Cardiac dysfunction in cancer patients: beyond direct cardiomyocyte damage of anticancer drugs: novel cardio-oncology insights from the joint 2019 meeting of the ESC Working Groups of Myocardial Function and Cellular Biology of the Heart

Cardiovasc Res. 2020 Sep 1;116(11):1820-1834. doi: 10.1093/cvr/cvaa222.

Abstract

In western countries, cardiovascular (CV) disease and cancer are the leading causes of death in the ageing population. Recent epidemiological data suggest that cancer is more frequent in patients with prevalent or incident CV disease, in particular, heart failure (HF). Indeed, there is a tight link in terms of shared risk factors and mechanisms between HF and cancer. HF induced by anticancer therapies has been extensively studied, primarily focusing on the toxic effects that anti-tumour treatments exert on cardiomyocytes. In this Cardio-Oncology update, members of the ESC Working Groups of Myocardial Function and Cellular Biology of the Heart discuss novel evidence interconnecting cardiac dysfunction and cancer via pathways in which cardiomyocytes may be involved but are not central. In particular, the multiple roles of cardiac stromal cells (endothelial cells and fibroblasts) and inflammatory cells are highlighted. Also, the gut microbiota is depicted as a new player at the crossroads between HF and cancer. Finally, the role of non-coding RNAs in Cardio-Oncology is also addressed. All these insights are expected to fuel additional research efforts in the field of Cardio-Oncology.

Keywords: Cardio-Oncology; Common pathways in heart failure and cancer; Multicellular and multiorgan mechanisms.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Antineoplastic Agents / adverse effects*
  • Cardiotoxicity
  • Cell Communication
  • Gastrointestinal Microbiome
  • Gene Expression Regulation
  • Heart Diseases / chemically induced*
  • Heart Diseases / metabolism
  • Heart Diseases / pathology
  • Heart Diseases / physiopathology
  • Humans
  • Inflammation Mediators / metabolism
  • Myocytes, Cardiac / drug effects*
  • Myocytes, Cardiac / metabolism
  • Myocytes, Cardiac / pathology
  • Neoplasms / complications
  • Neoplasms / drug therapy*
  • Neoplasms / metabolism
  • RNA, Untranslated / genetics
  • RNA, Untranslated / metabolism
  • Risk Assessment
  • Risk Factors
  • Signal Transduction

Substances

  • Antineoplastic Agents
  • Inflammation Mediators
  • RNA, Untranslated