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Review

Anthracycline chemotherapy, Vascular Dysfunction and Cognitive Impairment: Burgeoning Topics and Future Directions

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Pages 547-566 | Received 09 Sep 2022, Accepted 17 Oct 2022, Published online: 10 Nov 2022
 

Abstract

Anthracyclines, chemotherapeutic agents used to treat common forms of cancer, increase cardiovascular (CV) complications, thereby necessitating research regarding interventions to improve the health of cancer survivors. Vascular dysfunction, which is induced by anthracycline chemotherapy, is an established antecedent to overt CV diseases. Potential treatment options for ameliorating vascular dysfunction have largely been understudied. Furthermore, patients treated with anthracyclines have impaired cognitive function and vascular dysfunction is an independent risk factor for the development of mild cognitive impairment. Here, we will focus on: anthracycline chemotherapy associated CV diseases risk; how targeting mechanisms underlying vascular dysfunction may be a means to improve both CV and cognitive health; and research gaps and potential future directions for the field of cardio-oncology.

Plain language summary

Cancer and cardiovascular diseases are highly prevalent in the USA and are inter-related issues. Drugs that are used to treat common cancers effectively destroy harmful cancer cells but negatively impact the function of the heart and blood vessels. Cancer patients treated with these drugs are at a high risk of developing problems within the blood vessels that prevent the vessels from dilating properly. Cancer treatments are also associated with impaired memory and brain function later in life. It is important to understand how and why these cancer treatments increase the risk of developing cardiovascular diseases and cognitive impairment. Current research is examining the mechanisms (i.e., potential therapeutic targets) underlying the negative effects of these drugs with the goal of developing interventions and additional treatments to improve the quality of life of cancer survivors.

Acknowledgments

The authors would like to thank all the individuals that have contributed and are currently contributing to the work described throughout this review. Authors would also like to thank https://flaticon.com/, which was used to acquire images used throughout the figures.

Financial & competing interests disclosure

Work from the authors research was supported by NIH awards T32 DK007135, F32 HL151022 and K99 HL159241. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.

No writing assistance was utilized in the production of this manuscript.

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