| Peer-Reviewed

Bevacizumab Induced Cardiomyopathy in a Patient with Adult Congenital Heart Disease: A Case Report and Brief Review

Received: 3 March 2015     Accepted: 23 March 2015     Published: 21 April 2015
Views:       Downloads:
Abstract

Background: Cardiac dysfunction is an unusual but documented side effect of many forms of antineoplastic therapy. Bevacizumab is a novel antineoplastic agent that inhibits VEGF-A with a low reported incidence of cardiotoxicity (1.7 - 3%) derived primarily from clinical trials of women with breast cancer which captured adverse events of symptomatic heart failure. Subsequent studies suggest the incidence of asymptomatic decline in cardiac function may be closer to 20%. Untreated declines in cardiac function are associated with increased morbidity and mortality, early recognition and treatment can improve outcomes. Case Report: Here we describe a case of a 51 year old male being treated with Bevacizumab for metastatic neuroendocrine cancer of the colon who developed a severe asymptomatic decline in cardiac function. With interruption of Bevacizumab and implementation of heart failure therapy his cardiac function returned to baseline. Conclusion: Early recognition and application of heart failure disease modifying therapy can decrease the risk and improve the likelihood of recovery in cases of chemotherapy induced cardiac dysfunction. Baseline cardiac testing and standardized surveillance can increase the opportunities for early intervention and may improve long term outcomes.

Published in Journal of Cancer Treatment and Research (Volume 3, Issue 3)
DOI 10.11648/j.jctr.20150303.12
Page(s) 32-36
Creative Commons

This is an Open Access article, distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution and reproduction in any medium or format, provided the original work is properly cited.

Copyright

Copyright © The Author(s), 2015. Published by Science Publishing Group

Keywords

Heart Failure, Chemotherapy, Cardiotoxic Agents, Bevacizumab, Cardiac Remodeling, Ventricular

References
[1] Shih T, Lindley C. Bevacizumab: an angiogenesis inhibitor for the treatment of solid malignancies. Clinical therapeutics. 2006;28(11):1779-802.
[2] Eschenhagen T, Force T, Ewer MS, et al. Cardiovascular side effects of cancer therapies: a position statement from the Heart Failure Association of the European Society of Cardiology. European journal of heart failure. 2011;13(1):1-10.
[3] Force T, Kerkela R. Cardiotoxicity of the new cancer therapeutics--mechanisms of, and approaches to, the problem. Drug discovery today. 2008;13(17-18):778-84.
[4] Grazette LP, Boecker W, Matsui T, et al. Inhibition of ErbB2 causes mitochondrial dysfunction in cardiomyocytes: implications for herceptin-induced cardiomyopathy. Journal of the American College of Cardiology. 2004;44(11):2231-8.
[5] Kerkela R, Grazette L, Yacobi R, et al. Cardiotoxicity of the cancer therapeutic agent imatinib mesylate. Nature medicine. 2006;12(8):908-16.
[6] Force T. Double-edged sword of the new cancer therapeutics. Circulation. 2012;125(17):2057-8.
[7] Folkman J. Tumor angiogenesis: therapeutic implications. The New England journal of medicine. 1971;285(21):1182-6.
[8] Ferrara N, Henzel WJ. Pituitary follicular cells secrete a novel heparin-binding growth factor specific for vascular endothelial cells. Biochemical and biophysical research communications. 1989;161(2):851-8.
[9] Senger DR, Galli SJ, Dvorak AM, et al. Tumor cells secrete a vascular permeability factor that promotes accumulation of ascites fluid. Science. 1983;219(4587):983-5.
[10] Koch S, Claesson-Welsh L. Signal transduction by vascular endothelial growth factor receptors. Cold Spring Harbor perspectives in medicine. 2012;2(7):a006502.
[11] Giordano FJ, Gerber HP, Williams SP, et al. A cardiac myocyte vascular endothelial growth factor paracrine pathway is required to maintain cardiac function. Proceedings of the National Academy of Sciences of the United States of America. 2001;98(10):5780-5.
[12] Zentilin L, Puligadda U, Lionetti V, et al. Cardiomyocyte VEGFR-1 activation by VEGF-B induces compensatory hypertrophy and preserves cardiac function after myocardial infarction. FASEB journal : official publication of the Federation of American Societies for Experimental Biology. 2010;24(5):1467-78.
[13] Izumiya Y, Shiojima I, Sato K, et al. Vascular endothelial growth factor blockade promotes the transition from compensatory cardiac hypertrophy to failure in response to pressure overload. Hypertension. 2006;47(5):887-93.
[14] Taimeh Z, Loughran J, Birks EJ, Bolli R. Vascular endothelial growth factor in heart failure. Nature reviews Cardiology. 2013;10(9):519-30.
[15] Mukherji SK. Bevacizumab (Avastin). AJNR American journal of neuroradiology. 2010;31(2):235-6.
[16] Choueiri TK, Mayer EL, Je Y, et al. Congestive heart failure risk in patients with breast cancer treated with bevacizumab. Journal of clinical oncology : official journal of the American Society of Clinical Oncology. 2011;29(6):632-8.
[17] Chen XL, Lei YH, Liu CF, et al. Angiogenesis inhibitor bevacizumab increases the risk of ischemic heart disease associated with chemotherapy: a meta-analysis. PloS one. 2013;8(6):e66721.
[18] Stopeck AT, Unger JM, Rimsza LM, et al. A phase 2 trial of standard-dose cyclophosphamide, doxorubicin, vincristine, prednisone (CHOP) and rituximab plus bevacizumab for patients with newly diagnosed diffuse large B-cell non-Hodgkin lymphoma: SWOG 0515. Blood. 2012;120(6):1210-7.
[19] Qi WX1, Fu S, Zhang Q, Guo XM. Bevacizumab increases the risk of severe congestive heart failure in cancer patients: an up-to-date meta-analysis with a focus on different subgroups.Clin Drug Investig. 2014 Oct;34(10):681-90
[20] Williams SP, Gerber HP, Giordano FJ, et al. Dobutamine stress cine-MRI of cardiac function in the hearts of adult cardiomyocyte-specific VEGF knockout mice. Journal of magnetic resonance imaging : JMRI. 2001;14(4):374-82.
[21] Minotti G, Salvatorelli E, Menna P. Pharmacological foundations of cardio-oncology. The Journal of pharmacology and experimental therapeutics. 2010;334(1):2-8.
[22] Lionetti V, Matteucci M, Ribezzo M, et al. Regional mapping of myocardial hibernation phenotype in idiopathic end-stage dilated cardiomyopathy. Journal of cellular and molecular medicine. 2014;18(3):396-414.
[23] Naranjo CA, Busto U, Sellers EM, et al. A method for estimating the probability of adverse drug reactions. Clin Pharmacol Ther. 1981;30(2):239-45.
[24] Centre TUM. The use of the WHO-UMC system for standardised case causality assessment.
[25] J.V. McMurray JEM, Pamela N. Peterson, Barbara Riegel, Flora Sam, Lynne W., Johnson EKK, Wayne C. Levy, Frederick A. Masoudi, Patrick E. McBride, John, Drazner GCF, Stephen A. Geraci, Tamara Horwich, James L. Januzzi, Maryl R., et al. 2013 ACCF/AHA Guideline for the Management of Heart Failure: A Report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines Circulation. 2013;128:: e240-e327.
[26] Bovelli D, Plataniotis G, Roila F, Group EGW. Cardiotoxicity of chemotherapeutic agents and radiotherapy-related heart disease: ESMO Clinical Practice Guidelines. Annals of oncology : official journal of the European Society for Medical Oncology / ESMO. 2010;21 Suppl 5:v277-82.
Cite This Article
  • APA Style

    Hemalatha Narayanasamy, Nikky Bardia, Michael Fong, Luanda Grazette. (2015). Bevacizumab Induced Cardiomyopathy in a Patient with Adult Congenital Heart Disease: A Case Report and Brief Review. Journal of Cancer Treatment and Research, 3(3), 32-36. https://doi.org/10.11648/j.jctr.20150303.12

    Copy | Download

    ACS Style

    Hemalatha Narayanasamy; Nikky Bardia; Michael Fong; Luanda Grazette. Bevacizumab Induced Cardiomyopathy in a Patient with Adult Congenital Heart Disease: A Case Report and Brief Review. J. Cancer Treat. Res. 2015, 3(3), 32-36. doi: 10.11648/j.jctr.20150303.12

    Copy | Download

    AMA Style

    Hemalatha Narayanasamy, Nikky Bardia, Michael Fong, Luanda Grazette. Bevacizumab Induced Cardiomyopathy in a Patient with Adult Congenital Heart Disease: A Case Report and Brief Review. J Cancer Treat Res. 2015;3(3):32-36. doi: 10.11648/j.jctr.20150303.12

    Copy | Download

  • @article{10.11648/j.jctr.20150303.12,
      author = {Hemalatha Narayanasamy and Nikky Bardia and Michael Fong and Luanda Grazette},
      title = {Bevacizumab Induced Cardiomyopathy in a Patient with Adult Congenital Heart Disease: A Case Report and Brief Review},
      journal = {Journal of Cancer Treatment and Research},
      volume = {3},
      number = {3},
      pages = {32-36},
      doi = {10.11648/j.jctr.20150303.12},
      url = {https://doi.org/10.11648/j.jctr.20150303.12},
      eprint = {https://article.sciencepublishinggroup.com/pdf/10.11648.j.jctr.20150303.12},
      abstract = {Background: Cardiac dysfunction is an unusual but documented side effect of many forms of antineoplastic therapy. Bevacizumab is a novel antineoplastic agent that inhibits VEGF-A with a low reported incidence of cardiotoxicity (1.7 - 3%) derived primarily from clinical trials of women with breast cancer which captured adverse events of symptomatic heart failure. Subsequent studies suggest the incidence of asymptomatic decline in cardiac function may be closer to 20%. Untreated declines in cardiac function are associated with increased morbidity and mortality, early recognition and treatment can improve outcomes. Case Report: Here we describe a case of a 51 year old male being treated with Bevacizumab for metastatic neuroendocrine cancer of the colon who developed a severe asymptomatic decline in cardiac function. With interruption of Bevacizumab and implementation of heart failure therapy his cardiac function returned to baseline. Conclusion: Early recognition and application of heart failure disease modifying therapy can decrease the risk and improve the likelihood of recovery in cases of chemotherapy induced cardiac dysfunction. Baseline cardiac testing and standardized surveillance can increase the opportunities for early intervention and may improve long term outcomes.},
     year = {2015}
    }
    

    Copy | Download

  • TY  - JOUR
    T1  - Bevacizumab Induced Cardiomyopathy in a Patient with Adult Congenital Heart Disease: A Case Report and Brief Review
    AU  - Hemalatha Narayanasamy
    AU  - Nikky Bardia
    AU  - Michael Fong
    AU  - Luanda Grazette
    Y1  - 2015/04/21
    PY  - 2015
    N1  - https://doi.org/10.11648/j.jctr.20150303.12
    DO  - 10.11648/j.jctr.20150303.12
    T2  - Journal of Cancer Treatment and Research
    JF  - Journal of Cancer Treatment and Research
    JO  - Journal of Cancer Treatment and Research
    SP  - 32
    EP  - 36
    PB  - Science Publishing Group
    SN  - 2376-7790
    UR  - https://doi.org/10.11648/j.jctr.20150303.12
    AB  - Background: Cardiac dysfunction is an unusual but documented side effect of many forms of antineoplastic therapy. Bevacizumab is a novel antineoplastic agent that inhibits VEGF-A with a low reported incidence of cardiotoxicity (1.7 - 3%) derived primarily from clinical trials of women with breast cancer which captured adverse events of symptomatic heart failure. Subsequent studies suggest the incidence of asymptomatic decline in cardiac function may be closer to 20%. Untreated declines in cardiac function are associated with increased morbidity and mortality, early recognition and treatment can improve outcomes. Case Report: Here we describe a case of a 51 year old male being treated with Bevacizumab for metastatic neuroendocrine cancer of the colon who developed a severe asymptomatic decline in cardiac function. With interruption of Bevacizumab and implementation of heart failure therapy his cardiac function returned to baseline. Conclusion: Early recognition and application of heart failure disease modifying therapy can decrease the risk and improve the likelihood of recovery in cases of chemotherapy induced cardiac dysfunction. Baseline cardiac testing and standardized surveillance can increase the opportunities for early intervention and may improve long term outcomes.
    VL  - 3
    IS  - 3
    ER  - 

    Copy | Download

Author Information
  • Keck School of Medicine of USC, Department of Medicine, Los Angles, California, USA

  • Keck School of Medicine of USC, Department of Medicine, Los Angles, California, USA

  • Division of Cardiovascular Medicine, Keck Medical Center of USC, University of Southern California, Los Angeles, California, USA

  • Division of Cardiovascular Medicine, Keck Medical Center of USC, University of Southern California, Los Angeles, California, USA

  • Sections