In this review, we discuss the incidence, risk factors, types, and . Insights of CECCY Trial: Should Troponin be the Target for Anthracycline Cardiotoxicity Prevention? Preventing cardiotoxicity might allow for escalation of the anthracycline dose, which would further enhance the anticancer effects. Source/Disclosures. Dexrazoxane is the only FDA- approved drug for preventing anthracycline-induced cardiotoxicity [ 46 ]. prevention of anthracycline-induced cardiotoxicity is of paramount importance. Currently, there are several ongoing debates on the role of different measures in the primary prevention of cardiotoxicity in cancer survivors. Anthracycline-induced cardiotoxicity in children with cancer: strategies for prevention and management. 25,26 The pathophysiology of cardiotoxicity is unclear, but it is thought to be mediated by the generation of reactive oxygen species following anthracycline . Cardiovascular complications are a leading cause of therapy-related morbidity and mortality in long-term survivors of childhood malignancy. 15. Pharmacodynamic approaches can be applied for primary prevention of anthracycline-induced cardiotoxicity. Listing a study does not mean it has been evaluated by the U.S. Federal Government. Regarding pharmacological therapy there are two approaches in primary prevention of anthracycline-induced cardiotoxicity: to reduce the cardiotoxic effects ANT and initiate a cardioprotective medication. Cumulative anthracycline dose: Cumulative doses >500 mg/m 2 associated with marked long-term risk [38,52,54,57] The optimal chemotherapy for this lymphoma subtype has not been established. Drug-induced cardiotoxicity is a major adverse effect that has been encountered for some clinically important drugs especially antineoplastic agents. Anthracyclines are highly effective chemotherapeutic agents, used for a wide variety of malignancies. Despite its effectiveness, cardiotoxicity is a major late effect that compromises the survival and quality of life of survivors of this and other cancers. "Probably, anthracycline-induced cardiotoxicity is a single and continuous phenomenon, from cellular to clinical stage, starting with myocardial cell injury, followed by progressive LVEF decline and, potentially, overt heart failure." I was diagnosed with a blood cancer, multiple myeloma, in early 1994. Currently, assessing the cardiotoxicity potential is a crucial parameter in drug . There is little doubt that cardiac damage is related to total cumulative dose, with those receiving more than 400 mg/m 2 being at significant risk.21 There is also evidence of a cumulative affect with other chemotherapeutic agents, leading to severe and fatal cardiotoxicity even at doses below 400 mg/m 2.22 Mediastinal . Clinical heart failure may ensue in up to 5% of high-risk patients. 1 Although anthracycline-induced cardiotoxicity was . We propose that Top2β is a promising molecular target that can be used to design interventions to . 8.Design and baseline characteristics for the ACE Inhibitor After Anthracycline (AAA) study of cardiac dysfunction in long-term pediatric cancer survivors. Tel +966503225121. This paper provides an overview of anthracycline-induced cardiotoxicity in terms of definition, classification, incidence, risk factors, possible mechanisms, diagnosis, and treatment. Paediatr Drugs. Ivabradine selectively reduces heart rate through inhibition of the cardiac pace maker IF channel, thus prolonging the duration of spontaneous depolarization in the sinus node. Anthracycline-induced heart failure has been traditionally attributed to direct iron-catalyzed oxidative damage. Dive into the research topics of 'Anthracycline-induced cardiotoxicity: Course, pathophysiology, prevention and management'. Email halkofide@ksu.edu.sa. Purpose: Although clinical trials have provided some data on the benefit of angiotensin-converting enzyme inhibitors (ACEIs) or β-blockers (BBs) in patients with chemotherapy-induced cardiotoxicity, evidence of ACEIs/BBs on prevention of trastuzumab and/or anthracycline-induced cardiotoxicity outside trials is limited. Doxorubicin is an anthracycline and one of the more effective chemotherapy agents used in the treatment of children, adolescents, and adults with osteosarcoma. The anthracyclines and related compounds (doxorubicin, daunorubicin, idarubicin, epirubicin, and the anthraquinone mitoxantrone) are among the chemotherapeutic agents implicated in cardiotoxicity. Previous studies suggest that enalapril, and or carvedilol, protect against cardiovascular effects of these drugs. Dexrazoxane is the only option recommended for cardiotoxicity prevention in high-risk patients supported by randomised trials but its cost-effectiveness in paediatric cancer patients has not been established. However, despite an established dose-dependent association, there is interpatient variability in risk for CHF for exposure to anthracycline at any dose, such that clinical variables alone yield moderate predictive power in detecting CHF. Due to advances in detection and treatment, 50% of cancer patients will live 10 or more years with 18 million survivors in USA with a similar estimated survivor population in Europe. In the OVERCOME trial, combined treatment with enalapril and carvedilol was compared with no treatment in patients with malignant hemopathies treated with intensive CT. Prevention of anthracycline-induced cardiotoxicity, while maintaining the drugs' therapeutic effectiveness, can be achieved by pharmacological and non-pharmacological means. Anthracycline-induced cardiotoxicity has been classified based on its onset into acute, early, and late. A research team at the American Heart Association (AHA) Scientific Sessions 2021, held virtually from November 13 to 15, 2021, presented new data on anthracycline cardiotoxicity in a . It may indeed affect the quality of life and survival of patients with cancer, regardless of oncological prognosis. Diagnosis and treatment of primary and metastatic cardiac tumours as well as cardiac amyloidosis can be considered 'less classical . By Alexandra (Sasha) Todak. Anthracyclines are the cornerstone of many chemotherapy regimens for a variety of cancers. Two approaches for primary prevention of anthracycline-induced cardiotoxicity are: 1) reduce cardiotoxic potency by administering via continuous infusion, liposome encapsulation, or using a less cardiotoxic derivative (e.g., epirubicin or idarubicin); and 2) use a cardioprotective agent (e.g., dexrazoxane) in conjunction with treatment. Prevention of anthracycline-induced cardiotoxicity in adult cancer patients In a systematic review of cardioprotective agents used during anthracycline therapy, the authors concluded that of the eight different agents for which there were randomized controlled trials, only dexrazoxane could be recommended for clinical practice [ 29 ]. Anthracycline-induced cardiotoxicity (AIC) persists as a significant cause of morbidity and mortality in cancer survivors. Cardiotoxicity is a well‑recognized side effect of anthracycline therapy that limits the total amount of drug administered and can cause heart failure in some patients. Perspective from Fatima Cardoso, MD. Anthracycline cardiotoxicity: an update on mechanisms, monitoring and prevention Anthracycline chemotherapy causes dose-related cardiomyocyte injury and death leading to left ventricular dysfunction. Despite more than five decades of research, the biological mechanisms underlying anthracycline cardiotoxicity are not completely understood. Prevention of Anthracycline-induced Cardiotoxicity Edward T.H. [4,5,7]. Non-pharmacological prevention Cardiovascular risk factors should be identified and treated appropriately as soon as cancer is diagnosed. Non-pharmacological prevention Cardiovascular risk factors should be identified and treated appropriately as soon as cancer is diagnosed. The classic cardio-oncology paradigm is the prevention, diagnosis and treatment of cardiotoxicity resulting from chemotherapy and/or radiotherapy. The primary cause of chemotherapy-induced cardiotoxicity is anthracycline compounds, which are used extensively to treat lymphoma, sarcoma, breast cancer, and pediatric leukemia . Wittayanukorn S, Qian J, Westrick SC, Billor N, Johnson B, Hansen RA (2018) Prevention of trastuzumab and anthracycline-induced cardiotoxicity using angiotensin-converting enzyme inhibitors or β-blockers in older adults with breast cancer. Anthracycline-Induced Cardiotoxicity in Young Cancer Patients: The Role of Carnitine SaroH.Armenian Division of Outcomes Research, Department of Population Sciences, City of Hope, Duarte , Calif., USA preliminary studies suggest a role for carnitine in primary prevention (during treatment) and secondary prevention (to 8.Design and baseline characteristics for the ACE Inhibitor After Anthracycline (AAA) study of cardiac dysfunction in long-term pediatric cancer survivors. It may have a significant burden on the quality and quantity of life of those exposed to this class of medication. 2005;7(2):67-76. Cardiotoxicity is a feared side effect that may limit the clinical use of anthracyclines. Primary mediastinal B-cell lymphoma (PMBCL) is a relatively rare lymphoma subtype affecting mainly young adults. Although many protective strategies have been evaluated, cardiotoxicity remains an ongoing threat. Anthracycline-induced cardiotoxicity in children with cancer: strategies for prevention and management. We searched PubMed, Embase and Cochrane Library for randomized controlled trials of the comparison of β blockers versus placebo in patients undergoing anthracycline chemotherapy. Use of PEGylated liposomal doxorubicin has been shown to decrease the cardiotoxicity of this anthracycline, even at doses >500 mg/m2[64,65]. The antioxidant, probucol, has been shown to prevent the decrease in LVEF in animal models of doxorubicin cardiotoxicity [66,67]. In the anthracycline-damaged mitochondria, iron accumulation and iron-dependent reactive oxygen species (ROS) generation induced are[8,9]. Anthracycline-induced cardiotoxicity starts from the first dose. 2005;7(2):67-76. Anthracyclines are the cornerstone of many chemotherapy regimens for a variety of cancers. Cardinale et al 133a demonstrated that in high-risk patients, defined by an increased troponin I (TnI) value (> 0.07 ng/mL) during treatment, early initiation of enalapril (ACE inhibitor . Risk factors for anthracycline cardiotoxicity. Barry E, Alvarez JA, Scully RE, et al: Anthracycline-induced cardiotoxicity: Course, pathophysiology, prevention and management. Unfortunately, their use is limited by a cumulative dose-dependent cardiotoxicity. Risk factor Aspects Ref. Although anthracycline-induced cardiotoxicity is dose dependent, it can also occur early at the onset of treatment and even up to several years following completion of treatment. The following are summary points from this review of anthracycline cardiotoxicity mechanisms, monitoring, and prevention:. As the number of survivors of childhood cancer increase, so too will be the number of survivors with adverse effects from cancer therapy. Purpose: Cardiotoxicity is a common complication associated with anthracyclines. Treating anthracycline-induced cardiotoxicity. They were first isolated from cultures of Streptomyces peucetius by Dr. Federico . The effects of β blockers on the primary prevention of anthracycline-induced cardiotoxicity were controversial. Doxorubicin is an anthracycline and one of the more effective chemotherapy agents used in the treatment of children, adolescents, and adults with osteosarcoma. Anthracyclines are the cornerstone of many chemotherapy regimens for a variety of cancers. Ivabradine to Prevent Anthracycline-induced Cardiotoxicity. Part of this success is due to the effective use of anthracycline (AC) chemotherapy, but at the potential expense of damage to the patient's heart. I underwent local radiation, induction chemotherapy, and an autologous stem cell . To date, the main strategies that seem to be effective in reducing its incidence and severity include screening and treating preexisting cardiovascular risk factors, limiting the cumulative anthracycline dose with a preference for less toxic analogues, and . Table 1. Anthracycline is a mainstay in treatment of many cancers including lymphoma and breast cancer among many others. Despite its effectiveness, cardiotoxicity is a major late effect that compromises the survival and quality of life of survivors of this and other cancers. Doxorubicin is an anthracycline and one of the more effective chemotherapy agents used in the treatment of children, adolescents, and adults with osteosarcoma. Its molecular signature and clinical features resemble classical Hodgkin lymphoma. Cardio-oncology is an emerging field of cardiology that focuses on cardiovascular diseases in patients with cancer. Iarussi D, Indolfi P, Casale F, et al. - Trials secondary prevention anthracycline-induced cardiotoxicity RELATED TOPICS Adjuvant systemic therapy for HER2-positive breast cancer Cardiotoxicity of cancer chemotherapy agents other than anthracyclines, HER2-targeted agents, and fluoropyrimidines Cardiotoxicity of trastuzumab and other HER2-targeted agents CAS PubMed Google Scholar 99. When the central role of topoisomerase 2<i>β</i . Prevention of cardiomyopathy REDUCTION OF CUMULATIVE ANTHRACYCLINE DOSE. Despite its effectiveness,. Doxorubicin poisons Topoisomerase 2 (Top2) causes DNA double strand breaks (DSBs) J Clin Cardiol. The safety and scientific validity of this study is the responsibility of the study sponsor and investigators. Anthracycline Cardiotoxicity After Breast Cancer Treatment. Conclusions: Although a protective effect of enalapril on myocardial toxicity was observed in terms of the LVEF values and TnI, CK-MB and NT-proBNP levels, its use in the prevention and treatment of cardiotoxicity caused by anthracycline needs to be investigated by more scientific research. In August 2014, the FDA designated dexrazoxane as an orphan drug for "prevention of cardiomyopathy for children and adolescents 0 through 16 years of age treated with anthracyclines" [ 47 ]. Based on clinical investigation, although limited, a cumulative dose of doxorubicin of up to 900 mg/m 2 , and possibly higher, can be administered safely during chemotherapy as long as coenzyme Q10 is administered . Dexrazoxane (DEX)—the only drug approved for its prevention—has been believed to protect the heart via its iron-chelating metabolite ADR-925. Anthracycline is a commonly prescribed antineoplastic agent. Lisinopril may prevent cardiotoxicity of anthracycline, trastuzumab use in breast cancer. Third, inhibiting and deleting Top2β in the heart should also be tested as primary prevention strategies. Materials and Methods: A cohort study of 142,990 women (66 y and above . Prevention of anthracycline-induced cardiotoxicity, while maintaining the drugs' therapeutic effectiveness, can be achieved by pharmacological and non-pharmacological means. Listing a study does not mean it has been evaluated by the U.S. Federal Government. Prevention of Anthracycline-induced Cardiotoxicity (ICOS-ONE) The safety and scientific validity of this study is the responsibility of the study sponsor and investigators. 16 Besides that, it is also important to know that some patients show a higher predisposition to develop HF and individual genotyping . Cancers responsive to anthracyclines include carcinoma (breast, small . Childhood cancer survivors are at a five- to 15-fold increased risk for congestive heart failure compared with the general population. The role of biomarkers, in particular troponins, in identifying subclinical cardiotoxicity and its therapy with angiotensin-converting enzyme inhibitors (mainly enalapril) to prevent LVEF reduction is a recognized and effective strategy. RegionalCentrefor . Dexrazoxane (DRZ) has proven protective activity against anthracycline cardiotoxicity by minimising or completely preventing LVEF fall and reducing cardiac marker release. Discovered in the 1960s, anthracyclines are still among the most widely used chemotherapy drugs, but are associated with cardiotoxicity. In this review, we discuss the incidence, risk factors, types, and . In this review, important insight into the current state of the evidence on the use of different cardioprotective agents, different anthracycline analogues, and different anthracycline infusion durations to reduce or prevent cardiotoxicity in children treated with anthracyclines is . In the intervention group, enalapril and carvedilol were started simultaneously at . Prophylactic use of ACE inhibitors, β-blockers, or ARBs for prevention of anthracycline-induced cardiotoxicity is an ongoing area of active investigation. Anthracycline-induced cardiotoxicity can be detected at a preclinical phase. Bocchi EA, Belfort DP, Avila MS. 16. Published by: Source . March 16, 2009. Anthracycline-treated childhood cancer survivors are at higher risk of cardiotoxicity, especially with cumulative doses received above 250 mg/m2. A cohort study [4] enrolling 318 breast cancer patients with anthracycline and trastuzu-mab indicated that β blockers were associated with lower risk of new HF events (HR 0.2, 95% confidence 1,2 However, data are lacking on anthracycline cardiotoxicity in racially and ethnically diverse populations. Anthracyclines are among the most effective and widely prescribed anticancer agents. Together they form a unique fingerprint. The mechanisms of AIC remain unclear; however, several pathways have been proposed, suggesting a multifactorial origin. 36 41 DRZ is taken up rapidly by the myocardium following infusion and competes with ATP-binding sites on Top 2β. Oncology, ONCOLOGY Vol 23 No 3, Volume 23, Issue 3. Despite more than five decades of research, the biological mechanisms underlying anthracycline cardiotoxicity are not completely understood. Dawn L. Hershman, MD, MS , Theresa Shao, MD. In the contemporary cohort of 2625 anthracycline-treated patients, who were followed for a median time of 5.2 years after chemotherapy, the incidence of cardiotoxicity was 9% (cardiotoxicity was defined as reduction in left ventricular [LV] ejection fraction >10% from baseline and <50%).
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