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Rapidly developing heart failure from capecitabine cardiotoxicity: a case study

Capecitabine is a pyrimidine analogue used as an anti‐neoplastic agent. It is a fluoropyrimidine‐based oral prodrug of 5‐fluorouracil (5‐FU). It exerts its effect by selectively activating a three step enzymatic pathway. The last step is catalysed by the enzyme thymidine phosphorylase 1. 
 
As compared to normal tissues, this enzyme has higher activity in neoplasms than in normal tissues. Hence, 5‐FU tends to accumulate in tumour cells. Capecitabine is currently approved for treatment of metastatic breast cancer and is included in the WHO list of essential medicines. Though 5‐FU has been associated with cardiotoxicity, there have only been a handful of reports linking capecitabine to cardiac dysfunction. Generally speaking, capecitabine is known as a relatively safe drug. However, the most common reversible side effects are hand–foot syndrome (17%), gastrointestinal upset (17%), and nausea (15%) 1. Though 5‐FU has been associated with cardiotoxic effects, capecitabine‐induced myocardial toxicity is rare and has not been much reported. Its incidence is on the rise due to a burgeoning geriatric population and more widespread use of capecitabine 2. In this case report, we describe a male with metastatic breast cancer and no pre‐existing heart disease, who was being treated with capecitabine. Before initiation of chemotherapy, his cardiac function was normal with an ejection fraction of 70%. However, over the next 12 months, he developed progressive exertional dyspnoea. Repeat Transthoracic Echocardiography (TTE) revealed an ejection fraction of 10%.