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Review
. 2020 Sep 7;9(9):2885.
doi: 10.3390/jcm9092885.

Management of Cardiac Toxicity Induced by Chemotherapy

Affiliations
Review

Management of Cardiac Toxicity Induced by Chemotherapy

Dario Trapani et al. J Clin Med. .

Abstract

Cardiotoxicity encompasses a spectrum of adverse cardiological effects experienced by cancer patients during and after receiving antineoplastic treatments. The intersection of cancer care with the management of the multiple comorbid non-communicable diseases carried by patients or related to cancer treatments motivates the need for an integrated and multidisciplinary approach to therapeutic clinical decision-making. This present review aimed to provide a perspective and an update of the current pharmacotherapy approaches for the prevention and management of cardiotoxicity from antiblastic chemotherapy; as such, it addresses myocardial, vascular, and arrhythmic disorders associated to chemotherapy, by navigating the current knowledge and clinical indications in support of the medical interventions. Clinical scenarios of pharmacological interventions take place with patients receiving anthracycline and, by extrapolation, other agents with cardiotoxic potentials and non-chemotherapy agents, including various small molecules and immunotherapy agents. Analysis of these scenarios aims to provide practical evidence-based guidance for the management of drug-induced cardiac dysfunctions. The possible role of new biomarkers for the early recognition of cardiotoxicity is mentioned across the clinical studies, with reference to the pharmacological biomarker-driven interventions delivered. To best inform survivorship care, the management and context of cardio-oncology services are discussed within the broader network of providers and settings of care.

Keywords: cardio-oncology; cardiotoxicity; chemotherapy; pharmacotherapy; treatment-related adverse events.

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Conflict of interest statement

G.C. has received honoraria from Pfizer, Novartis, Lilly, and Roche; fees for expert testimony and medical education from Pfizer; has participated in advisory boards for Pfizer, Roche, Lilly, Novartis, Seattle Genetics, and Celltrion. G.P., D.T., P.Z., and E.N. have no potential conflicts of interest to disclose regarding this paper. Although the declaration of interests has been provided to allow for the highest standard for transparency, the authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest for this specific work.

Figures

Figure 1
Figure 1
The spectrum of cardiac toxicity and the most common related causative antineoplastic agents.
Figure 2
Figure 2
Overview of the current clinical use of cardiac protective agents across the continuum of cardiotoxicity. ACE-Is: angiotensin-converting enzyme inhibitors, bBs: beta blockers, CV: cardiovascular, DXR: dexrazoxane, HF: heart failure, HFT: heart-failure-specific therapy, LVEF: left ventricular ejection fraction, RFC: risk factors control, RFs: risk factors.
Figure 3
Figure 3
Proposed framework to identify the critical points for medical interventions to prevent and treat cardiotoxicity. The identification of cancer patients that are more susceptible to cardiac toxicity can prompt the development of interventions of primary prevention, which is adjusted for cancer types, previous treatments, and planned therapies. Validating prognostic and predictive biomarkers is critical for defining the benefits of early interventions, based on quality endpoints of cardiovascular mortality. The current strategy of the management of cardio-toxicity commonly takes the form of a tertiary type, treating patients with functional-structural alterations and cardiovascular symptoms. Eventually, the risk-adapted plans of follow-up can reduce the excessive medicalization and medical harms.

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