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Cancer Therapy-Induced Cardiomyopathy

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Essential Cardiology

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Abstract

Modern advances in cancer treatment have resulted in a steady improvement in life expectancy in cancer patients. However, cardiovascular toxicity is one of the most devastating complications threatening to offset the substantive reductions in cancer-related morbidity and mortality that has been achieved with novel chemotherapeutic agents. Cardiologists and oncologists must collaborate closely to provide effective cancer therapy to kill cancer cells while minimizing toxicity to the cardiovascular system. Structural, functional, or biochemical indicators of cardiac injury are emerging as potential markers for early detection of cardiotoxicity. Imaging modalities such as tissue Doppler imaging, strain imaging, and cardiac magnetic resonance imaging have shown promise in earlier detection of cardiotoxicity. Biomarkers such as troponin I may also play an adjunctive role in earlier recognition of cardiotoxicity and identifying high-risk patients. There have been significant advances in the understanding of the mechanisms of cancer therapy-induced cardiotoxicity. These new pathways have been instrumental in the testing of preventive therapies. Several agents have been investigated in their ability to protect normal cardiac tissue during cancer therapy. These include dexrazoxane, angiotensin-converting enzyme inhibitors, and beta-blockers. However, further studies are warranted to clarify the efficacy, safety, and cancer treatment-related effects of these agents. Once clinical signs or symptoms of cardiac dysfunction develop, the patients should be promptly treated with standard heart failure therapy, and offending agents should be stopped. In some patients, cancer therapy may be resumed following the restoration of cardiac function. Close collaboration between the cardiologists and oncologists will herald in a new era where cancer patients will have a healthy heart to enjoy life after cancer therapy.

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Recommended Readings

  • Cardinale D et al. Anthracycline-induced cardiomyopathy: clinical relevance and response to pharmacologic therapy. J Am Coll Cardiol. 2010;55:213–20.

    Article  PubMed  CAS  Google Scholar 

  • Ewer MS, Lippman SM. Type II chemotherapy-related cardiac dysfunction: time to recognize a new entity. J Clin Oncol. 2005;23:2900–2.

    Article  PubMed  CAS  Google Scholar 

  • Hare JL et al. Use of myocardial deformation imaging to detect preclinical myocardial dysfunction before conventional measures in patients undergoing breast cancer treatment with trastuzumab. Am Heart J. 2009;158:294–301.

    Article  PubMed  CAS  Google Scholar 

  • Lyu YL et al. Topoisomerase IIbeta mediated DNA double-strand breaks: Implications in doxorubicin cardiotoxicity and prevention by dexrazoxane. Cancer Res. 2007;67:8839–46.

    Article  PubMed  CAS  Google Scholar 

  • Yeh ET, Bickford CL. Cardiovascular complications of cancer therapy: incidence, pathogenesis, diagnosis, and management. J Am Coll Cardiol. 2009;53:2231–47.

    Article  PubMed  CAS  Google Scholar 

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Authors and Affiliations

  1. Department of Cardiology, The University of Texas, MD Anderson Cancer Center, Houston, TX, USA

    Peter Kim MD, Pimprapa Vejpongsa MD & Edward T. H. Yeh MD

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  1. Peter Kim MD
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  2. Pimprapa Vejpongsa MD
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  3. Edward T. H. Yeh MD
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Correspondence to Edward T. H. Yeh MD .

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  1. The Mount Sinai School of Medicine, The James J. Peters VA Medical Center, Department of Medicine, West Kingsbridge Rd 130, Bronx, 10468, New York, USA

    Clive Rosendorff

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Kim, P., Vejpongsa, P., Yeh, E.T.H. (2013). Cancer Therapy-Induced Cardiomyopathy. In: Rosendorff, C. (eds) Essential Cardiology. Springer, New York, NY. https://doi.org/10.1007/978-1-4614-6705-2_42

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