Coronary artery spasm induced by 5-fluorouracil

Luwaert, R.; Descamps, Olivier; Majois, F.; Chaudron, J M; Beauduin, M.

doi:10.1093/oxfordjournals.eurheartj.a059919

Cited by 65 publications

(39 citation statements)

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“…Coronary vasospasm has historically been accepted as the main contributor to this clinical entity. Ultrasound and angiographic studies demonstrate both coronary artery and brachial artery vasospasm following 5-FU infusion [6,7,8]. 5-FU has also been shown to induce the vasoconstriction of vascular smooth muscle cells in vitro via the activation of protein kinase C, which resolves with administration of protein kinase inhibitors [9].…”

Section: Discussionmentioning

confidence: 99%

Role of Urotensin-2 in 5-Fluorouracil-Related Arterial Vasoconstriction in Cancer Patients

et al. 2018

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Background: The aim of this study was to identify the possible relationship of 5-fluorouracil (5-FU)-related arterial vasoconstriction with urotensin-2 (UT-2), which has a high potential as an endogenic vasoconstrictor. Methods: We assigned the patients to 1 of 3 groups. Patients in group 1 received a bolus of 5-FU, those in group 2 a continuous infusion (CI) of 5-FU, and those in group 3 no 5-FU, which was also a control group. Pre- and post-treatment UT-2 levels and brachial arterial diameters were measured and recorded in all patients. Results: 132 patients were included in the study. Pre- and post-treatment brachial artery diameters were similar in all groups: in group 1 (3.28 ± 0.52 vs. 3.25 ± 0.44 mm, p = 0.740), in group 2 (3.57 ± 0.47 vs. 3.46 ± 0.45 mm, p = 0.441) and in the control group (3.51 ± 0.52 vs. 3.25 ± 0.44 mm, p = 0.818). Pre- and post-treatment UT-2 levels were significantly different in each group: in group 1 (39.5 ± 30.9 vs. 56.7 ± 27.1 ng/ml, p = 0.0001), in group 2 (37.7 ± 33.7 vs. 62.5 ± 37.7 ng/ml, p = 0.0001) and in the control group (52.9 ± 40.2 vs. 60.8 ± 40.7 ng/ml, p = 0.006). Conclusion: Our findings suggest that UT-2 has a high potential as a vasoconstrictor agent in our bodies and its level increases through a bolus or CI 5-FU. Increased UT-2 levels are likely to play a role in 5-FU-related cardiac toxicity pathogenesis.

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Section: Discussionmentioning

confidence: 99%

Role of Urotensin-2 in 5-Fluorouracil-Related Arterial Vasoconstriction in Cancer Patients

et al. 2018

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“…Ultrasound and angiographic studies demonstrate both coronary artery and brachial artery vasospasm following 5-FU infusion [21][22][23]. Prior case reports reveal disease-free coronary arteries on angiography [24].…”

Section: Coronary Vasospasmmentioning

confidence: 95%

5-fluorouracil induced cardiotoxicity: Review of the literature

Sorrentino

Kim²,

Foderaro³

et al. 2012

Cardiol J

176

138

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“…Although the mechanism of cardiotoxic eff ects of 5-FU is not clear, coronary artery spasm, autoimmunemediated injury of the myocardium, endothelial damage, thrombogenic eff ects or thrombus formation, direct myocardial toxicity causing necrosis and accumulation of metabolites have been suggested to play a role 4 . Th e most frequently suggested mechanism is the coronary vasospasm caused by 5-FU itself or its metabolites (fl uoro beta alanine and fl uoro acetate).…”

Section: Discussionmentioning

confidence: 99%

“…Th e therapy was discontinued and the patient was transferred to our intensive care unit because the electrocardiogram (ECG) showed ischemic changes. Th e fi rst ECG showed ST elevation and peaked T waves in D I-III , aVL, aVF and V [2][3][4][5][6] derivations as well as reciprocal changes in aVR and V I ( Figure 1). Detailed history revealed that a coronary angiography revealing non-pathological fi ndings was performed two weeks ago as a result of a similar clinical picture in another center.…”

Section: Case Presentationmentioning

confidence: 99%