Abstract

Trastuzumab prolongs progression-free and overall survival in patients with human epidermal growth factor receptor 2 (HER2) positive breast cancer. However, trastuzumab treatment is hampered by cardiotoxicity, defined as a left ventricular ejection fraction (LVEF) decline with a reported incidence ranging from 3 to 27% depending on variable factors. Early identification of patients at increased risk of trastuzumab-induced myocardial damage is of great importance to prevent deterioration to irreversible cardiotoxicity. Although current cardiac monitoring with multi gated acquisition (MUGA) scanning and/or conventional 2D-echocardiography (2DE) have a high availability, their reproducibility are modest, and more sensitive and reliable techniques are needed such as 3D-echocardiography (3DE) and speckle tracking echocardiography (STE). But which other diagnostic imaging modalities are available for patients before and during trastuzumab treatment? In addition, what is the optimal frequency and duration of cardiac monitoring? At last, which biomarker monitoring strategies are currently available for the identification of cardiotoxicity in patients treated with trastuzumab?

PMID: 32361151 [PubMed - as supplied by publisher]

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Plasma metabolite biomarkers predictive of radiation induced cardiotoxicity.


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Plasma metabolite biomarkers predictive of radiation induced cardiotoxicity.


Radiother Oncol. 2020 Apr 20;:


Authors: Unger K, Li Y, Yeh C, Barac A, Srichai MB, Ballew EA, Girgis M, Jayatilake M, Sridharan V, Boerma M, Cheema AK


Abstract

PURPOSE: Although advancements in cancer treatments using radiation therapy (RT) have led to improved outcomes, radiation-induced heart disease (RIHD) remains a significant source of morbidity and mortality in survivors of cancers in the chest. Currently, there are no diagnostic tests in clinical use due to a lack of understanding of the natural history and mechanisms of RIHD development. Few studies have examined the utility of using metabolomics to prospectively identify cancer survivors who are at risk of developing cardiotoxicity.

METHODS: We analyzed plasma and left ventricle heart tissue samples collected from a cohort of male Sprague Dawley (SD) rats that were either sham irradiated or received fractionated doses (9 Gy per day × 5 days) of targeted X-ray radiation to the heart. Metabolomic and lipidomic analyses were utilized as a correlative approach for delineation of novel biomarkers associated with radiation-induced cardiac toxicity. Additionally, we used high-resolution mass spectrometry to examine the metabolomic profiles of plasma samples obtained from patients receiving high dose thoracic RT for esophageal cancer.

RESULTS: Metabolic alterations in the rat model and patient plasma profiles, showed commonalities of radiation response that included steroid hormone biosynthesis and vitamin E metabolism. Alterations in patient plasma profiles were used to develop classification algorithms predictive of patients at risk of developing RIHD.

CONCLUSION: Herein, we report the feasibility of developing a metabolomics-based biomarker panel that is associated with adverse outcomes of cardiac function in patients who received RT for the treatment of esophageal cancer.

PMID: 32360032 [PubMed - as supplied by publisher]

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Perioperative Cardiothoracic and Vascular Risk in Childhood Cancer and its Survivors.


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Perioperative Cardiothoracic and Vascular Risk in Childhood Cancer and its Survivors.


J Cardiothorac Vasc Anesth. 2020 Mar 07;:


Authors: Ketterl TG, Latham GJ


Abstract

CHILDREN with cancer and survivors of childhood cancer have an increased risk of cardiovascular disease, and this risk in the perioperative period must be understood. During diagnosis and treatment of pediatric cancer, multiple acute cardiovascular morbidities are possible, including anterior mediastinal mass, tamponade, hypertension, cardiomyopathy,and heart failure. Childhood cancer survivors reaching late childhood and adulthood experience substantially increased rates of cardiomyopathy, heart failure, valvular disease, pericardiac disease, ischemia, and arrhythmias. Despite considerable advances in the understanding and therapeutic options of pediatric malignancies, cardiac disease remains the most common treatment-related, noncancer cause of death in childhood cancer survivors. Increasingly, molecularly targeted agents, including small molecule inhibitors, are being incorporated into pediatric oncology. The acute and chronic risks associated with these newer therapeutic options in children are not yet well-described, which poses challenges for clinicians caring for these patients. In the present review, the unique risks factors, prevention strategies, and treatment of cardiovascular toxicities of the child with cancer and the childhood cancer survivor are examined, with an emphasis on the perioperative period.

PMID: 32360009 [PubMed - as supplied by publisher]

6 May 2020

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Effect of Cardioprotective Drugs on Chemotherapy-Induced Heart Failure and New Risk Stratification.


//www.ncbi.nlm.nih.gov/corehtml/query/egifs/https:--linkinghub.elsevier.com-ihub-images-PubMedLink.gif Related Articles

Effect of Cardioprotective Drugs on Chemotherapy-Induced Heart Failure and New Risk Stratification.


J Am Coll Cardiol. 2019 10 01;74(13):1736


Authors: Sun J, Shang H, Yang X, Xing Y


PMID: 31558260 [PubMed - indexed for MEDLINE]

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pubmed: tutte cardiotoxicity...

Strategies to Prevent Cardiotoxicity.


//www.ncbi.nlm.nih.gov/corehtml/query/egifs/https:--linkinghub.elsevier.com-ihub-images-PubMedLink.gif Related Articles

Strategies to Prevent Cardiotoxicity.


J Am Coll Cardiol. 2019 10 01;74(13):1737


Authors: Ozkalayci F, Tanboga IH


PMID: 31558262 [PubMed - indexed for MEDLINE]

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Carnitine Supplementation Attenuates Sunitinib-Induced Inhibition of AMP-Activated Protein Kinase Downstream Signals in Cardiac Tissues.


//www.ncbi.nlm.nih.gov/corehtml/query/egifs/http:--production.springer.de-OnlineResources-Logos-springerlink.gif //www.ncbi.nlm.nih.gov/corehtml/query/egifs/https:--www.ncbi.nlm.nih.gov-corehtml-pmc-pmcgifs-pubmed-pmc.png Related Articles

Carnitine Supplementation Attenuates Sunitinib-Induced Inhibition of AMP-Activated Protein Kinase Downstream Signals in Cardiac Tissues.


Cardiovasc Toxicol. 2019 08;19(4):344-356


Authors: Sayed-Ahmed MM, Alrufaiq BI, Alrikabi A, Abdullah ML, Hafez MM, Al-Shabanah OA


Abstract

This study has been initiated to investigate whether sunitinib (SUN) alters the expression of key genes engaged in mitochondrial transport and oxidation of long chain fatty acids (LCFA), and if so, whether these alterations should be viewed as a mechanism of SUN-induced cardiotoxicity, and to explore the molecular mechanisms whereby carnitine supplementation could attenuate SUN-induced cardiotoxicity. Adult male Wister albino rats were assigned to one of the four treatment groups: Rats in group 1 received no treatment but free access to tap water for 28 days. Rats in group 2 received L-carnitine (200 mg/kg/day) in drinking water for 28 days. Rats in group 3 received SUN (25 mg/kg/day) in drinking water for 28 days. Rats in group 4 received the same doses of L-carnitine and SUN in drinking water for 28 days. Treatment with SUN significantly increased heart weight, cardiac index, and cardiotoxicity enzymatic indices, as well as severe histopathological changes. Moreover, SUN significantly decreased level of adenosine monophosphate-activated protein kinase (AMPKα2), total carnitine, adenosine triphosphate (ATP) and carnitine palmitoyltransferase I (CPT I) expression and significantly increased acetyl-CoA carboxylase-2 (ACC2) expression and malonyl-CoA level in cardiac tissues. Interestingly, carnitine supplementation resulted in a complete reversal of all the biochemical, gene expression and histopathological changes-induced by SUN to the control values. In conclusion, data from this study suggest that SUN inhibits AMPK downstream signaling with the consequent inhibition of mitochondrial transport of LCFA and energy production in cardiac tissues. Carnitine supplementation attenuates SUN-induced cardiotoxicity.

PMID: 30644033 [PubMed - indexed for MEDLINE]

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pubmed: tutte cardiotoxicity...

Fulminant Vascular and Cardiac Toxicity Associated with Tyrosine Kinase Inhibitor Sorafenib.


//www.ncbi.nlm.nih.gov/corehtml/query/egifs/http:--production.springer.de-OnlineResources-Logos-springerlink.gif Related Articles

Fulminant Vascular and Cardiac Toxicity Associated with Tyrosine Kinase Inhibitor Sorafenib.


Cardiovasc Toxicol. 2019 08;19(4):382-387


Authors: Sudasena D, Balanescu DV, Donisan T, Hassan S, Palaskas N, Kim P, Karimzad K, Lopez-Mattei J, Arain S, Gould KL, Iliescu C


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