Search results for "CARDIOTOXICITY"

showing 10 items of 104 documents

Drug-related cardiotoxicity for the treatment of haematological malignancies in elderly.

2010

Several publications have focused on the cardiotoxicity of specific classes of haematological therapeutic agents such as antracyclines and cyclofosfamide. Cardiotoxicity of cancer chemotherapeutics is a problem for patients of all ages, but it increases with age. Toxicity can also be developed months after the last chemotherapy dose, and late reactions can be seen years later when they present new-onset cardiomyopathy. No data are available about the cardiotoxicity of non-chemotherapy agents currently used as preferred therapy for haematological malignancy in elderly. In this review we have provided a summary of the cardiovascular toxic effects produced by different drugs and therapeutic ag…

Drugmedicine.medical_specialtyHeart diseaseHeart Diseasesmedicine.medical_treatmentmedia_common.quotation_subjectCardiomyopathyAntineoplastic AgentsPharmacologyCardiotoxinsDrug Delivery SystemsDrug DiscoverymedicineAnimalsHumansIntensive care medicinedrug cardiotoxicity haematological malignanciesmedia_commonAgedPharmacologyCardiotoxicityChemotherapybusiness.industryAge FactorsCancerImatinibmedicine.diseaseHematologic NeoplasmsRituximabbusinessmedicine.drugCurrent pharmaceutical design
researchProduct

Acute myocardial effects of mitoxantrone in the rabbit

1987

Some clinical studies that were performed for the purpose of assessing the potential cardiotoxicity of mitoxantrone (DHAD) have shown that repeated administrations of the drugs in some patients cause a mild impairment of cardiac functions and morphological changes in the myocardial cells qualitatively similar to those elicited by anthracyclines. Since doxorubicin has been reported to cause acute cardiac effects, probably related to its chronic cardiotoxicity, experiments were carried out on the rabbit heart to investigate whether DHAD is also able to induce acute cardiac effects. Our results show that this drug caused a reversible dose-related impairment of cardiac contractility on the isol…

ElectrocardiographyDHADDrug Evaluation PreclinicalAnimalsHeartRabbitsIn Vitro TechniquesMitoxantroneantitumor drugsMyocardial ContractionCardiotoxicity
researchProduct

Gp91phox-containing NAD(P)H oxidase increases superoxide formation by doxorubicin and NADPH

2006

Doxorubicin is a highly effective antineoplastic drug associated with a dose-dependent cardiotoxicity that may result in irreversible cardiomyopathy and heart failure. Gene variants of the superoxide-generating enzyme NAD(P)H oxidase have recently been associated with this phenotype. We investigated the mechanism of this association using lucigenin-enhanced chemiluminescence, spectrophotometry, electrochemical sensor, and electron paramagnetic resonance spectroscopy. Superoxide production was measured in female wild-type and NAD(P)H oxidase-deficient (gp91phox knockout) mice. The magnitude of the increase in superoxide production on the addition of doxorubicin was much higher in hearts of w…

LuminescenceGene ExpressionAntineoplastic AgentsPolymerase Chain ReactionBiochemistryMicechemistry.chemical_compoundSuperoxidesPhysiology (medical)medicineAnimalsDoxorubicinNADPH-Ferrihemoprotein ReductaseMice Knockoutchemistry.chemical_classificationCardiotoxicityOxidase testMembrane GlycoproteinsDose-Response Relationship DrugSuperoxideMyocardiumNADPH OxidasesMolecular biologyMice Inbred C57BLEnzymechemistryBiochemistryDoxorubicinNAD(P)H oxidaseNADPH Oxidase 2Knockout mouseNAD+ kinaseNADPmedicine.drugFree Radical Biology and Medicine
researchProduct

Cardiovascular Toxicity in Cancer Patients Treated with Tyrosine Kinase Inhibitors: A Real-World Single-Center Experience

2019

<b><i>Background:</i></b> Target therapy can cause various cardiovascular complications. The aim of this study was to evaluate the burden of cardiovascular complications related to treatment with anti-BCR-ABL tyrosine kinase inhibitors (TKIs) and to determine if there are differences between the latest- and first-generation TKIs. <b><i>Methods:</i></b> A retrospective observational study was carried out on 55 patients (39 men, 16 women; mean age ± SD: 58 ± 11 years) treated with TKIs targeting Bcr-Abl for a median period of 3.5 years. Patients were divided in two groups according to the type of treatment. Group A included patients treated with…

MaleCancer Researchmedicine.medical_specialtyGastrointestinal Stromal TumorsDasatinibFusion Proteins bcr-ablCoronary Artery DiseasePulse Wave AnalysisCardio-oncology Cardiotoxicity Tyrosine kinase inhibitors Chronic myeloid leukemia Arterial stiffness03 medical and health scienceschemistry.chemical_compound0302 clinical medicineInternal medicineLeukemia Myelogenous Chronic BCR-ABL PositiveMedicineHumans030212 general & internal medicineAdverse effectPulse wave velocityProtein Kinase InhibitorsAgedGastrointestinal NeoplasmsRetrospective Studiesbusiness.industryPonatinibImidazolesRetrospective cohort studyGeneral MedicineMiddle Agedmedicine.diseaseThrombosisrespiratory tract diseasesDasatinibPyridazinesPyrimidinesTreatment OutcomeOncologyNilotinibchemistry030220 oncology & carcinogenesisArterial stiffnessCardiologyImatinib MesylateFemalebusinessmedicine.drugFollow-Up Studies
researchProduct

Sex differences in anthracycline-induced cardiotoxicity: the benefits of estrogens

2019

Anthracyclines are the cornerstone for many oncologic treatments, but their cardiotoxicity has been recognized for several decades. Female subjects, especially before puberty and adolescence, or after menopause, seem to be more at increased risk, with the prognostic impact of this sex issue being less consistent compared to other cardiovascular risk factors. Several studies imply that sex differences could depend on the lack of the protective effect of sex hormones against the anthracycline-initiated damage in cardiac cells, or on differential mitochondria-related oxidative gene expression. This is also reflected by the results obtained with different diagnostic methods, such as cardiovascu…

MaleCardiac & Cardiovascular SystemsMagnetic Resonance Spectroscopyand protection from anthracycline cardiotoxicitymedicine.disease_causeBioinformaticsRisk FactorsAnthracycline cardiotoxicityGender differenceGender differencesAnthracyclinesGonadal Steroid Hormones1102 Cardiorespiratory Medicine and HaematologyAMERICAN SOCIETYCardioprotectionSex CharacteristicsHeartPrognosisMitochondriaMenopauseEchocardiographyReperfusion InjuryHEART-FAILUREAnthracycline cardiotoxicity; Gender differences; Pathophysiology monitoring and protection from anthracycline cardiotoxicity; Anthracyclines; Biomarkers; Cardiotonic Agents; Cardiotoxicity; Echocardiography; Female; Gonadal Steroid Hormones; Heart; Heart Failure; Humans; Magnetic Resonance Spectroscopy; Male; Mitochondria; Nuclear Medicine; Oxidative Stress; Prognosis; Reperfusion Injury; Risk Factors; Sex CharacteristicsFemaleCardiology and Cardiovascular MedicineLife Sciences & BiomedicinePOSITION PAPERCARDIAC DYSFUNCTIONCardiotonic AgentsAnthracyclineSPECKLE-TRACKINGIschemiaDRUG CARDIOTOXICITYPathophysiologymedicineHumansCHILDHOOD-CANCER SURVIVORSBREAST-CANCERPathophysiology monitoring and protection from anthracycline cardiotoxicityHeart FailureCardiotoxicityScience & Technologybusiness.industryWORKING GROUPmedicine.diseaseCardiotoxicityOxidative StressmonitoringCardiovascular System & HematologyHeart failureCardiovascular System & CardiologyRISK-FACTORSNuclear MedicinebusinessOxidative stressAnthracycline cardiotoxicity; Gender differences; Pathophysiology monitoring and protection from anthracycline cardiotoxicityBiomarkersHormone
researchProduct

Acute Administration of Epirubicin Induces Myocardial Depression in Isolated Rat Heart and Production of Radical Species Evaluated by Electron Spin R…

2007

The aim of our study was to evaluate the acute effect of epirubicin (EPI), an anthracycline anticancer drug, on the evolution of cardiac functional parameters and production of reactive oxygen/nitrogen species (RONS). Isolated perfused rat hearts were subjected to 70 minutes of EPI (10.3 microM) infusion and to 5 minutes of isoproterenol (ISO, 0.1 microM) at the end of the protocol. Coronary flow (CF), left ventricular developed pressure (LVDP), and lactate dehydrogenase (LDH) release in the coronary effluents were evaluated throughout the protocol. RONS were detected in the coronary effluents by electron spin resonance spectroscopy with a spin probe, 1-hydroxy-3-carboxy-pyrrolidine (CP-H, …

MaleCardiac function curveTime FactorsFree RadicalsAnthracyclineIn Vitro TechniquesPharmacologymedicine.disease_causeVentricular Function Leftchemistry.chemical_compoundHeart RateCoronary CirculationLactate dehydrogenasemedicineAnimalsRats WistarEpirubicinPharmacologyAnalysis of VarianceCardiotoxicityAntibiotics AntineoplasticDose-Response Relationship DrugL-Lactate DehydrogenaseMolecular StructureChemistryMyocardiumElectron Spin Resonance SpectroscopyIsoproterenolHeartReactive Nitrogen SpeciesRatsPerfusionOxidative StressDose–response relationshipAnesthesiaReactive Oxygen SpeciesCardiology and Cardiovascular MedicinePerfusionOxidative stressEpirubicinmedicine.drugJournal of Cardiovascular Pharmacology
researchProduct

Distinct influence of atypical 1,4-dihydropyridine compounds in azidothymidine-induced neuro- and cardiotoxicity in mice ex vivo.

2008

This study demonstrates the effective protection by compounds of atypical 1,4-dihydropyridine (DHP) series cerebrocrast, glutapyrone and tauropyrone against neuro- and cardiotoxicity caused by the model compound azidothymidine, a well-known mitochondria-compromising anti-HIV drug. In previous in vitro experiments, we have demonstrated distinct effects of these DHP compounds to influence mitochondrial functioning. In the present in vivo experiments, DHP compounds were administered intraperitoneally in mice daily for 2 weeks, per se and in combinations with azidothymidine at doses: azidothymidine 50 mg/kg; cerebrocrast 0.1 mg/kg; glutapyrone 1 mg/kg; and tauropyrone 1 mg/kg. At the end of the…

MaleDihydropyridinesHeart DiseasesRatónAnti-HIV AgentsTaurineApoptosisBiologyPharmacologyToxicologyMiceGlutamatesIn vivomedicineAnimalsPharmacologyCerebral CortexInflammationCardiotoxicityMice Inbred ICRCaspase 3DihydropyridineTranscription Factor RelAGeneral MedicineBiochemistryGene Expression RegulationEnzyme inhibitorApoptosisToxicitybiology.proteinNeurotoxicity SyndromesZidovudineEx vivomedicine.drugBasicclinical pharmacologytoxicology
researchProduct

Molecular mechanisms of carfilzomib-induced cardiotoxicity in mice and the emerging cardioprotective role of metformin

2019

AbstractCarfilzomib (Cfz), an irreversible proteasome inhibitor licensed for relapsed/refractory myeloma, is associated with cardiotoxicity in humans. We sought to establish the optimal protocol of Cfz-induced cardiac dysfunction, to investigate the underlying molecular-signaling and, based on the findings, to evaluate the cardioprotective potency of metformin (Met). Mice were randomized into protocols 1 and 2 (control and Cfz for 1 and 2 consecutive days, respectively); protocols 3 and 4 (control and alternate doses of Cfz for 6 and 14 days, respectively); protocols 5A and 5B (control and Cfz, intermittent doses on days 0, 1 [5A] and 0, 1, 7, and 8 [5B] for 13 days); protocols 6A and 6B (p…

MaleImmunologymTORC1AMP-Activated Protein Kinases030204 cardiovascular system & hematologyPharmacologyBiochemistryMice03 medical and health scienceschemistry.chemical_compound0302 clinical medicinemedicineAnimalsHypoglycemic AgentsProtein Phosphatase 2Protein kinase BCardiotoxicitybiologybusiness.industryBortezomibCell BiologyHematologyCarfilzomibCardiotoxicityMetforminMetforminMice Inbred C57BLNitric oxide synthasechemistry030220 oncology & carcinogenesisProteasome inhibitorbiology.proteinbusinessOligopeptidesSignal Transductionmedicine.drugBlood
researchProduct

General oxidative stress during doxorubicin-induced cardiotoxicity in rats: Absence of cardioprotection and low antioxidant efficiency of alpha-lipoi…

2012

International audience; To evaluate the effects of alpha-lipoic acid (AL) in a model of doxorubicin (DOX)-induced cardiotoxicity, male Wistar rats were treated with DOX (1 mg/kg/d; 10 d) in combination or not with AL (50 mg/kg/d; 15 d). Plasma oxidative stress was determined by hydroperoxides (ROOH) and the ascorbyl radical/ascorbate ratio. One and two months later, the functional parameters of the hearts were determined in vivo by catheterization and cardiac oxidative stress was assessed by malonedialdehyde (MDA) and O₂*⁻ (dihydroethidium fluorescence) content in tissue. After two months, body weight was higher in the DOX-AL group than in DOX (+16%), but this was due to ascites. Histologic…

MaleMESH : Oxidative StressAntioxidantmedicine.medical_treatmentMESH : HematocritMESH : Thioctic AcidBiochemistryAntioxidants0302 clinical medicineSuperoxidesAscitic FluidMESH: AnimalsMESH : Body WeightComputingMilieux_MISCELLANEOUS0303 health sciencesThioctic AcidCumulative doseMESH: Heart DiseasesHeartGeneral Medicine3. Good healthMESH: Ascitic Fluid[SDV] Life Sciences [q-bio]030220 oncology & carcinogenesisMESH : Ascitic FluidMESH: Hydrogen PeroxideMESH : AntioxidantsMESH: Thioctic Acidmedicine.medical_specialtyCardiotonic AgentsCardiotoxinsMESH: Hematocrit03 medical and health sciencesMESH: Doxorubicin[SDV.MHEP.CSC]Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular systemIn vivoRats Wistar[ SDV ] Life Sciences [q-bio]MyocardiumMESH: AntioxidantsHydrogen PeroxideMESH: Cardiotonic AgentsMESH : Organ SizeMESH: Body WeightMESH: Heartcarbohydrates (lipids)EndocrinologyMESH: LiverMESH : SuperoxidesMESH: Organ Size[SDV]Life Sciences [q-bio]MESH : Cardiotonic AgentsAscorbic AcidMESH: Superoxidesmedicine.disease_causeMESH: EatingEatingpolycyclic compoundsMESH : MyocardiumMESH: Thiobarbituric Acid Reactive SubstancesMESH: Ascorbic AcidAntibiotics AntineoplasticMESH: Oxidative StressChemistryMESH : RatsOrgan SizeMESH : Antibiotics Antineoplastic[SDV.MHEP.CSC] Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular systemBiochemistryHematocritLiverMESH : Cardiotoxinsmedicine.drugMESH : EatingMESH: MyocardiumHeart DiseasesMESH: RatsMESH : MaleMESH : Thiobarbituric Acid Reactive SubstancesMESH : Rats WistarThiobarbituric Acid Reactive SubstancesContractilityMESH : HeartInternal medicinemedicineTBARSAnimalsMESH : DoxorubicinDoxorubicinMESH: Antibiotics AntineoplasticMESH : Ascorbic Acid030304 developmental biologyCardiotoxicityBody WeightMESH : LiverMESH : Heart DiseasesMESH: Rats WistarMESH: MaleRatsOxidative StressMESH: CardiotoxinsDoxorubicinMESH : AnimalsMESH : Hydrogen PeroxideOxidative stress
researchProduct

Mitochondria as the target for mildronate's protective effects in azidothymidine (AZT)-induced toxicity of isolated rat liver mitochondria

2008

Previously mildronate, an aza-butyrobetaine derivative, was shown to be a cytoprotective drug, through its mechanism of action of inhibition of carnitine palmitoyltransferase-1, thus protecting mitochondria from long-chain fatty acid accumulation and subsequent damage. Recently in an azidothymidine (AZT)-induced cardiotoxicity model in vivo (in mice), we have found mildronate's ability of protecting heart tissue from nuclear factor kappaB abnormal expression. Preliminary data also demonstrate cerebro- and hepatoprotecting properties of mildronate in AZT-toxicity models. We suggest that mildronate may target its action predominantly to mitochondria. The present study in isolated rat liver mi…

MaleMitochondrial DiseasesBioenergeticsAntimetabolitesCell RespirationClinical BiochemistryMitochondria LiverIn Vitro TechniquesMitochondrionPharmacologyBiologymedicine.disease_causeBiochemistryPermeabilityRespiratory electron transport chainDrug Delivery SystemsmedicineAnimalsCarnitineRats WistarCardiotoxicityCell BiologyGeneral MedicineRatsDisease Models AnimalMechanism of actionBiochemistryToxicitymedicine.symptomEnergy MetabolismZidovudineOxidative stressMethylhydrazinesmedicine.drug
researchProduct