Cardiovascular Complications of Cancer Therapy

Abstract

Abstract-The cardiotoxicity of anticancer agents can lead to significant complications that can affect patients being treated for various malignancies. The severity of such toxicity depends on many factors such as the molecular site of action, the immediate and cumulative dose, the method of administration, the presence of any underlying cardiac condition, and the demographics of the patient. Moreover, toxicity can be affected by current or previous treatment with other antineoplastic agents. Cardiotoxic effects can occur immediately during administration of the drug, or they may not manifest themselves until months or years after the patient has been treated. In this article we review commonly used chemotherapy agents, including several recently approved medications, for their propensity to cause cardiotoxicity. Further research will be required to more accurately predict which patients are at risk for developing cardiotoxicity. In addition, management plans, as well as strategies to reduce cardiotoxicity, need to be developed.

Transactivation of the epidermal growth factor receptor in responses to myocardial stress and cardioprotection

“…Shifts in EGFR functionality may contribute to pathogenesis of ischaemic heart disease and cardiomyopathies. This is consistent with the cardiotoxicity of anti-cancer therapies targeting EGFR tyrosine kinase (Yeh and Bickford, 2009), and cardiac dysfunction with EGFR (ErbB1) mutation (Rajagopalan et al, 2008) or inhibition (Barrick et al, 2008).…”

Gemcitabine induced cardiomyopathy: a case of multiple hit cardiotoxicity

“…The delayed toxicity of doxorubicin, in combination with the direct cytotoxic effects and apoptosis seen with cyclophosphamide, led to her initial drop in LVEF 4, 15. Subsequent exposure to cisplatin in May 2014 further damaged DNA repair mechanisms and quickly depressed our patient's LVEF to 25%.…”

“…The mechanism of cardio‐toxicity here involves disruption of topoisomerase‐II‐mediated DNA repair and generation of oxygen‐derived free radicals 4, 5, 6, 7. Serial echocardiograms during several years after doxorubicin administration showed stable LVEF.…”

“…Cyclophosphamide can cause endothelial and myocyte injury mediated through its toxic metabolic phosphoramide mustard that leads to DNA crosslinking and subsequent apoptosis 4. The patient was then exposed to R‐DHAP, of which, cisplatin has been shown to cause congestive heart failure, particularly in the elderly.…”

“…The patient was then exposed to R‐DHAP, of which, cisplatin has been shown to cause congestive heart failure, particularly in the elderly. Its mode of toxicity involves crosslinking with purine bases on the DNA and thus interfering with DNA repair mechanisms, causing DNA damage and cell apoptosis 4, 6…”