A Case of Severe Coronary Spasm Associated with 5-Fluorouracil Chemotherapy

Kim, Sang-Min; Kwak, Cheol-Hoon; Lee, Bora; Kim, Seong Beom; Sir, Jung-Ju; Cho, Wook-Hyun; Choi, Soon-Kun

doi:10.3904/kjim.2012.27.3.342

Cited by 29 publications

(22 citation statements)

References 10 publications

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“…Several reports described patients who developed myocardial ischaemia after infusion of 5-FU [64,65]. The possible explanation is that 5-FU causes protein kinase C-mediated vascular smooth muscle constriction [66].…”

Section: The Influence Of Anti-cancer Agents On Endothelial Homeostasismentioning

confidence: 99%

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Anti-cancer agents and endothelium

et al. 2018

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Recent advances in oncology have improved the treatment outcomes and life expectancy of cancer patients; therefore, late effects of oncological treatment are of high clinical importance. Recent studies have shown that cardiovascular events are among the leading causes of premature morbidity in cancer survivors. Cardiotoxicity of some chemotherapeutic agents have been already confirmed; however, this issue seems to be more complex. Endothelium dysfunction is one of the first recognisable signs of atherosclerosis, which occurs long before the development of overt cardiovascular disease. Thus, it could be considered as an initial step, leading to increased risk of cardiovascular events. This process is not easy to recognise; however, there are some laboratory tests and imagining techniques that provide an insight into the progression of endothelial dysfunction. In this review we discuss the influence of oncological treatment on endothelium, according to the hypothesis that it increases cardiovascular morbidity and mortality in cancer survivors. Additionally, we present diagnostic and therapeutic measures that could reduce cardiovascular risk in cancer patients.

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Section: The Influence Of Anti-cancer Agents On Endothelial Homeostasismentioning

confidence: 99%

“…Vasospasm caused by cisplatin has been successfully treated with calcium channel blockers [105]. Discontinuation of 5-FU infusion together with administration of a calcium channel blocker and nitrate usually gives a good outcome in the case of signs of myocardial ischaemia [65].…”

Section: Other Medicationsmentioning

confidence: 99%

Anti-cancer agents and endothelium

et al. 2018

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“…There are strategies for the protection of cardiac function during anthracycline treatment: primary and secondary prevention [ 4 ]. Primary strategies for the prevention of cardiotoxicity include the continuous infusion of anthracycline and the use of liposomal doxorubicin and the cardioprotective agent dexrazoxane.…”

Section: Strategies For the Protection Of Cardiac Functionmentioning

confidence: 99%

“…Liposomal doxorubicin is approved for limited cancer types. Dexrazoxane is approved only for women with metastatic breast cancer who received at least 300 mg/m 2 doxorubicin and need additional doxorubicin for the maintenance of tumor control [ 4 ]. In animal studies, the concomitant administration of insulin-like growth factor 1 reduced apoptosis in doxorubicin-treated mouse myocardium [ 48 ], and candesartan prevented elastin degradation ( Fig.…”

Section: Strategies For the Protection Of Cardiac Functionmentioning

confidence: 99%

“…Cardiotoxicity can increase mortality not only due to cancer itself but also due to heart failure even if the patient has survived cancer. Many types of cardiotoxicity have been reported, including bradycardia, QT interval prolongation, myocardial ischemia, and cardiomyopathy [ 3 ], and one type of anti-cancer drug may cause various types of cardiotoxicity [ 2 - 4 ]. The pathogenesis of cardiotoxicity is different for each drug.…”

Section: Introductionmentioning

confidence: 99%

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Pathophysiology and preventive strategies of anthracycline-induced cardiotoxicity

Chung

Youn

2016

Korean J Intern Med

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Cardiotoxicity is a well-known complication following treatment with anthracyclines. However, they are still widely used in chemotherapy for breast cancer, lymphoma, leukemia, and sarcoma, among others. Patient clinical characteristics, such as age, sex, comorbidities, anthracycline dose and infusion schedule, and the combined anti-cancer agents used, are diverse among cancer types. It is difficult to recommend guidelines for the prevention or management of anthracycline-induced cardiotoxicity applicable to all cancer types. Therefore, anthracycline-induced cardiotoxicity remains a major limitation in the proper management of cancer patients treated with an anthracycline-combined regimen. Efforts have been extensive to determine the mechanism and treatment of anthracycline-induced cardiotoxicity. Because cardiotoxicity causes irreversible damage to the myocardium, prevention is a more effective approach than treatment of cardiotoxicity after symptomatic or asymptomatic cardiac dysfunction develops. This article will review the pathophysiological mechanisms of anthracycline-induced cardiotoxicity and strategies for protecting the myocardium from anthracycline.

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Myocardial Ischemia Induced by 5-Fluorouracil: A Prospective Electrocardiographic and Cardiac Biomarker Study

et al. 2020

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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-FUbased 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.

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A Case of Severe Coronary Spasm Associated with 5-Fluorouracil Chemotherapy

Cited by 29 publications

References 10 publications

Anti-cancer agents and endothelium

Anti-cancer agents and endothelium

Pathophysiology and preventive strategies of anthracycline-induced cardiotoxicity

Myocardial Ischemia Induced by 5-Fluorouracil: A Prospective Electrocardiographic and Cardiac Biomarker Study

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