Overview of current guidelines
Susan F. Dent in Practical Cardio-Oncology, 2019
This chapter aims to provide an overview of the current major societal guidelines and recommendations within the field of cardio-oncology. These include the (a) definition of cancer therapeutics related cardiac dysfunction (CTRCD); (b) diagnosis of CTRCD with a multimodality imaging approach and serum biomarkers; (c) identification of patients at high risk of cardiotoxicity; (d) prevention of cardiotoxicity; (e) monitoring of cardiotoxicity; and (f) treatment of cardiotoxicity. Guidelines and position statements reviewed include the 2016 European Society of Cardiology (ESC) Position Paper (3); the 2016 American Society of Clinical Oncology (ASCO) Practice Guidelines (4); the 2016 Canadian Cardiovascular Society (CCS) Guidelines (5); the 2014 Report from the American Society of Echocardiography (ASE) and the European Association of Cardiovascular Imaging (EACVI) (6); and the 2012 European Society of Medical Oncology (ESMO) Clinical Practice Guidelines (7). The guidelines aim to provide some consensus on the general management of patients with cardiotoxicity. Minor discrepancies exist owing to differences in each society's focus and target audience.
Drug Analysis of Protein Microspheres: From Pharmaceutical Preparation to In Vivo Fate
Neville Willmott, John Daly in Microspheres and Regional Cancer Therapy, 2020
Daunorubicin (daunomycin, rubidomycin) was the first anthracycline antibiotic to be discovered (in 1963) followed by doxorubicin (adriamycin) (in 1969), and together these two remain the most useful clinically.5 Both drugs are used extensively in combination chemotherapy, with doxorubicin having the wider spectrum of clinical activity. Both exhibit the classic toxicity profiles of cytotoxic drugs: nausea and vomiting, gastrointestinal tract toxicity, hair loss, and myelosuppression. In addition, they induce a unique toxicity to the heart, which is related to cumulative dose and peak plasma drug concentrations and is irreversible. Originally, this cardiotoxicity stimulated the drive for new compounds and analog development, but drug resistance, both in the form of the multidrug resistance phenotype6,7 and the atypical (altered topoisomerase II) multidrug resistance phenotype,8 is generally considered the major clinical problem to be overcome by the pharmacologist. Cardiotoxicity can be controlled by altering dose schedules without loss of anticancer activity.9 Because doxorubicin is the more active drug and has been incorporated in microspheres, the following sections will deal exclusively with doxorubicin.
A Review on Medicinal Plants used in Cardioprotective Remedies in Traditional Medicine
Anne George, Oluwatobi Samuel Oluwafemi, Blessy Joseph, Sabu Thomas, Sebastian Mathew, V. Raji in Holistic Healthcare, 2017
Cardiovascular diseases (CVD) are the leading cause of death in developing countries. CVD causes over 1.5 million deaths in the European Union (EU) and is the main cause of years of life lost from early death. CVD include coronary heart disease, myocardial infarction (MI), peripheral artery disease, rheumatic heart disease, and congenital heart disease.1 Coronary heart disease is the most common type of heart disease, killing more than 385,000 people annually.2 More than half of the deaths due to heart disease were reported in men.2 The risk factors for the growing burden of CVD includes hypertension, dyslipidemia, diabetes, obesity, change of life style, physical inactivity, use of tobacco and some chemotherapeutics.3 The drugs which induce cardiotoxicity include anthracyclines, isoproterenol, trastuzumab, 5-fluorouracil, CP and heavy metals like arsenic, cadmium, and lead. These drugs enhance the formation of free radicals leading to oxidative stress, which results in cardiac damage.4
Radiation metabolomics in the quest of cardiotoxicity biomarkers: the review
Published in International Journal of Radiation Biology, 2020
Michalina Gramatyka, Maria Sokół
From a molecular perspective, the most important cause of cardiotoxicity at low doses are free radicals (primarily reactive oxygen species; ROS) generated by radiation. They induce oxidative stress, disrupt metabolic processes and trigger inflammatory response in living cells (Jang et al. 2016; Tapio 2016). At low, physiological concentrations, free radicals play an important role in regulating protein kinases and phosphatases, as well as in maintaining cellular homeostasis, cardiomyocytes contractility and proper functioning of endothelial cells (Bhattacharya and Asaithamby 2016). Higher concentrations of free radicals lead to cellular death by damaging cell structures, disturbing enzymatic activity, and causing lipid peroxidation (Ishikawa et al. 2010). ROS also lead to impaired mitochondrial functioning and damage of their structure (Barjaktarovic et al. 2013b; Azimzadeh et al. 2017).
Trimetazidine ameliorates sunitinib-induced cardiotoxicity in mice via the AMPK/mTOR/autophagy pathway
Published in Pharmaceutical Biology, 2019
Yi Yang, Na Li, Tongshuai Chen, Chunmei Zhang, Lingxin Liu, Yan Qi, Peili Bu
Cardiovascular adverse effects of SU commonly include hypertension, LVEF declines, and congestive heart failure (Chu et al. 2007). Initially designed as a selective tyrosine kinase inhibitor, SU primarily inhibits vascular endothelial cell growth factor receptors (VEGFRs) 1-3, platelet-derived growth factor receptors (PDGRF) α and β, FMS-like tyrosine kinase-3 (Flt-3), the stem cell factor receptor c-kit, colony-stimulating factor 1 receptor (CSF1R), and the ret oncogene product, RET (Chu et al. 2007), as molecular targets. However, recent kinome and transcriptome profiling revealed that cytotoxic effects of SU are not limited to inhibition of these targets, but are instead far more broad-targeted (Stuhlmiller et al. 2017). Cardiomyocytes constitute the cellular component of the myocardium and are highly energy-consumptive and sensitive to SU cytotoxicities. Recent studies revealed the mechanisms of cardiomyocyte toxicities of SU to include mitochondrial dysfunction (Varga et al. 2015), hypertrophy influenced by mitogen-activated protein kinases pathways and aryl hydrocarbon receptor signaling pathway (Maayah et al. 2014; Korashy et al. 2015), autophagy (Zhao et al. 2010), and AMP-activated protein kinase inhibition (Kerkela et al. 2009). Cardioprotective strategies should, therefore, be designed to counteract these mechanisms of cardiotoxicity.
UR-144, synthetic cannabinoid receptor agonist, induced cardiomyoblast toxicity mechanism comprises cytoplasmic Ca2+ and DAPK1 related autophagy and necrosis
Published in Toxicology Mechanisms and Methods, 2023
Muzeyyen Akar, Merve Ercin, Tugce Boran, Selda Gezginci-Oktayoglu, Gül Özhan
The molecular mechanisms of UR-144’s cytotoxic effects are still unknown. There are limited studies on the toxic profile of UR-144. Studies have shown that UR-144 induced ROS and apoptotic cell death in different cell lines (Fonseca et al. 2019; Almada et al. 2020). Cardiomyocyte death plays a major role in cardiotoxicity and it affects cardiotoxic progression. There are many types of cell death mechanisms. The most common types of cardiotoxicity induced by drugs/chemicals are apoptosis, necrosis, and autophagy (Ma et al. 2020). Apoptosis (caspase-dependent) and autophagy (caspase-independent) are also known as programmed cell death, whereas necrosis is considered to be unregulated and sudden cell death (Nikoletopoulou et al. 2013). Complex signalization processes interconnect these pathways to decide cell fate (Chen et al. 2018).
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