Merna A Armanious1,2, Shreya Mishra1, Michael G Fradley3,4. 1. Division of Cardiovascular Medicine, University of South Florida, 2 Tampa General Circle, Tampa, FL, 33606, USA. 2. Cardio-Oncology Program, H. Lee Moffitt Cancer Center & Research Institute, 12902 Magnolia Drive, Tampa, FL, 33612, USA. 3. Division of Cardiovascular Medicine, University of South Florida, 2 Tampa General Circle, Tampa, FL, 33606, USA. mfradley@health.usf.edu. 4. Cardio-Oncology Program, H. Lee Moffitt Cancer Center & Research Institute, 12902 Magnolia Drive, Tampa, FL, 33612, USA. mfradley@health.usf.edu.
Abstract
PURPOSE OF REVIEW: There is growing awareness of the link between oncology treatments and cardiovascular (CV) complications. This has led to the development of cardio-oncology, a specialty aimed at managing CV risk and disease in cancer patients and survivors. Cardiac arrhythmias are potential adverse CV complications of cancer treatments; however, these cardiotoxicities are often underappreciated due to the uncertain arrhythmogenic mechanisms of various chemotherapeutic agents. RECENT FINDINGS: Chemotherapeutic agents can induce arrhythmias via direct electrophysiological effects on ion channels or intracellular signaling pathways, or indirectly from cardiac tissue damage. As more drugs are being linked to the development of arrhythmias, a deeper understanding of the pathophysiology of their electrophysiological (EP) effects will be necessary. Expanding research in this field has allowed for the identification of novel agents with potential arrhythmogenic properties and the development of preventative measures, early recognition, and closer surveillance of patients more susceptible to these EP side effects.
PURPOSE OF REVIEW: There is growing awareness of the link between oncology treatments and cardiovascular (CV) complications. This has led to the development of cardio-oncology, a specialty aimed at managing CV risk and disease in cancerpatients and survivors. Cardiac arrhythmias are potential adverse CV complications of cancer treatments; however, these cardiotoxicities are often underappreciated due to the uncertain arrhythmogenic mechanisms of various chemotherapeutic agents. RECENT FINDINGS: Chemotherapeutic agents can induce arrhythmias via direct electrophysiological effects on ion channels or intracellular signaling pathways, or indirectly from cardiac tissue damage. As more drugs are being linked to the development of arrhythmias, a deeper understanding of the pathophysiology of their electrophysiological (EP) effects will be necessary. Expanding research in this field has allowed for the identification of novel agents with potential arrhythmogenic properties and the development of preventative measures, early recognition, and closer surveillance of patients more susceptible to these EP side effects.
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