Capecitabine can induce acute coronary syndrome similar to5-fluorouracil

Frickhofen, N.; Beck, François; Jung, Bo‐Hyun; Fuhr, H. G.; Andrasch, H.; Sigmund, Martin

doi:10.1093/annonc/mdf035

Cited by 141 publications

(83 citation statements)

References 19 publications

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“…22 Capecitabine is currently used in the treatment of breast and gastrointestinal cancers and is believed to be less toxic than 5-FU. Other reported cardiotoxic effects associated with capecitabine include angina or MI, 23 arrhythmias, ECG changes, and cardiomyopathy.…”

Section: Antimetabolitesmentioning

confidence: 99%

Cardiovascular Complications of Cancer Therapy

et al. 2004

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Abstract-The cardiotoxicity of anticancer agents can lead to significant complications that can affect patients being treated for various malignancies. The severity of such toxicity depends on many factors such as the molecular site of action, the immediate and cumulative dose, the method of administration, the presence of any underlying cardiac condition, and the demographics of the patient. Moreover, toxicity can be affected by current or previous treatment with other antineoplastic agents. Cardiotoxic effects can occur immediately during administration of the drug, or they may not manifest themselves until months or years after the patient has been treated. In this article we review commonly used chemotherapy agents, including several recently approved medications, for their propensity to cause cardiotoxicity. Further research will be required to more accurately predict which patients are at risk for developing cardiotoxicity. In addition, management plans, as well as strategies to reduce cardiotoxicity, need to be developed.

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Section: Antimetabolitesmentioning

confidence: 99%

Cardiovascular Complications of Cancer Therapy

et al. 2004

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“…103 Moreover, severe adverse events have also been observed with capecitabine, which is an orally bioavailable prodrug of 5-FU. 104 Three-to-five percent of Caucasians have been reported to show a reduced enzymatic activity potentially leading to severe 5-FU-related toxicity in cancer patients. 105 However, measuring individual DPD activity in peripheral mononuclear blood cells does not provide a valid phenotyping approach since the correlation with hepatic DPD activity and 5-FU-pharmacokinetics is poor.…”

Section: -Fluorouracilmentioning

confidence: 99%

The clinical role of genetic polymorphisms in drug-metabolizing enzymes

et al. 2007

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“…3 In the last ten years several case reports of induced cardiotoxicity by the oral 5-FU analogue capecitabine have been published. 2,[4][5][6][7][8][9][10][11][12][13][14] In these reports, the exact pathophysiology of cardiac injury is not elucidated. It has been postulated that capecitabine has the same mechanism of side effects as IV 5-FU.…”

Section: Discussionmentioning

confidence: 99%

Acute chest pain in a patient treated with capecitabine

Camaro¹,

Danse²,

Bosker³

2009

NHJL

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A 61-year-old male with a history of metastatic colorectal cancer was referred to our hospital for primary coronary intervention because of acute ST-elevation myocardial infarction. Coronary angiography, however, revealed no significant stenoses. When asked, the patient revealed that capecitabine (Xeloda ® ) was started by his oncologist one day before admission. It is known that this oral 5-FU analogue drug, used in metastatic colorectal cancer, can cause coronary artery spasms. A 61-year-old male was admitted to a referring hospital because of acute chest pain. Three years ago he had suffered an acute coronary syndrome. Coronary angiography (CAG) showed focal coronary sclerosis in the right coronary artery, but no obstructive lesions and the patient was treated conservatively with aspirin, metoprolol, isosorbide-5-mononitrate and rosuvastatin. Furthermore, he had colon cancer with metastases in the liver and the lungs.After dinner the patient experienced 30 minutes of retrosternal chest pain without radiation. Because the chest pain was not relieved by sublingual nitroglycerin he contacted his general practitioner who sent him to hospital for observation. At the referring hospital he had no symptoms. The electrocardiogram (ECG) at admittance showed sinus rhythm with early repolarisation (figure 1). Four hours after admission, while waiting for the second troponin, there was recurrence of heavy retrosternal chest discomfort with radiation to the left arm. A new ECG was taken immediately and revealed sinus rhythm with ST-segment elevation in the inferolateral leads and peaked T-waves ( figure 2). An ST-elevation myocardial infarction was diagnosed and he was sent to our hospital for primary coronary intervention. Immediate treatment with 600 mg clopidogrel, 5000 units heparin and 160 mg aspirin was initiated and he was sent directly to our catheterisation laboratory. At presentation to the catheterisation laboratory he was free of symptoms. CAG revealed diffuse coronary sclerosis, but no significant stenosis in the coronary arteries with TIMI 3 flow in all vessels. In comparison with his CAG performed three years ago, no changes were seen. He was admitted to the coronary care unit. His blood pressure was 134/70 mmHg and the pulse 77 beats/min. There was no fever. No abnormalities were discovered on physical examination. The cardiac enzymes and the inflammation parameters were not elevated. His renal function was normal. Transthoracic echocardiography showed normal left and right ventricular function and no pericardial effusion. Two hours later, the severe chest discomfort returned with ST-segment elevation similar to the ECG at the referring hospital and nitroglycerin IV was started. Because of the intermittent character of his complaints with concomitant ST-segment changes, coronary artery vasospasms were now suspected as the cause of the symptoms. When asked, the patient revealed that capecitabine (Xeloda ® ) 1500 mg twice a day had been started just one day earlier. Capecitabine can indeed cause coronary arte...

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Capecitabine can induce acute coronary syndrome similar to5-fluorouracil

Cited by 141 publications

References 19 publications

Cardiovascular Complications of Cancer Therapy

Cardiovascular Complications of Cancer Therapy

The clinical role of genetic polymorphisms in drug-metabolizing enzymes

Acute chest pain in a patient treated with capecitabine

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