Key result
Capecitabine treatment was associated with an 8% incidence of myocardial ischemia and a 9% incidence of clinical cardiotoxicity, though the increase in ischemia compared to baseline was not statistically significant.
Why the study?
Fluoropyrimidines can cause cardiotoxicity and 5-fluorouracil is known to cause myocardial ischemia, but the incidence of ischemia and clinical cardiotoxicity with capecitabine was not established.
Does capecitabine treatment induce myocardial ischemia or clinical cardiotoxicity in patients with breast or colorectal cancer?
Cohort (n=81)
No
Does capecitabine treatment induce myocardial ischemia or clinical cardiotoxicity in patients with breast or colorectal cancer?
Absolute Event Rate: 8% vs 1%
p-value: p=0.22
First-time capecitabine treatment is associated with a 9% rate of clinical cardiotoxicity and increased NSVT, though the incidence of myocardial ischemia appears lower than historically reported for 5-fluorouracil.
Capecitabine was associated with 8-9% ischemia/cardiotoxicity rates; leaves open need for prospective monitoring trials before practice change.
BACKGROUND AND PURPOSE: Treatment with fluoropyrimidines can lead to cardiotoxicity. For 5-fluorouracil, silent myocardial ischemia and effort-related myocardial ischemia have been demonstrated. We investigated the incidence of myocardial ischemia and clinical cardiotoxicity during treatment with capecitabine, a pro-drug of 5-fluorouracil. PATIENTS AND METHODS: We included patients with breast- or colorectal cancer, who received first-time treatment with capecitabine. Holter recording, clinical evaluation, 12-lead electrocardiogram, and measurement of plasma cardiac troponin I and copeptin were performed before and during treatment. RESULTS: A total of 42 patients with breast cancer and 39 with colorectal cancer were included. Seven patients (9%) experienced clinical cardiotoxicity; five with unstable angina, one with dyspnoea, ST elevations and anterolateral hypokinesia, and one with cardiac arrest. Six patients (8%) had myocardial ischemia on Holter recording during treatment. Among these were two with clinical cardiotoxicity, and four (5.0%) with silent myocardial ischemia. More patients had myocardial ischemia on Holter recording during treatment compared to before, but the difference was not statistically significant (1st cycle: p = 0.22, 3rd/4th cycle: p = 0.50). Plasma copeptin increased during 1st cycle (p = 0.004), while cardiac troponin I remained unchanged (p = 0.92). More patients had non-sustained ventricular tachycardia during 1st cycle of treatment than before (p = 0.020). INTERPRETATION: Treatment with capecitabine was associated with an incidence of myocardial ischemia of 8%, an incidence of clinical cardiotoxicity of 9%, and an increase in plasma copeptin and the frequency of non-sustained ventricular tachycardia episodes. Increases in cardiac troponin I were rare. The incidence of myocardial ischemia was lower than previously reported for 5-fluorouracil.
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Dyhl-Polk et al. (2025) conducted a cohort in Breast or colorectal cancer (n=81). Capecitabine vs. Baseline (before treatment) was evaluated on Myocardial ischemia on Holter recording or 12-lead ECG (p=0.22). Capecitabine treatment was associated with an 8% incidence of myocardial ischemia and a 9% incidence of clinical cardiotoxicity, though the increase in ischemia compared to baseline was not statistically significant.
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