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)

5-Fluorouracil (5FU) cardiotoxicity is thought to be an infrequent toxic effect, usually related to coronary vasospasm. Among 198 patients (pts) receiving 5FU as a continuous infusion (CI) over 96 or 120 h, at a daily dose of 1,000 mg/m2, 13 new cases of 5FU--cardiotoxicity are reported. In all cases but 1, cardiovascular symptoms occurred at the first 5FU-CI course, with mean time of onset of 3 d. Chest pain was the prominent inaugural symptom with angor pectoris (6 pts) and pericarditis (3 pts). Five pts developed cardiogenic shock, which was irreversible in 3 cases. The severity of such an evolution requires prompt 5FU discontinuation, if symptoms occur, and careful hemodynamic supervision during 5FU therapy. One patient experienced typical myocardial infarction, another one epicardo myocardiopathic process with adiastolia. Disorders of repolarisation on electrocardiographic tracing were the prominent abnormalities, associated with a significant increase of QT segment in 3 cases. Re-introduction of 5FU-CI resulted in chest pain recurrence in 2 out of 4 pts, despite calcium antagonist "prevention". In our retrospective study, the incidence of 5FU-CI cardiotoxicity is 6.5%, which is consistent with recent reports (10%). Whether 5FU-induced cardiotoxicity mechanism is related to vasospastic or direct effect remains unclear. However, our series suggests a 5FU-induced post ischaemic myocardial dysfunction as described in the "stunned myocardium" syndrome.
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PMID:[Cardiotoxicity of continuous intravenous infusion of 5-fluorouracil: clinical study, prevention and physiopathology. Apropos of 13 cases]. 220 12

Although there have been anecdotal reports of cardiac toxicity associated with fluorouracil (5-FU) therapy, this phenomenon has not been studied in a systematic fashion. We prospectively performed continuous ambulatory ECG monitoring on 25 patients undergoing 5-FU infusion for treatment of solid tumors in order to assess the incidence of ischemic ST changes. Patients were monitored for 23 +/- 4 hours before 5-FU infusion, and 98 +/- 9 hours during 5-FU infusion. Anginal episodes were rare: only one patient had angina (during 5-FU infusion). However, asymptomatic ST changes (greater than or equal to 1 mm ST deviation) were common: six of 25 patients (24%) had ST changes before 5-FU infusion v 17 (68%) during 5-FU infusion (P less than .002). The incidence of ischemic episodes per patient per hour was 0.05 +/- 0.02 prior to 5-FU infusion v 0.13 +/- 0.03 during 5-FU infusion (P less than .001); the duration of ECG changes was 0.6 +/- 0.3 minutes per patient per hour before 5-FU v 1.9 +/- 0.5 minutes per patient per hour during 5-FU (P less than .01). ECG changes were more common among patients with known coronary artery disease. There were two cases of sudden death, both of which occurred at the end of the chemotherapy course. We conclude that 5-FU infusion is associated with a significant increase in silent ST segment deviation suggestive of ischemia, particularly among patients with coronary artery disease. The mechanism and clinical significance of these ECG changes remain to be determined.
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PMID:Continuous ambulatory ECG monitoring during fluorouracil therapy: a prospective study. 246 60

Five fluoro-uracil (5-FU) is a cytotoxic drug which has been extensively used for chemotherapy since 1957. Ischaemic heart disease resulting from its administration is rare. Spontaneous angina during infusions of 5-FU was observed in two patients with electrocardiographic changes suggesting coronary spasm. After treatment, clinical examination, electrocardiogram, echocardiogram, stress test, coronary angiography with left ventriculography were all normal. An Ergonovine test was performed in one patient but failed to elicit coronary spasm. In the other patient, intravenous trinitrin and diltiazem were ineffective in preventing the ischaemic changes. A review of the literature is presented (51 cases). The pathophysiology of 5-FU-induced ischaemic heart disease is not fully understood. In 9 cases, coronary angiography was normal and coronary spasm was suggested as a possible cause. However, antispastic drugs are usually ineffective. It has been shown experimentally that 5-FU has a direct toxic effect on the myocardium.
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PMID:[Cardiotoxicity of 5-fluorouracil: coronary spasm? Apropos of 2 cases with normal coronarography]. 266 Jun 65

5-fluorouracil is potentially cardiotoxic to man. To date, 47 patients have been reported with undesired heart disorders after the administration of this cytotoxic drug. The incidence of cardiotoxicity due to 5-FU is 1.6%. Angina-type precordial pain with electrocardiographic changes suggesting myocardial ischemia is the common clinical feature. Generally it disappears spontaneously or after the use of coronary vasodilators. Acute left ventricular failure, pericarditis and rythm disorders are not often found. The pathogenesis is unknown however, cardiac spasm as well as the direct or indirect effect of the drug on myocardium, are possible responsible mechanisms.
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PMID:[Cardiotoxicity induced by 5-fluorouracil. Review of the literature]. 267 49

Infusion of 5'-dFUrd (2.0-3.0 g/m2 over 1 h on days 1-5 every 3rd week) resulted in one partial response in 21 patients with advanced and progressing colorectal cancer. No patient had received chemotherapy before the 5'-dFUrd trial. Hematological and gastrointestinal toxicity were generally mild. In 4 patients peripheral neurotoxicity was diagnosed during treatment, whereas transient cerebellopathy was observed in one. Cardiac side effects (repeated angina pectoris following 5'-dFUrd infusion) led to discontinuation of treatment after two courses in one patient. It is concluded that 5'-dFUrd at the above doses is not superior to conventional 5-FU treatment in colorectal cancer. Neurological and cardiac side effects are rare but may be a problem in individual patients.
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PMID:Doxifluridine (5'-dFUrd) in patients with advanced colorectal carcinoma. A phase II study. 299 Jul 50

Two cases of 5-Fluorouracil (5FU) cardiotoxicity, chest pain with changes in ECG the former, and myocardial infarction the latter, are described. Review of literature shows the existence of 49 cases of cardiotoxicity due to 5FU (38 angina = 77.5% 8 myocardial infarction = 16.3%). This complication seems due to a "coronary toxicity" whose onset is very precocious and not dose-dependent. Since 5FU therapy could result very dangerous when cardiotoxicity occurs, it is strictly advisable to withdraw further administration of the drug. As a matter of fact 18 patients out of 21 who again were treated with 5FU, had more serious complications which resulted in 3 myocardial infarctions (2 deaths).
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PMID:[Cardiotoxicity of 5-fluorouracil. Personal cases and review of the literature]. 331 58

Cardiotoxicity is an uncommon side-effect of 5-FU-based chemotherapy. Coronary artery vasospasms have been postulated to be involved in the pathogenesis of this rare but serious problem. We found high plasma levels of ET-1, a potent natural vasoconstrictor, in two patients who experienced two of the commonest clinical manifestations of 5-FU-induced cardiac toxicity--i.e., angina pectoris and chronic heart failure. We, therefore, propose ET-1 as the ultimate mediator of this toxicity, even though the mechanism of ET-1 increase in peripheral venous blood is still unknown. Finally, another important question still remains unresolved: is the release of ET-1 from normal coronary endothelial cells the prime cause or simply the consequence of 5-FU-related cardiotoxicity?
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PMID:Endothelin-1 and 5-fluorouracil-induced cardiotoxicity. 968 87

The antimetabolite fluorouracil (5-FU) is frequently administered for chemotherapy of various malignant neoplasms. The drug is well known for its adverse effects involving bone marrow, skin, mucous membranes, intestinal tract and central nervous system, whereas its cardiotoxicity is less familiar to clinicians. The pathophysiology of fluorouracil-associated cardiac adverse events is controversial and conclusions are based on clinical studies and case reports more than on solid experimental evidence. While clinical and electrocardiographic features suggest myocardial ischaemia as a main aetiological factor, possibly induced by coronary vasospasm, histomorphological and biochemical studies indicate a more direct drug-mediated cytotoxic action. Estimates of the overall incidence of fluorouracil cardiotoxicity have varied widely from 1.2 to 18% of patients. Patients may present with angina-like chest pain, cardiac arrhythmias or myocardial infarction. There is no unequivocally effective prophylaxis or treatment in this syndrome. Once fluorouracil administration is discontinued symptoms are usually reversible, although fatal events have been described. The overall mortality rate has been estimated to be between 2.2 and 13.3%. There is a high risk of relapse when patients are re-exposed to this drug following previous cardiac incidents. From the present data it is concluded that cardiotoxicity is a relevant but underestimated problem in fluorouracil treatment. Since the mechanisms of fluorouracil-associated cardiotoxicity are not yet fully understood, all patients undergoing this chemotherapy have to be carefully evaluated and monitored for cardiac risk factors and complaints. After cardiotoxic events, fluorouracil should definitely be withdrawn and replaced by an alternative antiproliferative regimen.
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PMID:Cardiotoxicity of the antiproliferative compound fluorouracil. 1023 88

Cardiovascular emergencies in oncology patients include all of the usual cardiac problems, as well as complications of cancer and its therapy. Pericardial effusions and tamponade, cardiac masses, and extrinsic compression of the heart and great vessels by tumor masses, or fluid collections may all occur. Certain tumors may secrete mediators that are directly toxic to the heart; for example, catecholamines are secreted by pheochromocytomas and serotonin is secreted by carcinoid tumors. Tumors can also cause arrhythmias due to the mediators they secret or to direct mechanical irritation of the heart or pericardium. Cancer therapy is also associated with cardiac emergencies. Perioperative myocardial ischemia or infarction, as well as arrhythmias, may complicate surgery. Pericardial effusions and tamponade can follow surgery, radiation, or chemotherapy. Chemotherapy with anthracyclines, mitoxantrone, and trastuzumab may prompt acute and chronic heart failure. 5-Fluorouracil causes coronary spasm in some patients, leading to angina, myocardial infarction, arrhythmias, and/or sudden death. Cyclophosphamide, particularly in high doses, may produce acute myopericarditis. Radiation may cause acute pericardial disease and late sequelae such as myocardial infarction, acute valvular insufficiency, or effusive constrictive pericarditis. Endocarditis also occurs in cancer patients in association with vascular access devices and immune compromise. This review will discuss each of these complications of cancer and its therapy.
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PMID:Cardiovascular emergencies in the cancer patient. 1086 14

5-Fluorouracil (5-FU) is the backbone of the chemotherapy regimens approved for treatment of colorectal cancer. Incidence of cardiotoxicity associated with 5-FU ranges between 1.5% to 18%; 48% as anginal symptoms and 2% as cardiogenic shock. Cardiotoxicity is unpredictable and no alternatives have been defined so far. A 35-year-old man treated for stage III A rectal cancer developed chest pain typical of angina on treatment with capecetabine initially and 5-FU infusion afterwards. Scheduled dosing of 5-FU was changed from infusion to a bolus type. He was asymptomatic with no electrocardiographic (ECG) changes on 24-h Holter monitoring after changing the mode of administration to bolus 5-FU. Here, we report the first case in the English literature where a change in the mode of 5-FU administration to bolus is an alternative to infusion 5-FU-induced cardiotoxicity. In conclusion, Bolus 5-FU can be used in patients developing cardio-toxicity due to 5-FU infusion.
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PMID:Bolus 5-Fluorouracil as an alternative modality to infusion 5-Fluorouracil in a patient with rectal cancer and capecitabine-induced cardiotoxicity. 1977 18


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