scholarly journals Cancer Therapy–Related Cardiac Dysfunction and Heart Failure

2016 ◽  
Vol 9 (2) ◽  
Author(s):  
Carine E. Hamo ◽  
Michelle W. Bloom ◽  
Daniela Cardinale ◽  
Bonnie Ky ◽  
Anju Nohria ◽  
...  
Keyword(s):  
Heart Failure ◽  
Cancer Therapy ◽  
Cardiac Dysfunction

Very early detection of low dose anti-cancer therapy-related cardiotoxicity in lymphoma patients

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
Y.W Liu ◽  
H.Y Chang ◽  
C.H Lee ◽  
W.C Tsai ◽  
P.Y Liu ◽  
...  
Keyword(s):  
Heart Failure ◽  
Cancer Therapy ◽  
Cardiac Dysfunction ◽  
Systolic Dysfunction ◽  
Multivariable Analysis ◽  
Cardiopulmonary Exercise Test ◽  
Left Ventricular ◽  
Funding Source ◽  
Anti Cancer ◽  
All Cause Mortality

Abstract Background and purpose Left ventricular (LV) global peak systolic longitudinal strain (GLS) by speckle-tracking echocardiography is a sensitive modality for the detection of subclinical LV systolic dysfunction and a powerful prognostic predictor. However, the clinical implication of LV GLS in lymphoma patients receiving anti-cancer therapy remains unknown. Methods We prospectively enrolled 74 patients (57.9±17.0 years old, 57% male) with lymphoma who underwent echocardiography prior to chemotherapy, post 3rd and 6th cycle and 1 year after chemotherapy. Cancer therapy-related cardiac dysfunction (CTRCD) is defined as the reduction of absolute GLS value from baseline of ≥15%. All the eligible patients underwent a cardiopulmonary exercise test (CPET) upon completion of 3 cycles of anti-cancer therapy. The primary outcome was defined as a composite of all-cause mortality and heart failure events. Results Among 36 (49%) patients with CTRCD, LV GLS was significantly decreased after the 3rd cycle of chemotherapy (20.1±2.6% vs. 17.5±2.3%, p<0.001). In the multivariable analysis, male sex and anemia (hemoglobin <11 g/dL) were found to be independent risk factors of CTRCD. Objectively, patients with CTRCD had lower minute oxygen consumption/kg (VO2/kg) and lower VO2/kg value at anaerobic threshold in the CPET. The incidence of the primary composite outcome was higher in the CTRCD group than in the non-CTRCD group (hazard ratio 3.21; 95% CI, 1.04–9.97; p=0.03). Conclusion LV GLS is capable of detecting early cardiac dysfunction in lymphoma patients receiving anti-cancer therapy. Patients with CTRCD not only had a reduced exercise capacity but also a higher risk of all-cause mortality and heart failure events. Change of LVEF and GLS after cancer Tx Funding Acknowledgement Type of funding source: Public grant(s) – National budget only. Main funding source(s): The Ministry of Science and Technology (MOST), Taiwan

scholarly journals Cancer Therapy–Related Cardiac Dysfunction and Heart Failure

2016 ◽  
Vol 9 (1) ◽  
Author(s):  
Michelle W. Bloom ◽  
Carine E. Hamo ◽  
Daniela Cardinale ◽  
Bonnie Ky ◽  
Anju Nohria ◽  
...  
Keyword(s):  
Heart Failure ◽  
Cancer Therapy ◽  
Cardiac Dysfunction

scholarly journals Time to switch angiotensin-converting enzyme inhibitors/angiotensin receptor blockers to sacubitril/valsartan in patients with cancer therapy-related cardiac dysfunction

2022 ◽  
Vol 50 (1) ◽  
pp. 030006052110679
Author(s):  
Qianlan Xi ◽  
Zijun Chen ◽  
Tingming Li ◽  
Liya Wang
Keyword(s):  
Heart Failure ◽  
Cancer Therapy ◽  
Cardiac Dysfunction ◽  
Enzyme Inhibitors ◽  
Angiotensin Receptor Blockers ◽  
Angiotensin Converting Enzyme Inhibitors ◽  
Angiotensin Receptor ◽  
Efficacy And Safety ◽  
Converting Enzyme Inhibitors ◽  
Receptor Blockers

Advances in cancer therapy have resulted in more cancer therapy-related cardiac dysfunction (CTRCD), which is the main cause of death in older female survivors of breast cancer. Traditionally, guideline-recommended medications for heart failure, such as beta-blockers and angiotensin-converting enzyme inhibitors/angiotensin receptor blockers (ACEIs/ARBs), are commonly used to prevent or attenuate CTRCD. However, sometimes their effectiveness is not satisfactory. Recently, the drug combination of sacubitril plus valsartan has been proven to be more beneficial for heart failure with reduced ejection fraction in the long term compared with an ACEI/ARB alone. However, there is a lack of evidence of the efficacy and safety of this drug combination in CTRCD. We report a case of worsening CTRCD, despite treatment with traditional medications, in which the patient improved after changing perindopril to sacubitril/valsartan. The patient’s heart function greatly improved after changing this ACEI to sacubitril/valsartan. Changing an ACEI/ARB to sacubitril/valsartan in patients with worsening chemotherapy-induced heart failure is appropriate. Further studies with a high level of evidence are required to assess the efficacy and safety of sacubitril/valsartan for CTRCD.

scholarly journals Management of Advanced Heart Failure in Children with Cancer Therapy-Related Cardiac Dysfunction

Children ◽  
2021 ◽  
Vol 8 (10) ◽  
pp. 872
Author(s):  
Hari P. Tunuguntla ◽  
Kriti Puri ◽  
Susan W. Denfield
Keyword(s):  
Heart Failure ◽  
Cancer Therapy ◽  
Cardiac Dysfunction ◽  
Late Onset ◽  
Advanced Heart Failure ◽  
Cancer Therapies ◽  
Children With Cancer ◽  
Pericardial Disease ◽  
Symptomatic Heart Failure ◽  
Childhood Malignancies

The evolution of cancer therapies has led to marked improvement in survival of those affected by childhood malignancies, while also increasing the recognition of early and late toxicities associated with cancer therapies. Cardiotoxicity can include cardiomyopathy/heart failure, coronary artery disease, stroke, pericardial disease, arrhythmias, and valvular and vascular dysfunction as a result of exposure to chemotherapy and/or radiation. Anthracyclines remain the most common cause of chemotherapy-induced cardiomyopathy (CCM) with varying clinical presentations including: acute, early onset, and late-onset. Many individuals develop cardiac dysfunction over the long-term, ranging from subclinical cardiac dysfunction to end-stage symptomatic heart failure. The focus of this review is on characterization of symptomatic heart failure in children with cancer therapy-related cardiac dysfunction (CTRCD) primarily due to CCM and utilization of advanced heart failure therapies, including ventricular assist device (VAD) support and heart transplantation, with consideration of unique patient-related factors.

scholarly journals Impact of Cancer Therapy-Related Cardiac Dysfunction on Risk of Heart Failure in Pregnancy

2020 ◽  
Vol 2 (2) ◽  
pp. 153-162
Author(s):  
Mark Nolan ◽  
Evangelos K. Oikonomou ◽  
Candice K. Silversides ◽  
Melissa R. Hines ◽  
Kara A. Thompson ◽  
...  
Keyword(s):  
Heart Failure ◽  
Cancer Therapy ◽  
Cardiac Dysfunction ◽  
In Pregnancy

scholarly journals The Cancer Therapy-Related Clonal Hematopoiesis Driver Gene Ppm1d Promotes Inflammation and Non-Ischemic Heart Failure in Mice

2021 ◽  
Author(s):  
Yoshimitsu Yura ◽  
Emiri Miura-Yura ◽  
Yasufumi Katanasaka ◽  
Kyung-Duk Min ◽  
Nicholas W Chavkin ◽  
...  
Keyword(s):  
Heart Failure ◽  
Stem Cells ◽  
Dna Damage ◽  
Cancer Therapy ◽  
Mouse Model ◽  
Cardiac Dysfunction ◽  
Ischemic Heart Failure ◽  
Hematopoietic Stem ◽  
Cardiac Stress ◽  
Clonal Hematopoiesis

Rationale: Cancer therapy can be associated with short- and long-term cardiac dysfunction. Cancer patients often exhibit therapy-related clonal hematopoiesis (t-CH), an aggressive form of clonal hematopoiesis that can result from somatic mutations in genes encoding regulators of the DNA-damage response (DDR) pathway. Gain-of-function mutations in exon 6 the protein phosphatase Mg2+/Mn2+ dependent 1D (PPM1D) gene are the most frequently mutated DDR gene associated with t-CH. Whether t-CH can contribute to cardiac dysfunction is unknown. Objective: We evaluated the causal and mechanistic relationships between Ppm1d-mediated t-CH and non-ischemic heart failure in an experimental system. Methods and Results: To test whether gain-of-function hematopoietic cell mutations in Ppm1d can increase the susceptibility to cardiac stress, we evaluated cardiac dysfunction in a mouse model where clonal hematopoiesis-associated mutations in exon 6 of Ppm1d were produced by CRISPR-Cas9 technology. Mice transplanted with hematopoietic stem cells containing the mutated Ppm1d gene exhibited augmented cardiac remodeling following the continuous infusion of angiotensin II (AngII). Ppm1d-mutant macrophages were impaired in DDR pathway activation and displayed greater DNA damage, higher reactive oxygen species generation and an augmented proinflammatory profile with elevations in IL-1β and IL-18. The administration of an NLRP3 inflammasome inhibitor to mice reversed the cardiac phenotype induced by the Ppm1d-mutated hematopoietic stem cells under conditions of AngII-induced stress. Conclusions: A mouse model of Ppm1d-mediated t-CH was more susceptible to cardiac stress. Mechanistically, disruption of the DDR pathway led to elevations in inflammatory cytokine production, and the NLRP3 inflammasome was shown to be essential for this augmented cardiac stress response. These data indicate that t-CH involving activating mutations in PPM1D can contribute to the cardiac dysfunction observed in cancer survivors, and that anti-inflammatory therapy may have utility in treating this condition.

scholarly journals Interleukin-1 receptor-induced PGE2 production controls acetylcholine-mediated cardiac dysfunction and mortality during scorpion envenomation

2020 ◽  
Vol 11 (1) ◽  
Author(s):  
Mouzarllem B. Reis ◽  
Fernanda L. Rodrigues ◽  
Natalia Lautherbach ◽  
Alexandre Kanashiro ◽  
Carlos A. Sorgi ◽  
...  
Keyword(s):  
Heart Failure ◽  
Cardiac Dysfunction ◽  
Acetylcholine Release ◽  
Interleukin 1 ◽  
Clinical Manifestations ◽  
Prostaglandin E ◽  
High Dose ◽  
Scorpion Envenomation ◽  
Risk Of Death ◽  
Include Heart Failure

Abstract Scorpion envenomation is a leading cause of morbidity and mortality among accidents caused by venomous animals. Major clinical manifestations that precede death after scorpion envenomation include heart failure and pulmonary edema. Here, we demonstrate that cardiac dysfunction and fatal outcomes caused by lethal scorpion envenomation in mice are mediated by a neuro-immune interaction linking IL-1 receptor signaling, prostaglandin E2, and acetylcholine release. IL-1R deficiency, the treatment with a high dose of dexamethasone or blockage of parasympathetic signaling using atropine or vagotomy, abolished heart failure and mortality of envenomed mice. Therefore, we propose the use of dexamethasone administration very early after envenomation, even before antiserum, to inhibit the production of inflammatory mediators and acetylcholine release, and to reduce the risk of death.

scholarly journals Heart failure from cancer therapy: can we prevent it?

2019 ◽  
Vol 6 (4) ◽  
pp. 856-862 ◽  
Author(s):  
Matthias Totzeck ◽  
Raluca I. Mincu ◽  
Gerd Heusch ◽  
Tienush Rassaf
Keyword(s):  
Heart Failure ◽  
Cancer Therapy

scholarly journals Homogeneous 2D and 3D alignment of cardiomyocyte in dilated cardiomyopathy revealed by intravital heart imaging

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Kiyoshi Masuyama ◽  
Tomoaki Higo ◽  
Jong-Kook Lee ◽  
Ryohei Matsuura ◽  
Ian Jones ◽  
...  
Keyword(s):  
Heart Failure ◽  
Dilated Cardiomyopathy ◽  
Cardiac Dysfunction ◽  
Three Dimensional ◽  
Single Layer ◽  
Specific Pattern ◽  
Two Dimensional ◽  
Heart Imaging ◽  
Novel Method ◽  
2D And 3D

AbstractIn contrast to hypertrophic cardiomyopathy, there has been reported no specific pattern of cardiomyocyte array in dilated cardiomyopathy (DCM), partially because lack of alignment assessment in a three-dimensional (3D) manner. Here we have established a novel method to evaluate cardiomyocyte alignment in 3D using intravital heart imaging and demonstrated homogeneous alignment in DCM mice. Whilst cardiomyocytes of control mice changed their alignment by every layer in 3D and position twistedly even in a single layer, termed myocyte twist, cardiomyocytes of DCM mice aligned homogeneously both in two-dimensional (2D) and in 3D and lost myocyte twist. Manipulation of cultured cardiomyocyte toward homogeneously aligned increased their contractility, suggesting that homogeneous alignment in DCM mice is due to a sort of alignment remodelling as a way to compensate cardiac dysfunction. Our findings provide the first intravital evidence of cardiomyocyte alignment and will bring new insights into understanding the mechanism of heart failure.

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