Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0002962 (angina)
 21,142 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Capecitabine is a new chemotherapeutic agent considered highly specific for sensitive tumour cells, which convert the drug to 5-fluorouracil. Capecitabine is administered on an ambulatory basis for the treatment of metastatic breast and colorectal cancer, and both general practitioners and specialists are likely to deal with patients treated with this drug. We describe the case of a 44-year-old woman, with no cardiovascular risk factors, who started therapy with capecitabine for relapsing of breast carcinoma. She subsequently developed effort angina. Standard electrocardiogram and echocardiography were normal, whereas ST-segment elevation and angina were induced during exercise stress test. Capecitabine was withdrawn and therapy with diltiazem and transdermal nitroglycerine was started. The patient became asymptomatic and repeated symptom-limited exercise stress test did not induce any ST-segment changes or angina, even after withdrawal of anti-ischaemic therapy, thus confirming the hypothesis of capecitabine-induced coronary artery spasm as the cause of patient's symptoms.
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PMID:Coronary artery spasm induced by capecitabine. 1664 74

Capecitabine, an oral prodrug of 5-fluorouracil (5FU), has been integrated into the management of multiple cancer types because of convenience of administration and efficacy comparable with 5fu. Cardiotoxicity induced by 5FU-in particular angina-has been well described in the literature, but reports of adverse cardiac events with capecitabine are also emerging. The mechanism underlying 5FU cardiotoxicity has long been thought to result from coronary vasospasm, but animal-model studies and patient echocardiographic findings both suggest a cardiomyopathic picture. Although 5FU cardiotoxicity is often reversible and can be managed supportively, presentations that are more severe-including arrhythmias, acute ischemic events, and cardiogenic shock-have been documented. In this report, we describe the case of a patient who ultimately required a pacemaker after developing symptomatic bradycardia and sinus arrest while receiving capecitabine for colon cancer.
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PMID:Capecitabine-induced cardiotoxicity: case report and review of the literature. 2017 5

Capecitabine is a member of the fluoropyrimidine family of chemotherapeutic agents that selectively delivers 5-fluorouracil (5-FU) to tumors. It is increasingly used as part of combined modality treatment for gastrointestinal malignancies. Cardiotoxicity has been documented to occur with 5-FU, but due to an expansion in capecitabine use, reports exist of its propensity to coronary vasospasm. We report the case of a 28-year-old man, with no preceding angina, presenting with a reversible episode of ventricular fibrillation (VF) at rest in his fifth course of capecitabine chemotherapy for metastatic colorectal cancer. Emergency resuscitation successfully restored spontaneous circulation, with initial ST segment elevation in the inferolateral leads on electrocardiogram prompting emergency coronary angiography. This demonstrated normal coronary arteries. ST segments normalized post-angiography and the patient rapidly recovered with no myocardial damage sustained. An implantable cardioverter-defibrillator was placed for secondary prevention of sudden death, and capecitabine was implicated as the cause of coronary vasospasm which resulted in his presentation of VF. To our knowledge, this is the first episode of VF as a consequence of suspected capecitabine-induced coronary vasospasm occurring at rest. Our case highlights the potential for severe cardiotoxic consequences of capecitabine including sudden death from VF, and given the multi-disciplinary approach to managing oncology patients, health professionals should be aware of this.
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PMID:Ventricular fibrillation as a likely consequence of capecitabine-induced coronary vasospasm. 2202 Jun 60

Capecitabine is an oral prodrug of 5-fluorouracil (5-FU) which is converted in tumor cells to 5-FU by the enzyme thymidine phosphorylase. Nowadays, it is being widely used into the management of colorectal, breast and head and neck cancers because of its oral route and its comparable efficacy with 5-FU. 5-FU induced cardiotoxicity (angina and myocardial infarction) has been reported the literature, but capecitabine induced cardiotoxicity is less reported event. We report a patient with diagnosis of locally advanced adenocarcinoma of rectum who developed symptomatic bradycardia and acute ischemia while receiving oral capecitabine 825mg/m(2) twice daily with preoperative radiation.
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PMID:Capecitabine induced cardiotoxicity: a case report and review of literature. 2218 41

Capecitabine is a new oral chemotherapeutic agent that is considered highly specific for sensitive tumor cells. We present the case of a patient who, after treatment with capecitabine for colorectal cancer, presented to our hospital with angina pectoris and electrocardiographic changes indicative of myocardial ischemia. The absence of epicardial coronary stenosis on the coronary angiogram ruled out atherosclerotic coronary disease as the cause of ischemia. The occurrence of coronary spasm, although not evident during coronary angiography, seems to be a possible explanation of the patient's symptoms.
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PMID:Capecitabine may induce coronary artery vasospasm. 2430 88

5-fluorouracil is a chemotherapeutic agent that plays an important role in the treatment of various cancers including head and neck and gastrointestinal malignancies. Therapy with 5-fluorouracil is rarely associated with cardiotoxic effects including angina, heart failure, myocardial infarction and cardiac arrest, resulting in discontinuation at the expense of sub-optimal treatment of the targeted malignancy. In this article, we review the literature reported on 5-fluorouracil-associated cardiotoxicity and present a case of a patient who experienced chest pain on 5-fluorouracil. The cardiac symptoms subsided after initiation of capecitabine, the oral formulation of 5-fluorouracil. To our knowledge, this is only the second reported case where 5-fluorouracil was successfully replaced by capecitabine without recurrence of cardiac symptoms. Capecitabine may be a viable option for patients who develop 5-fluorouracil-induced chest pain. However, large clinical trials are warranted to confirm these findings. Currently, there is insufficient evidence to recommend an optimal approach for safe and effective alternative treatment for patients who experience 5-fluorouracil-induced cardiac adverse events.
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PMID:Paradoxical effect of capecitabine in 5-fluorouracil-induced cardiotoxicity: A case vignette and literature review. 2585 7