Anthracycline Cardiotoxicity

1983 ◽  
pp. 519-532 ◽  
Author(s):  
Victor J. Ferrans
Keyword(s):  
Anthracycline Cardiotoxicity

scholarly journals Selective protection of human cardiomyocytes from anthracycline cardiotoxicity by small molecule inhibitors of MAP4K4

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Pelin A. Golforoush ◽  
Priyanka Narasimhan ◽  
Patricia P. Chaves-Guerrero ◽  
Elsa Lawrence ◽  
Gary Newton ◽  
...  
Keyword(s):  
Small Molecule ◽  
Small Molecule Inhibitors ◽  
Anthracycline Cardiotoxicity ◽  
Human Cardiomyocytes ◽  
Selective Protection

scholarly journals The effects of doxorubicin on left and right atrial mechanics in patients with lymphoma

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
S Vahabi ◽  
E Kharati-Koopaei ◽  
M Stewart ◽  
H Hancock ◽  
M Norouzi ◽  
...  
Keyword(s):  
Strain Rate ◽  
Left Atrial ◽  
Left Ventricular ◽  
Right Atrial ◽  
Lv Function ◽  
Compensatory Mechanism ◽  
Research Association ◽  
Anthracycline Cardiotoxicity ◽  
Diastolic Strain Rate ◽  
Significant Change

Abstract Background Despite the associated dose-dependent cardiotoxicity, anthracyclines continue to form the backbone of modern chemotherapy regimens. Speckle Tracking Echocardiography (STE) has been a popular method of quantifying cardiac function but most studies have focused on left ventricular function. Research into the effects of anthracyclines on left atrial (LA) and right atrial (RA) function continues to be neglected. Purpose To investigate the effects of doxorubicin, a commonly used anthracycline, on both the LA and RA systolic and diastolic strain and strain-rate parameters in two groups of patients with lymphoma: Group 1 (G1) with a conventional drop in ejection fraction (EF <53%), and Group 2 (G2) without. Methods We retrospectively studied 46 patients treated for lymphoma between 2015 and 2018; G1 (n=12) and G2 (n=34). Echocardiograms performed at baseline (T0), mid-chemotherapy (T1), and post-chemotherapy (T2), were analysed by using offline vendor-independent software (TomTec, 2D Cardiac Performance Analysis). Using 2D STE, LA and RA reservoir, conduit and contractile strains, systolic and diastolic strain-rates were measured. Multi-level longitudinal model was used for statistical analysis.This study was ethically approved by the Health Research Association (REC Reference 18/SS/0139). Results Median age was 64 years (IQR 51–74 years) in G1, and 65 years (IQR 57–73 years) in G2. In G1, there was no significant change in LA reservoir strain with time, however a significant decline with an average mean difference of −7.52 was seen between T0 to T2 (p=0.016) in G2. LA conduit strain did not significantly change in either group with incremental doses of doxorubicin. However, LA contraction strain was seen to significantly increase in G1 between T1 to T2 (p=0.045) with an average change of 7.23. LA peak systolic strain rate, and late diastolic strain rate did not show any significant change with time in both groups. Yet, a significant increase was seen in LA early diastolic strain rate between T0 to T2 (p=0.017) in G1 but not G2. No significant changes were seen in the RA strain parameters in both groups. Conclusion In patient with a reduction in LV function, a significant change was noted in the left atrial contraction strain and early diastolic strain rate with incremental doses of doxorubicin. These changes shows the close relationship between the LA and LV, and the importance of LA in providing a compensatory mechanism for a decline in LV function secondary to anthracycline cardiotoxicity. Funding Acknowledgement Type of funding source: None

scholarly journals Targeted expression of cyclin D2 ameliorates late stage anthracycline cardiotoxicity

2018 ◽  
Vol 115 (5) ◽  
pp. 960-965 ◽  
Author(s):  
Wuqiang Zhu ◽  
Sean Reuter ◽  
Loren J Field
Keyword(s):  
Late Stage ◽  
Cyclin D2 ◽  
Anthracycline Cardiotoxicity ◽  
Targeted Expression

scholarly journals Subclinical Anthracycline Cardiotoxicity in Patients With Acute Promyelocytic Leukemia in Long-Term Remission After the AIDA Protocol

2012 ◽  
Vol 18 (4) ◽  
pp. 217-221 ◽  
Author(s):  
Pierpaolo Pellicori ◽  
Angela Calicchia ◽  
Francesco Lococo ◽  
Giuseppe Cimino ◽  
Concetta Torromeo
Keyword(s):  
Acute Promyelocytic Leukemia ◽  
Promyelocytic Leukemia ◽  
Anthracycline Cardiotoxicity

scholarly journals Dexrazoxane for Preventing Anthracycline Cardiotoxicity in Children with Solid Tumors

2010 ◽  
Vol 25 (9) ◽  
pp. 1336 ◽  
Author(s):  
Hyoung Soo Choi ◽  
Eun Sil Park ◽  
Hyoung Jin Kang ◽  
Hee Young Shin ◽  
Chung Il Noh ◽  
...  
Keyword(s):  
Solid Tumors ◽  
Anthracycline Cardiotoxicity

Late anthracycline cardiotoxicity protection by dexrazoxane (ICRF-187) in pediatric patients: echocardiographic follow-up

2005 ◽  
Vol 14 (2) ◽  
pp. 128-136 ◽  
Author(s):  
Lubomir Elbl ◽  
Hana Hrstkova ◽  
Iva Tomaskova ◽  
Jaroslav Michalek
Keyword(s):  
Pediatric Patients ◽  
Anthracycline Cardiotoxicity

scholarly journals p38δ genetic ablation protects female mice from anthracycline cardiotoxicity

2020 ◽  
Author(s):  
Sharon A George ◽  
Alexi Kiss ◽  
Sofian N Obaid ◽  
Aileen Venegas ◽  
Trisha Talapatra ◽  
...  
Keyword(s):  
Cardiac Injury ◽  
Mapk Signaling ◽  
Anthracycline Cardiotoxicity ◽  
Genetic Ablation ◽  
Female Mice ◽  
Echocardiographic Parameters ◽  
The Individual ◽  
And Function ◽  
First Time ◽  
Dose Dependent

ABSTRACTBACKGROUNDThe efficacy of an anthracycline antibiotic doxorubicin (DOX) as a chemotherapeutic agent is limited by dose-dependent cardiotoxicity. DOX is associated with activation of intracellular stress signaling pathways including p38 MAPKs. While previous studies have implicated p38 MAPK signaling in DOX-induced cardiac injury, the roles of the individual p38 isoforms, specifically, of the alternative isoforms p38γ and p38δ, remain uncharacterized.OBJECTIVESTo determine the potential cardioprotective effects of p38γ and p38δ genetic deletion in mice subjected to acute DOX treatment.METHODSMale and female wild-type (WT), p38γ-/-, p38δ-/- and p38γ-/-δ-/- mice were injected with 30 mg/kg DOX and their survival was tracked for ten days. During this period cardiac function was assessed by echocardiography and electrocardiography and fibrosis by PicroSirius Red staining. Immunoblotting was performed to assess the expression of signaling proteins and markers linked to autophagy.RESULTSSignificantly improved survival was observed in p38δ-/- female mice post-DOX relative to WT females, but not in p38γ-/- or p38γ-/-δ-/- male or female mice. The improved survival in DOX-treated p38δ-/- females was associated with decreased fibrosis, increased cardiac output and LV diameter relative to DOX-treated WT females, and similar to saline-treated controls. Structural and echocardiographic parameters were either unchanged or worsened in all other groups. Increased autophagy, as evidenced by increased LC3-II level, and decreased mTOR activation was also observed in DOX-treated p38δ-/- females.CONCLUSIONSp38δ plays a crucial role in promoting DOX-induced cardiotoxicity in female mice by inhibiting autophagy. Therefore, p38δ targeting could be a potential cardioprotective strategy in anthracycline chemotherapy.NEW AND NOTEWORTHYThis study for the first time identifies the roles of the alternative p38γ and p38δ MAPK isoforms in promoting DOX-cardiotoxicity in a sex-specific manner. While p38γ systemic deletion did not affect DOX-cardiotoxicity, p38δ systemic deletion was cardioprotective in female but not in male mice. Cardiac structure and function were preserved in DOX-treated p38δ-/- females and autophagy was increased.

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