Case report
In February 2012, a 59-year-old female patient was referred to the internal medicine emergency department after five days of …show more content…
Similarly to 5-FU, capecitabine belongs to the group of fluoropyrimidines (antimetabolites, i.e. pyrimidine analogues). It is an oral 5-FU analogue (a 5-FU precursor) that is enzymatically transformed into its active form, the 5-FU, within tumour cells. 5-FU inhibits DNA synthesis and thus the growth of tumour cells. Therefore, the possible adverse effects of both agents are similar. Capecitabine and fluoropyrimidines are associated with a wide range of cardiotoxic effects, including angina, myocardial infarction, congestive heart failure, cardiomyopathy, arrhythmias, sudden cardiac death, cardiogenic shock and coronary artery dissection.1 The mechanism of cardiotoxicity is unclear, but may include coronary artery vasospasm, autoimmune cardiomyopathy, direct endothelial damage, thrombogenic effect of the therapy, direct myocardial toxicity leading to necrosis, global dysfunction and the accumulation of metabolites.1,2,4 Until now, approximately 30 studies examining cardiotoxic effects of 5-FU and capecitabine were conducted. The most common fluoropyrimidines-induced cardiac symptom is angina, occurring in up to 20% of 5-FU-treated patients.5 When 5-FU is administered as infusion (half-life: 10–12 minutes), angina may last for as much as 12 hours after the infusion is completed, while with capecitabine, the effect may last even longer due to the accumulation of metabolites and precursors in the body. With prolonged infusions of 5-FU angina is more common.5 Typically, pain is felt behind the sternum and the ECG usually shows ST abnormalities, while troponin levels may not be elevated. Development of angina is more likely in patients with existing cardiovascular disease, although this is not a prerequisite.1–8 The angina-causing mechanism is supposed to be vascular smooth muscle constriction resulting from activation of the protein