Heart Failure With Targeted Cancer Therapies: Mechanisms and Cardioprotection

Oncology has seen growing use of newly developed targeted therapies. Although this has resulted in dramatic improvements in progression-free and overall survival, challenges in the management of toxicities related to longer-term treatment of these therapies have also become evident. Although a targe...

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Bibliographic Details
Published in:Circulation research 2021-05, Vol.128 (10), p.1576-1593
Main Authors: Hahn, Virginia S, Zhang, Kathleen W, Sun, Lova, Narayan, Vivek, Lenihan, Daniel J, Ky, Bonnie
Format: Article
Language:English
Subjects:
Androgen Antagonists - adverse effects
Anthracyclines - adverse effects
Antineoplastic Agents, Immunological - adverse effects
Cardiotonic Agents - therapeutic use
Cardiotoxicity - etiology
Cardiotoxicity - prevention & control
Heart Failure - chemically induced
Heart Failure - epidemiology
Heart Failure - prevention & control
Humans
Immunotherapy - adverse effects
Incidence
Molecular Targeted Therapy - adverse effects
Neoplasms - drug therapy
Proteasome Inhibitors - adverse effects
Protein Kinase Inhibitors - adverse effects
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Summary:Oncology has seen growing use of newly developed targeted therapies. Although this has resulted in dramatic improvements in progression-free and overall survival, challenges in the management of toxicities related to longer-term treatment of these therapies have also become evident. Although a targeted approach often exploits the differences between cancer cells and noncancer cells, overlap in signaling pathways necessary for the maintenance of function and survival in multiple cell types has resulted in systemic toxicities. In particular, cardiovascular toxicities are of important concern. In this review, we highlight several targeted therapies commonly used across a variety of cancer types, including HER2 (human epidermal growth factor receptor 2)+ targeted therapies, tyrosine kinase inhibitors, immune checkpoint inhibitors, proteasome inhibitors, androgen deprivation therapies, and MEK (mitogen-activated protein kinase kinase)/BRAF (v-raf murine sarcoma viral oncogene homolog B) inhibitors. We present the oncological indications, heart failure incidence, hypothesized mechanisms of cardiotoxicity, and potential mechanistic rationale for specific cardioprotective strategies.
ISSN:0009-7330
1524-4571
DOI:10.1161/CIRCRESAHA.121.318223