Journal
JOURNAL OF CLINICAL ONCOLOGY
Volume 28, Issue 36, Pages 5280-5286Publisher
AMER SOC CLINICAL ONCOLOGY
DOI: 10.1200/JCO.2009.27.3953
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Funding
- Augustinus Foundation
- Merchant M. Brogaard and Wife's Foundation
- Harboe Foundation
- Karen A. Tolstrup Foundation
- Dagmar Marshall's Foundation
- A.P. Moller Foundation for the Advancement of Medical Science
- Hartmann Brothers Foundation
- Director Michael Hermann Nielsen's Foundation
- Manufacturer Einar Willumsen Foundation
- Merchant Sven Hansen and wife Ina Hansen Foundation
- Torben and Alice Frimodt Foundation
- Mastersmith Niels Hansen and Wife Foundation
- Director Werner Richter and Wife Foundation
- Else and Mogens Wedell-Wedellsborg Foundation
- Desiree and Niels Yde Foundation
- Aase and Ejnar Danielsen Foundation
- Director Jacob Madsen and Wife Olga Madsen Foundation
- Director Ib Henriksen Foundation
- Merchant M. Kristian Kjaer and Wife Foundation
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Purpose Fluorouracil (FU) is a cornerstone of colorectal cancer treatment; however, it has clinical and subclinical influence on the heart. This study aimed to clarify the pathophysiology, risk factors, and long-term effects of FU cardiotoxicity. Patients and Methods The study prospectively accrued colorectal cancer patients (n = 106) completely resected and adjuvantly treated with FU and oxaliplatin according to the FOLFOX4 regimen (infusional FU, folinic acid, and oxaliplatin). Serial measurements were made of systolic and diastolic features of the left ventricle by radionuclide ventriculography, plasma levels of N-terminal pro-brain natriuretic peptide (NT-proBNP), lactic acid, and ECG before chemotherapy, immediately after a treatment infusion, and at follow-up 2 weeks after cessation of the intended 12 treatment courses and were further evaluated by multivariate regression analysis that included cardiovascular history and its risk factors. Results In the entire cohort, NT-proBNP significantly increased from baseline 14.5 +/- 3.2 pmol/L (mean +/- standard error) to 28.3 +/- 5.3 pmol/L during FU therapy (P < .001). Nine patients (8.5%) with cardiotoxicity had significantly higher NT-proBNP of 55.3 +/- 40.8 pmol/L compared with 25.4 +/- 4.1 pmol/L in those without (P < .001). In multivariate analysis, the FU-induced rise of NT-proBNP was significantly higher in females (P < .001). Plasma lactic acid significantly increased from baseline (1.3 +/- 0.1 mmol/L to 1.8 +/- 0.1 mmol/L) during FU therapy (P < .001). Left ventricular ejection fraction at baseline of 0.66 +/- 0.01 remained unchanged at 0.65 +/- 0.01 during FU therapy and 0.66 +/- 0.01 at follow-up (P = .4). Conclusion FU therapy generally induces myocardial neuroendocrine changes with increasing plasma NT-proBNP and lactic acid but without long-term dysfunction of the left ventricle. The usability of NT-proBNP as a predictive marker for FU cardiotoxicity remains to be clarified.
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