardo
AU - Coats, Andrew J. S.
AU - Čelutkienė, Jelena
AU - Chioncel, O.
AU - Dodion, Pierre
AU - Eschenhagen, Thomas
AU - Farmakis, D.
AU - Bayés-Genís, Antoni
AU - Jäger, Dirk
AU - Jankowska, Ewa A.
AU - Kitsis, Richard N.
AU - Konety, Suma H.
AU - Larkin, James
AU - Lehmann, Lorenz
AU - Lenihan, Daniel J.
AU - Maack, Christoph
AU - Moslehi, Javid J.
AU - Müller, Oliver J.
AU - Nowak-Sliwinska, Patrycja
AU - Piepoli, Massimo Francesco
AU - Ponikowski, Piotr
AU - Pudil, Radek
AU - Rainer, Peter P.
AU - Ruschitzka, Frank
AU - Sawyer, Douglas
AU - Seferovic, Petar M.
AU - Suter, Thomas
AU - Thum, Thomas
AU - van der Meer, Peter
AU - Van Laake, Linda W.
AU - von Haehling, Stephan
AU - Heymans, Stephane
AU - Lyon, Alexander R.
AU - Backs, Johannes
PY - 2020
Y1 - 2020
N2 - 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. We describe the co-occurrence of cancer and heart failure (HF), their potential shared risk factors, and their pathophysiological mechanisms. We advocate intense interaction between cardiologists and oncologists to achieve unifying hypotheses and collaborative pre-clinical and clinical studies.
AB - 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. We describe the co-occurrence of cancer and heart failure (HF), their potential shared risk factors, and their pathophysiological mechanisms. We advocate intense interaction between cardiologists and oncologists to achieve unifying hypotheses and collaborative pre-clinical and clinical studies.
KW - Heart failure
KW - Cancer
KW - Cardiotoxicity
KW - Inflammation
KW - Clonal haematopoiesis
KW - Angiogenesis
KW - Metabolism
KW - Cardio-oncology
KW - Extracellular matrix
U2 - 10.1002/ejhf.2029
DO - 10.1002/ejhf.2029
M3 - Review article
C2 - 33094495
SN - 1388-9842
VL - 22
SP - 2272
EP - 2289
JO - European Journal of Heart Failure
JF - European Journal of Heart Failure
ER -