Doc-to-Doc: Cardiotoxicity of Cancer Therapies
Ronald Witteles, MD is Assistant Professor of Medicine in the Division of Cardiovascular Medicine at Stanford University. He also serves as Associate Director of the Cardiac Care Unit and as Co-Director of the Stanford Amyloid Center. He specializes in advanced heart failure therapies and in the treatment of cardiac disease in patients with malignancies. To contact Dr. Witteles about speaking engagements please call 650-498-4343 or email. For patient referrals, please call the Referring Physician Concierge Service at 866-742-4811, or send an email.
Improvements in cancer therapies over the last several decades have revolutionized the treatment of malignancies – but at the cost of significant ‘off-target’ sideeffects. Cardiotoxicity has been a particularly troublesome issue, and one which has only grown in importance due to the introduction of new cardiotoxic agents, more sensitive methods of screening for cardiotoxicity, and increased survival times for patients with malignancy. Despite increased awareness,many myths exist regarding cardiotoxicity from cancer therapies.
The first myth is that cardiotoxicity is only associated with a small number of tumor types. It is in fact a significant risk with a wide variety of chemotherapy classes, including anthracyclines (e.g. doxorubicin/Adriamycin), anti-Her2 therapy (e.g. trastuzumab/Herceptin), and most tyrosine kinase inhibitors (e.g. sunitinib/Sutent, sorafenib/Nexavar, bevacizumab/ Avastin). These agents are used in the treatment of the vast majority of tumors – most commonly including breast cancer, lymphoma, leukemia, sarcoma, and renal cell carcinoma.
A second myth is that screening for cardiotoxicity has a limited role. In fact, the vast majority of left ventricular dysfunction remains asymptomatic for months-years after injury. By the time that frank heart failure symptoms develop, significant cardiac remodeling has often occurred, much of which may be irreversible. Cardiac imaging is therefore recommended during therapy with potentially cardiotoxic chemotherapeutic agents, and Stanford is exploring the role of biomarkers (e.g. BNP, troponin) for even earlier detection of cardiac injury.
A third myth is that chemotherapy remains the only type of cancer-therapy which causes cardiotoxicity. Chest irradiation used to treat many thoracic malignancies also leads to significant cardioxicity in the form of coronary artery disease, valvular disease, heart failure, pericardial disease, and arrhythmias – and usually manifests many years after the patient’s exposure. Patients with coronary artery disease from radiation exposure often have very proximal lesions in the coronary arteries (the site of the radiation exposure), and commonly present with atypical symptoms due to nerve damage from the irradiation.
A fourth myth is that ‘worrying too much’ about cardiotoxicity will ultimately lead to patients getting inadequate doses of chemotherapy. In fact, the opposite is true. Careful screening can not only help prevent the morbidity/mortality from cardiotoxicity, but can allow early treatment to be initiated such that patients can tolerate their indicated doses of chemotherapy. This minimization of dose-interruptions and/or discontinuations can lead to better cancer outcomes.
Early screening and treatment of cardiotoxicity can make an enormous difference in patient outcomes. Unfortunately, recent research from Stanford highlights the fact that such screening is performed in the minority of patients – and that indicated cardiac therapies are initiated in even fewer. This underscores the importance of a close collaboration between the treating oncologist and a cardiologist well-versed in the issues of cancertherapy- associated cardiotoxicity.
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