Abstract 1893P
Background
Treatment with flouropyrimidines can lead to cardiotoxicity, and for 5-fluorouracil silent myocardial ischemia and effort-related myocardial ischemia have been demonstrated. The present study investigated the incidence of myocardial ischemia and clinical cardiotoxicity during treatment with capecitabine.
Methods
We included patients with breast- or colorectal cancer, who received first-time treatment with capecitabine-based chemotherapy. Holter recording, clinical evaluation, 12-lead electrocardiogram, and assessment of plasma concentrations of troponin I and copeptin were performed before and during treatment (1st and 3rd/4th cycles).
Results
Fourty-two patients with breast cancer and 39 with colorectal cancer were included. Seven patients (8.6%) experienced symptomatic cardiotoxicity; five with unstable angina, one with dyspnea, ST elevations and anterolateral hypokinesia and one with cardiac arrest. Six patients (7.5%) had myocardial ischemia on Holter recording during treatment, whereof 4 patients (5.0%) had silent myocardial ischemia. Although numerically more patients had myocardial ischemia on Holter recording during treatment with capecitabine (5 in 1st cycle, 3 in 3rd/4th cycle) compared to before (1 before 1st cycle, 1 before 3rd/4th cycle), the difference was not statistically significant, neither in 1st cycle (P = .219) nor 3rd/4th cycle (P = .500). The incidence of myocardial ischemia during capecitabine treatment was lower than previously reported for 5-flourouracil (95% CI of the difference: 1.9%–20.6%, P = 0.029). Plasma copeptin increased during first cycle (P = .004), while troponin I remained unchanged (P = .924). More patients had non-sustained ventricular tachycardia during first cycle of treatment than before (P = .021).
Conclusions
The incidence of myocardial ischemia on Holter recording was significantly lower for capecitabine compared to 5-fluorouracil, but clinical events were comparable between the two treatments. Treatment with capecitabine was associated with an increase in plasma copeptin and an increase in the frequency of non-sustained ventricular tachycardia, while increases in troponin I were rare.
Clinical trial identification
Editorial acknowledgement
Legal entity responsible for the study
The authors.
Funding
University of Copenhagen, the Danish Heart Foundation (grant number 16-R107-A6601-22016), Manufacturer Einar Willumsen Foundation, Aase and Ejnar Danielsen Foundation, Engineer August Frederik Wedell Erichsen Foundation, The Foundation of 17-12-1981, The Foundation for the promotion of Clinical Cancer Research and The Højmosegaard Grant/The Danish Medical Research Grant (grant number 2017-1064/91).
Disclosure
All authors have declared no conflicts of interest.
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Abstract