AC-Mode of Chemotherapy as a Trigger of Cardiac Syndrome X: A Case Study

Avagimyan, Ashot; Mkrtchyan, L. G.; Abrahomovich, Orest; Sheibani, Mohammad; Guevorkyan, A. G.; Sarrafzadegan, Nizal; Kozhukhov, Sergey; Agati, Luciano; Astengiano, Ricardo; Zaritska, Valentina; Jndoyan, Zinaida

doi:10.1016/j.cpcardiol.2021.100994

Cited by 15 publications

(5 citation statements)

References 16 publications

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“…Other mechanisms associated with DXR cardiotoxicity include calcium hemostasis imbalance inducing DNA damage and disruption of the neuroglial/ErbB signaling pathway resulting in apoptosis and mitochondrial dysfunction ( 4 ). There were recent reports of an association between cardiac syndrome X and DXR-induced endothelial cell damage ( 29 ). DXR-induced endothelial cell damage triggers the onset and progression of cardiomyopathy by reducing the release and activity of critical endothelial factors and inducing endothelial cell death.…”

Section: Discussionmentioning

confidence: 99%

Late-onset doxorubicin-induced congestive heart failure in an elderly cancer survivor: A case report

Suto

Inui

et al. 2023

Front. Cardiovasc. Med.

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BackgroundRecently, the survival rate of patients with cancer has improved annually due to advancements in cancer diagnosis and treatment technologies. Meanwhile, late-onset complications associated with cancer treatment significantly affect survival and quality of life. However, different from pediatric cancer survivors, there is no unified view on the follow-up of late complications in elderly cancer survivors. We reported a case of congestive heart failure as a late-onset complication of doxorubicin (DXR) in an elderly cancer survivor.Case reportThe patient is an 80-year-old woman with hypertension and chronic renal failure. She received six cycles of chemotherapy for Hodgkin's lymphoma that started in January 201X-2. The total dose of DXR was 300 mg/m2, and a transthoracic echocardiogram (TTE) performed in October 201X-2, showed good left ventricular wall motion (LVWM). In April 201X, she suddenly developed dyspnea. Upon arrival at the hospital, a physical examination revealed orthopnea, tachycardia, and leg edema. A chest radiograph showed cardiac enlargement and pleural effusion. A TTE showed diffusely reduced LVWM and a left ventricular ejection fraction in the 20% range. After close examination, the patient was diagnosed with congestive heart failure due to late-onset DXR-induced cardiomyopathy.ConclusionLate-onset DXR-induced cardiotoxicity is considered high-risk from 250 mg/m2 or higher. Elderly cancer survivors are at higher risk of cardiotoxicity than non-elderly cancer survivors and may require closer follow-up.

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Section: Discussionmentioning

confidence: 99%

Late-onset doxorubicin-induced congestive heart failure in an elderly cancer survivor: A case report

Suto

Inui

et al. 2023

Front. Cardiovasc. Med.

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“…all manipulations were carried out following the European Convention's provisions for the при усредненных кумулятивных дозах развивается целый спектр кардиологической симптоматики. Нами подробно описаны клинические случаи развития фибрилляции предсердий (ФП) [6], липоматоза миокарда [7], микроваскулярной стенокардии [8] и атерогенной гипердислипидемии [9]. В связи с вышеотмеченным было решено исследовать кардиотоксический и проатерогенный потенциал АС-режима химиотерапии.…”

Section: Adherence To Ethical Standardsunclassified

Trimetazidine as a modifier of doxorubicin+cyclophosphamideinduced hyperdyslipidemia

Avagimyan

Kakturskiy

2022

SJCEM

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Aim. The present work aimed at studying the proatherogenic potential of doxorubicin-cyclophosphamide (AC) chemotherapy regimen while simultaneously substantiating the use of trimetazidine as a modifier of the changes induced.Material and Methods. The fundamental, randomized, controlled, experimental in vivo study was conducted. To perform the experimental work, 80 inbred Wistar rats were randomly divided into four groups with equal numbers of animals in each group. The course dosages doxorubicin, cyclophosphamide, and trimetazidine were 15, 150, and 42 mg/kg, respectively. The experiment lasted for 14 days. Trimetazidine was chosen as a probable stabilizer of endothelial functioning.Results. The deviations of the following parameters were evaluated in the framework of this study: total cholesterol, triglycerides, high-density lipoproteins, and low-density lipoproteins. Coronary index and atherogenic index (CA) were also analyzed as prognostic indicators. Statistically significant intergroup differences were recorded in lipid profiles (one-way ANOVA, p < 0.0001) two weeks after beginning the AC chemotherapy regimen. It is worthy of note that the AC chemotherapy regimen caused destabilization of all studied parameters of cholesterol metabolism while trimetazidine showed statistically and pathogenetically significant mild hypolipidemic effect. The study showed that the concentration of CA in group 2 was higher by 187.4 and 172.8%, and the values of coronary risk index (CRI) were higher by 115.8 and 113.9% than the corresponding parameters in groups 1 and 4, respectively. Comparative analysis of groups 3 and 2 showed that the use of TMZ was associated with decreases in CA by 55.5% and in CRI by 44.2% (Tukey’s post-hoc test, p < 0.05).Conclusions. (1) AC chemotherapy regimen was an inducer of atherogenic hyperdyslipidemia, and (2) trimetazidine had a hypolipidemic effect.

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“…CP metabolites stimulate oxidative stress and directly damage the endothelial cells resulting in edema, interstitial hemorrhage, and formation of microthrombosis. 3,4 Endothelial cell is more susceptible to CP-induced damage than other cells. In addition, CP induces release of reactive oxygen species (ROS) leading to diminishing of nitric oxide availability and decreasing the release of antioxidant molecules with induction of hypoxia.…”

Section: Introductionmentioning

confidence: 99%

Role of hypoxia inducible factor/vascular endothelial growth factor/endothelial nitric oxide synthase signaling pathway in mediating the cardioprotective effect of dapagliflozin in cyclophosphamide-induced cardiotoxicity

et al. 2023

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Background Cyclophosphamide (CP) is a commonly used chemotherapeutic and immunosuppressive alkylating agent. However, cardiac adverse effects of CP interfere with its clinical benefit. Cardio-oncology research is currently an important issue and finding effective cardiopreserving agents is a critical need. For the first time, we aimed to detect if dapagliflozin (DAP) could ameliorate CP-induced cardiac injury and investigated the role of hypoxia inducible factor α (HIF1α)/vascular endothelial growth factor (VEGF)/endothelial nitric oxide synthase (eNOS) pathway. Methods Forty male Wistar albino rats were included in the current model. Studied groups are: control group; CP-induced cardiotoxicity group; CP group treated with DAP; CP group treated with DAP and administered a nitric oxide synthase inhibitor; nitro-ω-L-arginine (L-NNA) before DAP to explore the role of eNOS. Results Our data revealed that CP could induce cardiac damage as manifested by significant increases in cardiac enzymes, blood pressure, malondialdehyde (MDA), tumor necrosis factor alpha (TNFα), HIF1α, sodium glucose co-transporter 2 (SGLT2) and cleaved caspase-3 levels with toxic histopathological changes. However, there are significant decreases in reduced glutathione (GSH), total antioxidant capacity (TAC), VEGF, and eNOS. On the opposite side, co-administration of DAP showed marked improvement of CP-induced cardiac damage that may be due to its ability to inhibit SGLT2, antioxidant, anti-inflammatory and anti-apoptotic properties. Results showed decreasing the cardioprotective effect of DAP on administration of L-NNA, reflecting the critical effect of eNOS in mediating such protection. Conclusion DAP could reduce CP cardiotoxicity based upon its ability to modulate SGLT2 and HIF1α/VEGF/eNOS signaling pathway.

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AC-Mode of Chemotherapy as a Trigger of Cardiac Syndrome X: A Case Study

Cited by 15 publications

References 16 publications

Late-onset doxorubicin-induced congestive heart failure in an elderly cancer survivor: A case report

Late-onset doxorubicin-induced congestive heart failure in an elderly cancer survivor: A case report

Trimetazidine as a modifier of doxorubicin+cyclophosphamideinduced hyperdyslipidemia

Role of hypoxia inducible factor/vascular endothelial growth factor/endothelial nitric oxide synthase signaling pathway in mediating the cardioprotective effect of dapagliflozin in cyclophosphamide-induced cardiotoxicity

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