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New Insights on the Toxicity on Heart and Vessels of Breast Cancer Therapies.

Abstract
Cardiovascular diseases are largely represented in patients with cancer and appear to be important side effects of cancer treatments, heavily affecting quality of life and leading to premature morbidity and death among cancer survivors. In particular, treatments for breast cancer have been shown to potentially play serious detrimental effects on cardiovascular health. This review aims to explore the available literature on breast cancer therapy-induced side effects on heart and vessels, illustrating the molecular mechanisms of cardiotoxicity known so far. Moreover, principles of cardiovascular risk assessment and management of cardiotoxicity in clinical practice will also be elucidated. Chemotherapy (anthracycline, taxanes, cyclophosphamide and 5-fluorouracil), hormonal therapy (estrogen receptor modulator and gonadotropin or luteinizing releasing hormone agonists) and targeted therapy (epidermal growth factor receptor 2 and Cyclin-dependent kinases 4 and 6 inhibitors) adverse events include arterial and pulmonary hypertension, supraventricular and ventricular arrhythmias, systolic and diastolic cardiac dysfunction and coronary artery diseases due to different and still not well-dissected molecular pathways. Therefore, cardiovascular prevention programs and treatment of cardiotoxicity appear to be crucial to improve morbidity and mortality of cancer survivors.
AuthorsOreste Lanza, Armando Ferrera, Simone Reale, Giorgio Solfanelli, Mattia Petrungaro, Giacomo Tini Melato, Massimo Volpe, Allegra Battistoni
JournalMedical sciences (Basel, Switzerland) (Med Sci (Basel)) Vol. 10 Issue 2 (05 25 2022) ISSN: 2076-3271 [Electronic] Switzerland
PMID35736347 (Publication Type: Journal Article, Review)
Chemical References
  • Anthracyclines
Topics
  • Anthracyclines (adverse effects)
  • Breast Neoplasms (chemically induced, drug therapy)
  • Cardiotoxicity (etiology, prevention & control)
  • Female
  • Heart
  • Humans
  • Quality of Life

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