Myocardial Ischemia Induced by 5-Fluorouracil: A Prospective Electrocardiographic and Cardiac Biomarker Study
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Myocardial Ischemia Induced by 5-Fluorouracil : A Prospective Electrocardiographic and Cardiac Biomarker Study. / Dyhl-Polk, Anne; Schou, Morten; Vistisen, Kirsten K.; Sillesen, Anne Sophie; Serup-Hansen, Eva; Faber, Jens; Klausen, Tobias W.; Bojesen, Stig E.; Vaage-Nilsen, Merete; Nielsen, Dorte L.
I: Oncologist, Bind 26, Nr. 3, 2021, s. e403-e413.Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › fagfællebedømt
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TY - JOUR
T1 - Myocardial Ischemia Induced by 5-Fluorouracil
T2 - A Prospective Electrocardiographic and Cardiac Biomarker Study
AU - Dyhl-Polk, Anne
AU - Schou, Morten
AU - Vistisen, Kirsten K.
AU - Sillesen, Anne Sophie
AU - Serup-Hansen, Eva
AU - Faber, Jens
AU - Klausen, Tobias W.
AU - Bojesen, Stig E.
AU - Vaage-Nilsen, Merete
AU - Nielsen, Dorte L.
PY - 2021
Y1 - 2021
N2 - Background: Cardiotoxicity induced by 5-fluorouracil (5-FU) is well known but poorly understood. In this study, we undertook ECG recording (Holter) and analyses of the biomarkers troponin and copeptin in patients receiving 5-FU to increase our understanding of the cardiotoxicity. Subjects, Materials, and Methods: Patients with colorectal or anal cancer that received first-time treatment with 5-FU-based chemotherapy were prospectively included. Holter recording, clinical evaluation, 12-lead electrocardiogram, and assessment of plasma concentrations of troponin I and copeptin were performed before (control) and during 5-FU treatment (intervention). Results: A total of 108 patients were included, 82 with colorectal and 26 with anal cancer. The proportion of patients with myocardial ischemia on Holter recording was significantly higher during the first 5-FU infusion (14.1%) than before (3.7%; p =.001). The ischemic burden per day (p =.001), the number of ST depression episodes per day (p =.003), and the total duration of ischemic episodes per day (p =.003) were higher during the first 5-FU infusion than before, as was plasma copeptin (p <.001), whereas plasma troponin I was similar (p > 0.999). Six patients (5.6%) developed acute coronary syndromes and two (1.8%) developed symptomatic arrhythmias during 5-FU treatment. Conclusion: 5-FU infusion is associated with an increase in the number of patients with myocardial ischemia on Holter recording. According to biomarker analyses, 5-FU is associated with an increase in copeptin, but rarely with increases in cardiac troponin I. However, 5%–6% of the patients developed acute coronary syndromes during treatment with 5-FU. Implications for Practice: Symptomatic 5-fluorouracil (5-FU) cardiotoxicity occurs in 0.6%–19% of patients treated with this drug, but a small electrocardiographic (Holter) study has revealed silent myocardial ischemia in asymptomatic patients, suggesting a more prevalent subclinical cardiac influence. This study demonstrated a significant increase in the number of patients with myocardial ischemia on Holter recording during 5-FU treatment and an increase in ischemic burden. Cardiac biomarker analyses suggested that 5-FU infusion results in endogenous stress (increased copeptin) but rarely induces myocyte injury (no change in troponin). These findings suggest a more prevalent cardiac influence from 5-FU and that Holter recording is an important tool in the evaluation of patients with suspected cardiotoxicity from 5-FU.
AB - Background: Cardiotoxicity induced by 5-fluorouracil (5-FU) is well known but poorly understood. In this study, we undertook ECG recording (Holter) and analyses of the biomarkers troponin and copeptin in patients receiving 5-FU to increase our understanding of the cardiotoxicity. Subjects, Materials, and Methods: Patients with colorectal or anal cancer that received first-time treatment with 5-FU-based chemotherapy were prospectively included. Holter recording, clinical evaluation, 12-lead electrocardiogram, and assessment of plasma concentrations of troponin I and copeptin were performed before (control) and during 5-FU treatment (intervention). Results: A total of 108 patients were included, 82 with colorectal and 26 with anal cancer. The proportion of patients with myocardial ischemia on Holter recording was significantly higher during the first 5-FU infusion (14.1%) than before (3.7%; p =.001). The ischemic burden per day (p =.001), the number of ST depression episodes per day (p =.003), and the total duration of ischemic episodes per day (p =.003) were higher during the first 5-FU infusion than before, as was plasma copeptin (p <.001), whereas plasma troponin I was similar (p > 0.999). Six patients (5.6%) developed acute coronary syndromes and two (1.8%) developed symptomatic arrhythmias during 5-FU treatment. Conclusion: 5-FU infusion is associated with an increase in the number of patients with myocardial ischemia on Holter recording. According to biomarker analyses, 5-FU is associated with an increase in copeptin, but rarely with increases in cardiac troponin I. However, 5%–6% of the patients developed acute coronary syndromes during treatment with 5-FU. Implications for Practice: Symptomatic 5-fluorouracil (5-FU) cardiotoxicity occurs in 0.6%–19% of patients treated with this drug, but a small electrocardiographic (Holter) study has revealed silent myocardial ischemia in asymptomatic patients, suggesting a more prevalent subclinical cardiac influence. This study demonstrated a significant increase in the number of patients with myocardial ischemia on Holter recording during 5-FU treatment and an increase in ischemic burden. Cardiac biomarker analyses suggested that 5-FU infusion results in endogenous stress (increased copeptin) but rarely induces myocyte injury (no change in troponin). These findings suggest a more prevalent cardiac influence from 5-FU and that Holter recording is an important tool in the evaluation of patients with suspected cardiotoxicity from 5-FU.
KW - 5-Flourouracil
KW - Anal cancer
KW - Cardiotoxicity
KW - Colorectal cancer
KW - Myocardial ischemia
U2 - 10.1002/onco.13536
DO - 10.1002/onco.13536
M3 - Journal article
C2 - 32959474
AN - SCOPUS:85092176300
VL - 26
SP - e403-e413
JO - Oncologist
JF - Oncologist
SN - 1083-7159
IS - 3
ER -
ID: 260243838