cardiovascular toxicity
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2022 ◽  
Vol 8 ◽  
Author(s):  
Silvio Antoniak ◽  
Sukanya Phungphong ◽  
Zhaokang Cheng ◽  
Brian C. Jensen

Anthracycline antineoplastic agents such as doxorubicin are widely used and highly effective component of adjuvant chemotherapy for breast cancer and curative regimens for lymphomas, leukemias, and sarcomas. The primary dose-limiting adverse effect of anthracyclines is cardiotoxicity that typically manifests as cardiomyopathy and can progress to the potentially fatal clinical syndrome of heart failure. Decades of pre-clinical research have explicated the complex and multifaceted mechanisms of anthracycline-induced cardiotoxicity. It is well-established that oxidative stress contributes to the pathobiology and recent work has elucidated important central roles for direct mitochondrial injury and iron overload. Here we focus instead on emerging aspects of anthracycline-induced cardiotoxicity that may have received less attention in other recent reviews: thrombosis, myocardial atrophy, and non-apoptotic programmed cell death.


Biomedicines ◽  
2022 ◽  
Vol 10 (1) ◽  
pp. 99
Author(s):  
Abderrahim Nemmar ◽  
Sumaya Beegam ◽  
Nur Elena Zaaba ◽  
Salem Alblooshi ◽  
Saleh Alseiari ◽  
...  

Inhaled particulate air pollution exerts pulmonary inflammation and cardiovascular toxicity through secondary systemic effects due to oxidative stress and inflammation. Catalpol, an iridiod glucoside, extracted from the roots of Rehmannia glutinosa Libosch, has been reported to possess anti-inflammatory and antioxidant properties. Yet, the potential ameliorative effects of catalpol on particulate air pollution—induced cardiovascular toxicity, has not been studied so far. Hence, we evaluated the possible mitigating mechanism of catalpol (5 mg/kg) which was administered to mice by intraperitoneal injection one hour before the intratracheal (i.t.) administration of a relevant type of pollutant particle, viz. diesel exhaust particles (DEPs, 30 µg/mouse). Twenty-four hours after the lung deposition of DEPs, several cardiovascular endpoints were evaluated. DEPs caused a significant shortening of the thrombotic occlusion time in pial microvessels in vivo, induced platelet aggregation in vitro, and reduced the prothrombin time and the activated partial thromboplastin time. All these actions were effectively mitigated by catalpol pretreatment. Likewise, catalpol inhibited the increase of the plasma concentration of C-reactive proteins, fibrinogen, plasminogen activator inhibitor-1 and P- and E-selectins, induced by DEPs. Moreover, in heart tissue, catalpol inhibited the increase of markers of oxidative (lipid peroxidation and superoxide dismutase) and nitrosative (nitric oxide) stress, and inflammation (tumor necrosis factor α, interleukin (IL)-6 and IL-1β) triggered by lung exposure to DEPs. Exposure to DEPs also caused heart DNA damage and increased the levels of cytochrome C and cleaved caspase, and these effects were significantly diminished by the catalpol pretreatment. Moreover, catalpol significantly reduced the DEPs-induced increase of the nuclear factor κB (NFκB) in the heart. In conclusion, catalpol significantly ameliorated DEPs–induced procoagulant events and heart oxidative and nitrosative stress, inflammation, DNA damage and apoptosis, at least partly, through the inhibition of NFκB activation.


2021 ◽  
Vol 9 (12) ◽  
pp. 326-328
Author(s):  
Oussama Hdioud ◽  
◽  
Benmessaoudfz MD ◽  
Doghmi Nawal MD ◽  
Oukerraj Latifa ◽  
...  

Despite the development of tests for the detection of doping, Anabolic steroids, are still used to increase sports performance. Unfortunately, studies have clearly shown that overdose of anabolic steroids can induce serious cardiovascular complications that can be life-threatening. This implies the determining role of health professionals in informing the general population and athletes in particular about the lethal effect of these substances. We report the case of a young high-level athlete who consults for palpitations and in whom cardiac imaging reveals abnormalities related to chronic consumption of anabolic steroids.


2021 ◽  
Vol 3 ◽  
Author(s):  
Lena Ekström ◽  
Susanne Broström ◽  
Marja-Liisa Dahl ◽  
Annica Börjesson

Anabolic Androgenic Steroid (AAS) abuse in the society is considered a health problem and has been associated with cardiovascular toxicity, endocrine disruption, as well as psychiatric symptoms such as aggression and cognitive dysfunction. Men and women abusing AAS, as well as persons in close relationship to AAS abusers, may encounter concerns. Subsequently, the Anti-Doping Hotline was formed 1993 to answers questions about doping in the society. Here we have reviewed 7,123 enquiries posted on the Anti-Doping Hotline website between 2005 and 2018 to see what type of questions were raised. Most questions (n = 2,924) involved AAS, 60% from abusers themselves, and 17% from a person close to an AAS abusers. Only 2.3% of the questions concerned AAS abusing women. Of the AAS specific questions most were from persons who sought personal advice regarding risks and side effects. Notably, the AAS abusers themselves were concerned about somatic side effects (e.g., gynecomastia) and problems related to the AAS injection. The persons in close relationship to an AAS abusers on the other hand, expressed concerns about psychiatric changes including mood swings and aggressivity. In addition to AAS, 26 and 13% of the questions involved dietary supplements and other doping substances, respectively. A gradual decrease of questions regarding ephedrine was noted, whereas the numbers of SARMs related questions increased during this time. Our results show that there is a continuous need to provide medical, nursing, and social support and counseling to AAS abusers and their next of kin.


2021 ◽  
Vol 135 (23) ◽  
pp. 2661-2663
Author(s):  
Ninian N. Lang ◽  
Rhian M. Touyz

Abstract Dramatic improvements in cancer survival have arisen because of the rapid development of novel anti-cancer therapies. The potential for cardiovascular toxicity associated with these drugs often reflects overlap between pathogenic cancer mechanisms and physiological pathways required for normal cardiovascular function. Clinical Science has, therefore, compiled a themed collection on Cardiovascular-Oncology. This collection examines the intersection between cancer treatments and their potentially harmful cardiovascular effects. By defining the mechanisms underlying unwanted cardiovascular effects of anti-cancer therapies, cardioprotective strategies can be developed. Only by doing so, will patients be able to achieve optimal cancer treatment at the minimum cost to cardiovascular health.


2021 ◽  
Vol 20 (7) ◽  
pp. 2923
Author(s):  
Yu. Yu. Kirichenko ◽  
I. S. Ilgisonis ◽  
T. V. Ivanova ◽  
A. S. Zolotukhina ◽  
N. V. Khabarova ◽  
...  

Aim. To study the effect of multiagent chemotherapy on structural and functional vascular, electrophysiological parameters and cardiac hemodynamics in patients with stomach cancer.Material and methods. The study included 3 groups of 25 people: healthy volunteers, those with established cardiac disease (hypertension + coronary artery disease), gastric adenocarcinoma (fluoropyrimidine/platinum-based chemotherapy). Cancer patients before and after chemotherapy courses underwent non-invasive assessment of vascular wall and endothelial dysfunction (videocapillaroscopy, digital photoplethysmography), as well as electrocardiography and echocardiography. Healthy volunteers and cardiac patients were examined once.Results. In cancer patients, even before chemotherapy courses, endothelial dysfunction (ED) (occlusal index, 1,7 (1,4; 1,9), normal values >1,8) and structural vascular disorders (stiffness index, 8,9 m/s (7,7; 9,7), normal values <8 m/s; refractive index, 32,4% (27,5; 37,7), normal values <30%). All above-mentioned parameters significantly worsened after multiagent chemotherapy (progression of ED and vascular wall remodeling: occlusal index, 1,3 (1,2; 1,5) (p<0,0002); stiffness index, 10,3 m/s (9,5; 11,2) (p<0,0001); reflection index, 40,2% (35,5; 43,6) (p<0,001) Decrease in left ventricular ejection fraction and diastolic function was detected. The number of supraventricular and ventricular premature beats during chemotherapy increased 9 and 10 times, respectively (p<0,05).Conclusion. The study for the first time assessed the effect of multiagent chemotherapy on ED, vascular stiffness and cardiac hemodynamics in patients with gastric cancer. A significant aggravation of all endothelial function parameters after treatment has been proven, which requires further study in order to develop criteria for early cardiovascular toxicity. 


2021 ◽  
Vol 431 ◽  
pp. 115742
Author(s):  
Marina V. Malovichko ◽  
Wesley T. Abplanalp ◽  
Samantha A. McFall ◽  
Breandon S. Taylor ◽  
Nalinie S. Wickramasinghe ◽  
...  

2021 ◽  
Vol 12 ◽  
Author(s):  
Shan Cheng ◽  
Pan Jin ◽  
Heying Li ◽  
Duanqing Pei ◽  
Xiaodong Shu

Tyrosine kinase inhibitors (TKIs) to BCR-ABL1 have been successfully used to treat chronic myeloid leukemia (CML), however, multiple TKI-associated adverse events have been reported and become an emerging problem in patients. The mechanisms of TKI-induced toxicity are not fully understood and it remains challenging to predict potential cardiovascular toxicity of a compound. In this study, we established a zebrafish model to evaluate potential in vivo cardiovascular toxicity of TKIs. We treated the endothelium labeled Tg(kdrl:EGFP) transgenic zebrafish embryos with TKIs then performed confocal imaging to evaluate their vascular structure and function. We found that among FDA approved CML TKIs, ponatinib (the only approved TKI that is efficacious to T315I mutation) is the most toxic one. We then evaluated safety profiles of several clinical stage kinase inhibitors that can target T315I and found that HQP1351 treatment leads to vasculopathies similar to those induced by ponatinib while the allosteric ABL inhibitor asciminib does not induce noticeable cardiovascular defects, indicating it could be a promising therapeutic reagent for patients with T315I mutation. We then performed proof-of-principle study to rescue those TKI-induced cardiovascular toxicities and found that, among commonly used anti-hypertensive drugs, angiotensin receptor blockers such as azilsartan and valsartan are able to reduce ponatinib or HQP1351 induced cardiovascular toxicities. Together, this study establishes a zebrafish model that can be useful to evaluate cardiovascular toxicity of TKIs as well as to develop strategies to minimize TKI-induced adverse events.


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