Journal
HEART FAILURE REVIEWS
Volume 27, Issue 1, Pages 295-319Publisher
SPRINGER
DOI: 10.1007/s10741-020-09977-1
Keywords
Doxorubicin; Cardiotoxicity; Angiotensin; RAAS; ACEI; ARB
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Millions of new cancer cases are diagnosed each year worldwide, and although advancements in cancer biology and therapies have reduced mortality rates, most patients still require chemotherapy, which can have high medical costs and adverse effects. Anthracyclines, commonly used in cancer treatment, are associated with a high risk of cardiotoxicity. The dysregulation of the renin-angiotensin-aldosterone system (RAAS), a major regulator of the cardiovascular system, may play a role in anthracycline-induced cardiotoxicity. Targeting this system with drugs has shown promise in the prevention and treatment of cardiac adverse events associated with anthracyclines.
Few millions of new cancer cases are diagnosed worldwide every year. Due to significant progress in understanding cancer biology and developing new therapies, the mortality rates are decreasing with many of patients that can be completely cured. However, vast majority of them require chemotherapy which comes with high medical costs in terms of adverse events, of which cardiotoxicity is one of the most serious and challenging. Anthracyclines (doxorubicin, epirubicin) are a class of cytotoxic agents used in treatment of breast cancer, sarcomas, or hematological malignancies that are associated with high risk of cardiotoxicity that is observed in even up to 30% of patients and can be diagnosed years after the therapy. The mechanism, in which anthracyclines cause cardiotoxicity are not well known, but it is proposed that dysregulation of renin-angiotensin-aldosterone system (RAAS), one of main humoral regulators of cardiovascular system, may play a significant role. There is increasing evidence that drugs targeting this system can be effective in the prevention and treatment of anthracycline-induced cardiotoxicity what has recently found reflection in the recommendation of some scientific societies. In this review, we comprehensively describe possible mechanisms how anthracyclines affect RAAS and lead to cardiotoxicity. Moreover, we critically review available preclinical and clinical data on use of RAAS inhibitors in the primary and secondary prevention and treatment of cardiac adverse events associated with anthracycline-based chemotherapy.
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