Subacute Anthracycline Cardiotoxicity

Hengel, Christopher; Russell, Prudence A.; Gould, Paul A.; Kaye, David M.

doi:10.1016/j.hlc.2005.06.003

Cited by 14 publications

(12 citation statements)

References 6 publications

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“…Overall, the causative role of epirubicin cardiotoxicity in the death of twin A is supported by various evidences including: 1- the post-mortem cardiac examination revealing the hallmarks of subacute anthracycline toxicity, i.e. massive interstitial edema without cellular infiltrates and myofibrillar damage/vacuolization [ 6 ]; 2- the histologic findings in both chorionic villi and extravillous throphoblast, well fitting the described placental effects of anthracycline exposure [ 7 ]; 3- the manifestation of acute myocardial diastolic dysfunction, evidenced by the enlarged right cardiac chambers and an elevated ductus venosus pulsatility index, preceding fetal death; 4 – the absence of structural or genomic abnormalities that may indicate an alternative etiology of fetal demise. Of note, neither arterial Doppler nor STV evaluation anticipated the impending fetal demise.…”

Section: Case Presentationmentioning

confidence: 99%

Epirubicin: a new entry in the list of fetal cardiotoxic drugs? Intrauterine death of one fetus in a twin pregnancy. Case report and review of literature

Framarino-dei-Malatesta

Perrone

Giancotti

et al. 2015

BMC Cancer

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BackgroundCurrent knowledge indicate that epirubicin administration in late pregnancy is almost devoid of any fetal cardiotoxicity. We report a twin pregnancy complicated by breast cancer in which epirubicin administration was causatively linked to the death of one twin who was small for gestational age (SGA) and in a condition of oligohydramnios and determined the onset of a transient cardiotoxicity of the surviving fetus/newborn.Case presentationA 38-year-old caucasic woman with a dichorionic twin pregnancy was referred to our center at 20 and 1/7 weeks for a suspected breast cancer, later confirmed by the histopathology report. At 31 and 3/7 weeks, after the second chemotherapy cycle, ultrasound examination evidenced the demise of one twin while cardiac examination revealed a monophasic diastolic ventricular filling, i.e. a diastolic dysfunction of the surviving fetus who was delivered the following day due to the occurrence of grade II placental abruption. The role of epirubicin cardiotoxicity in the death of the first twin was supported by post-mortem cardiac and placental examination and by the absence of structural or genomic abnormalities that may indicate an alternative etiology of fetal demise. The occurrence of epirubicin cardiotoxicity in the surviving newborn was confirmed by the report of high levels of troponin and transient left ventricular septal hypokinesia.ConclusionBased on our findings we suggest that epirubicin administration in pregnancy should be preceded by the screening of some fetal conditions like SGA and oligohydramnios that may increase its cardiotoxicity and that, during treatment, the diastolic function of the fetal right ventricle should be specifically monitored by a pediatric cardiologist; also, epirubicin and desamethasone for lung maturation should not be closely administered since placental effects of glucocorticoids may increase epirubicin toxicity.

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Section: Case Presentationmentioning

confidence: 99%

Epirubicin: a new entry in the list of fetal cardiotoxic drugs? Intrauterine death of one fetus in a twin pregnancy. Case report and review of literature

Framarino-dei-Malatesta

Perrone

Giancotti

et al. 2015

BMC Cancer

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“…Hengel, et al described a patient with subacute (17 days after chemotherapy) anthracycline cardiotoxicity who showed transient cardiac hypertrophy, diastolic dysfunction, and biopsy-proven interstitial myocardial edema. 13) Increased production of pro-inflammatory cytokines might contribute to the development of myocardial edema. 13) We suggest that myocardial edema might contribute to the quick recovery in our case as well, if the marked hypoproteinemia could worsen tissue edema by lowered colloid osmotic pressure.…”

Section: Discussionmentioning

confidence: 99%

“…13) Increased production of pro-inflammatory cytokines might contribute to the development of myocardial edema. 13) We suggest that myocardial edema might contribute to the quick recovery in our case as well, if the marked hypoproteinemia could worsen tissue edema by lowered colloid osmotic pressure. However, myocardial biopsy and CMR could not support this idea since they were demonstrated after improvement of hypoproteinemia.…”

Section: Discussionmentioning

confidence: 99%

Reversible Cardiomyopathy After Epirubicin Administration

et al. 2015

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SummaryAnthracycline-containing chemotherapy can cause irreversible and progressive left ventricular dysfunction. Epirubicin, which is widely used for breast cancer chemotherapy, is an anthracycline that has less cardiac toxicity than doxorubicin. The present report describes the case of a 70-year-old woman with breast cancer who developed severe congestive heart failure and severe cardiac dysfunction at 6 weeks from epirubicin final administration. Left ventricular function gradually improved after intensive treatment for heart failure and recovered completely within 2 months. To the best of our knowledge, this is the first report to describe epirubicin-induced subacute reversible cardiotoxicity. (Int Heart J 2015; 56: 466-468) Key words: Anthracycline cardiac injury, Breast cancer A nthracycline chemotherapies are effective against a wide spectrum of malignancies, including lymphoma, gastric cancer, small cell lung cancer, sarcomas, and breast cancer.1) Commonly used anthracyclines include doxorubicin, daunorubicin, and epirubicin. Unfortunately, these agents also have the most well-recognized cardiotoxic profile among all cancer treatments, which often limits their utility.1) Cardiomyopathy induced by anthracyclines is characterized by a dose-dependent, symptomatic, or asymptomatic progressive reduction in ventricular systolic function, which often results in congestive heart failure.1) The cardiomyopathy can be acute, subacute, or late.1) Acute toxicities during or immediately after drug administration are generally rare. Subacute cardiomyopathy typically occurs up to 8 months after the final dose, with peak onset of symptoms at 3 months. Late cardiomyopathy presents 5 or more years after therapy with anthracyclines. The latter two presentations are usually irreversible and progressive.1) Early retrospective studies showed that subacute and late cardiomyopathy were associated with poor outcomes and a mortality rate greater than 40%. 1) Even though recent progress in the treatment of congestive heart failure has resulted in improved outcomes in affected individuals, the cardiotoxicity of anthracycline still limits its overall utility in the treatment of cancer.Epirubicin (4'-epidoxorubicin) was developed in an effort to identify an anthracycline with less cardiotoxicity.2) The cumulative dose of chemotherapy at which cardiotoxicity occurs is higher for epirubicin (900 to 1000 mg/m 2 ) than for doxorubicin (450 to 500 mg/m 2 ).2) Several studies have shown that epirubicin produces anti-tumor responses similar to doxorubicin, but is associated with a lower cardiotoxicity rate in women with breast cancer.2) Epirubicin-based adjuvant chemotherapy (fluorouracil 500 mg/m 2 , cyclophosphamide 500 mg/ m 2 , and epirubicin 100 mg/m 2 [FEC100]) is the most effective and standard epirubicin-based regimen for women with nodepositive breast cancer. 2,3)The present report describes a rare case of a female patient with breast cancer who developed severe cardiomyopathy and congestive heart failure after FEC100 followed b...

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“…Therapy with cytarabine rarely causes cardiotoxicity. There are, however, reports on cytarabine-induced sinoatrial blockade and isolated myocardial infarction by concomitant therapy with cytarabine and idarubicin [12,13]. In a study of amsacrine and intermediate-dose cytarabine with or without etoposide, 1 patient suffered from heart failure caused by myocarditis [14].…”

Section: Discussionmentioning

confidence: 99%

Takotsubo Cardiomyopathy after Systemic Consolidation Therapy with High-Dose Intravenous Cytarabine in a Patient with Acute Myeloid Leukemia

et al. 2014

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Background: Takotsubo cardiomyopathy (TC) is characterized by the abrupt onset of cardiac dysfunction, with transient apical and midventricular hypo-/akinesia with a compensatory hypercontractility of the remaining segments. The clinical presentation appears to be similar to acute myocardial infarction (AMI). However, the myocardial dysfunction is reversible. Case Report: We report on the case of a 58-year-old man with acute myeloid leukemia (AML) who was admitted to our hospital to receive the second course of consolidation chemotherapy with intravenous cytarabine. Subsequently, the patient developed severe dyspnea at rest, with cardiogenic shock after the central venous catheter was removed. Echocardiography revealed severe dyskinesia of the mid and apical portions of both ventricles, accompanied by a highly reduced left ventricular function (LVF). 5 months later, 12-lead electrocardiography (ECG) did not show any evidence of repolar-ization disorders and echocardiographic evaluation revealed a normal LVF. We suppose that the underlying mechanism was TC. Conclusions: TC can occur in patients with AML under systemic chemotherapy, which possibly represents a triggering factor for TC development. Cardiogenic shock is a serious life-threatening complication of TC. Nevertheless, the prognosis of TC is favorable and a complete recovery of the LVF is possible.

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Subacute Anthracycline Cardiotoxicity

Cited by 14 publications

References 6 publications

Epirubicin: a new entry in the list of fetal cardiotoxic drugs? Intrauterine death of one fetus in a twin pregnancy. Case report and review of literature

Epirubicin: a new entry in the list of fetal cardiotoxic drugs? Intrauterine death of one fetus in a twin pregnancy. Case report and review of literature

Reversible Cardiomyopathy After Epirubicin Administration

Takotsubo Cardiomyopathy after Systemic Consolidation Therapy with High-Dose Intravenous Cytarabine in a Patient with Acute Myeloid Leukemia

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