title: [Cardioprotective treatment during adjuvant cancer therapy].
abstract: BACKGROUND
  Cardiac dysfunction in the form of reduced systolic and/or diastolic left ventricular function after adjuvant cancer therapy has recently attracted increasing attention. The best-known cardiotoxic agents are anthracyclines and the recombinant antibody trastuzumab. Patients treated with radiotherapy to the thorax are liable to develop coronary artery disease. There are no official guidelines for the preventive treatment of cardiac dysfunction induced by chemotherapy, antibody therapy or radiotherapy. The purpose of this article is to provide an overview of cardiac dysfunction caused by adjuvant cancer therapies and to review possible preventive therapeutic principles.
  
  
  METHODS
  This article is based on a review of the literature derived from a search in PubMed.
  
  
  RESULTS
  27% of those treated with anthracyclines and trastuzumab may develop some degree of cardiac dysfunction. The figure for patients receiving radiotherapy to the thorax is more uncertain. Small-scale studies suggest that anthracycline-induced cardiac dysfunction can be prevented wholly or partially by blocking the renin-angiotensin-aldosterone system and by beta-adrenergic blockade. As yet, there are no results of prospective studies on cardiopreventive treatment during trastuzumab therapy or thoracic radiotherapy.
  
  
  CONCLUSIONS
  There is a need for randomised, placebo-controlled studies of homogeneous groups of patients in order to determine whether treatment with cardioprotective medication in parallel with chemotherapy, antibody therapy or radiotherapy can prevent or reduce cardiac dysfunction.
authors.forename: Geeta
authors.initials: G
authors.lastname: Gulati
authors.forename: Siri Lagethon
authors.initials: SL
authors.lastname: Heck
authors.forename: Anne Hansen
authors.initials: AH
authors.lastname: Ree
authors.forename: Berit
authors.initials: B
authors.lastname: Gravdehaug
authors.forename: Helge
authors.initials: H
authors.lastname: Røsjø
authors.forename: Kjetil
authors.initials: K
authors.lastname: Steine
authors.forename: Åse
authors.initials: Å
authors.lastname: Bratland
authors.forename: Pavel
authors.initials: P
authors.lastname: Hoffmann
authors.forename: Jürgen
authors.initials: J
authors.lastname: Geisler
authors.forename: Torbjørn
authors.initials: T
authors.lastname: Omland
mesh_terms: D000319:Adrenergic beta-Antagonists / Q000494:pharmacology / Q000627:therapeutic use; D057911:Angiotensin Receptor Antagonists / Q000494:pharmacology / Q000627:therapeutic use; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000494:pharmacology / Q000627:therapeutic use; D018943:Anthracyclines / Q000009:adverse effects / Q000494:pharmacology; D000903:Antibiotics, Antineoplastic / Q000009:adverse effects / Q000494:pharmacology; D061067:Antibodies, Monoclonal, Humanized / Q000009:adverse effects / Q000494:pharmacology; D000970:Antineoplastic Agents / Q000009:adverse effects* / Q000494:pharmacology; D017024:Chemotherapy, Adjuvant / Q000009:adverse effects*; D006321:Heart / Q000187:drug effects / Q000528:radiation effects*; D006331:Heart Diseases / Q000139:chemically induced* / Q000188:drug therapy / Q000517:prevention & control; D006801:Humans; D009369:Neoplasms / Q000188:drug therapy / Q000532:radiotherapy; D018714:Radiotherapy, Adjuvant / Q000009:adverse effects*; D000068878:Trastuzumab; D018487:Ventricular Dysfunction, Left / Q000139:chemically induced / Q000188:drug therapy / Q000517:prevention & control
chemical_list: D000319:Adrenergic beta-Antagonists; D057911:Angiotensin Receptor Antagonists; D000806:Angiotensin-Converting Enzyme Inhibitors; D018943:Anthracyclines; D000903:Antibiotics, Antineoplastic; D061067:Antibodies, Monoclonal, Humanized; D000970:Antineoplastic Agents; D000068878:Trastuzumab