Search results for "CARDIOTOXICITY"

showing 10 items of 104 documents

Cardiovascular Damage in Clinical Trials

2018

The Cardio-oncology field has grown considerably in the last two decades. The remarkable increase in the number of molecules used in oncology has brought with it a huge set of cardiovascular adverse events. For this reason, it is necessary to intervene on the early stages of drug development. This is what the Food and Drug Administration aims to do. This purpose can be achieved through a more careful analysis of the adverse event, development of guidelines, and identification of objective parameters that could guide the researcher in defining precisely the adverse event. It is also necessary to use additional methods not yet used in clinical trials that can allow an early detection of adver…

Cardiotoxicitymedicine.medical_specialtybusiness.industryfood and beveragesEarly detectionClinical trialFood and drug administrationDrug developmentmedicineCardio oncologyIntensive care medicineAdverse effectSet (psychology)business
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Cardioprotection by gene therapy: A review paper on behalf of the Working Group on Drug Cardiotoxicity and Cardioprotection of the Italian Society of…

2015

Ischemic heart disease remains the leading cause of death worldwide. Ischemic pre-, post-, and remote conditionings trigger endogenous cardioprotection that renders the heart resistant to ischemic-reperfusion injury (IRI). Mimicking endogenous cardioprotection by modulating genes involved in cardioprotective signal transduction provides an opportunity to reproduce endogenous cardioprotection with better possibilities of translation into the clinical setting. Genes and signaling pathways by which conditioning maneuvers exert their effects on the heart are partially understood. This is due to the targeted approach that allowed identifying one or a few genes associated with IRI and cardioprote…

CardiotoxinIschemic heart diseaseCardiologyMyocardial IschemiaPreconditioningMyocardial Reperfusion InjuryCardioprotectionRemote conditioningCardiotoxinsPostconditioningGene therapyMedicalHumansMyocardialIschemic PreconditioningSocieties MedicalCardioprotection; Gene therapy; Genomics; Ischemic heart disease; Postconditioning; Preconditioning; Remote conditioning; Cardiology; Cardiotoxicity; Cardiotoxins; Gene Targeting; Genetic Therapy; Humans; Ischemic Preconditioning Myocardial; Italy; Myocardial Ischemia; Myocardial Reperfusion Injury; Oxidative Stress; Societies MedicalCardioprotection; Gene therapy; Genomics; Ischemic heart disease; Postconditioning; Preconditioning; Remote conditioning; Cardiology; Cardiotoxicity; Cardiotoxins; Gene Targeting; Genetic Therapy; Humans; Ischemic Preconditioning; Myocardial; Italy; Myocardial Ischemia; Myocardial Reperfusion Injury; Oxidative Stress; Societies; Medical; Cardiology and Cardiovascular MedicineOxidative StreGenomicsGenetic TherapyCardioprotection Gene therapy Genomics Ischemic heart disease Postconditioning Preconditioning Remote conditioningCardiotoxicityOxidative StressCardioprotection; Gene therapy; Genomics; Ischemic heart disease; Postconditioning; Preconditioning; Remote conditioningItalyIschemic Preconditioning MyocardialGene TargetingGenomicSocietiesCardiology and Cardiovascular MedicineHuman
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Cardio-oncology in multiple myeloma: is it time for a specific focus?

2017

It has been known for some time that some oncologic drugs can cause heart damage. The term ‘cardiotoxicity’ just refers to the presence of a cardiac event during therapy or at least related to ther...

Cardiovascular eventCancer Researchmedicine.medical_specialtyHeart DiseasesInterdisciplinary ResearchAntineoplastic Agents030204 cardiovascular system & hematology03 medical and health sciences0302 clinical medicinemedicineHumansCardio oncologyIntensive care medicineMultiple myelomaFocus (computing)Cardiotoxicitybusiness.industryDisease Managementfood and beveragesHematologymedicine.diseaseCardiotoxicityhumanitiesCardio-oncologyOncologyMultiple MyelomabusinessHeart damage030215 immunology
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Prevention and Clinical Management of Cardiovascular Damage Induced by Anticancer Drugs: Need gor Early Biomarkers snd Cardio- snd Vasculo-Protection…

2018

The use of chemotherapy has largely improved the prognosis of cancer patients in the past two decades. However, the advent of more effective anticancer therapies has led to a higher incidence of cardiovascular toxicity that shows an increased incidence and represents a significant determinant of quality of life and mortality during ongoing treatment and in long-term survivors of cancer. In this setting, the primary objective for cardiologists and oncologists is the early identification of patients at high risk for developing cardiovascular toxicity and the identification of the cardiovascular cardiotoxicity in the earliest stages to personalize cancer therapy, arrange preventive interventio…

Cardiovascular toxicityCardiotoxicitymedicine.medical_specialtyChemotherapyVascular Toxicitybusiness.industryIncidence (epidemiology)medicine.medical_treatmentBiomarkers Omics Cardioprotection Vasculoprotection Cardiotoxicity Vascular Toxicity Anticancer drugsVasculoprotectionCancerOmicsCardioprotectionmedicine.diseaseOmicsAnticancer drugsCardiotoxicityQuality of lifemedicinePersonalized therapyIntensive care medicinebusinessBiomarkers
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From molecular mechanisms to clinical management of antineoplastic drug-induced cardiovascular toxicity: A translational overview

2019

Significance: Antineoplastic therapies have significantly improved the prognosis of oncology patients. However, these treatments can bring to a higher incidence of side-effects, including the worrying cardiovascular toxicity (CTX). Recent Advances: Substantial evidence indicates multiple mechanisms of CTX, with redox mechanisms playing a key role. Recent data singled out mitochondria as key targets for antineoplastic drug-induced CTX; understanding the underlying mechanisms is, therefore, crucial for effective cardioprotection, without compromising the efficacy of anti-cancer treatments. Critical Issues: CTX can occur within a few days or many years after treatment. Type I CTX is associated…

Cardiovascular toxicityPhysiologymedicine.medical_treatmentAntineoplastic drugClinical BiochemistryAntineoplastic Agents030204 cardiovascular system & hematologyPharmacologyBiochemistryCardiac cellcancer immunotherapy; chemotherapy; ErbB2 inhibitors; oxidative/nitrosative stress; tyrosine kinase inhibitors; vascular endothelial growth factor; Antineoplastic Agents; Cardiotoxicity; Humans; Mitochondria; Oxidation-Reduction03 medical and health scienceschemistry.chemical_compoundErbB2 inhibitors cancer immunotherapy chemotherapy oxidative/nitrosative stress tyrosine kinase inhibitors vascular endothelial growth factor0302 clinical medicinetyrosine kinase inhibitorcancer immunotherapy; chemotherapy; ErbB2 inhibitors; oxidative/nitrosative stress; tyrosine kinase inhibitors; vascular endothelial growth factorChemotherapy; ErbB2 inhibitors; vascular endothelial growth factor; tyrosine kinase inhibitors; oxidative/nitrosative stress; cancer immunotherapyCancer immunotherapytyrosine kinase inhibitorsmedicineHumansChemotherapyMolecular BiologyGeneral Environmental ScienceCardioprotectionComprehensive Invited ReviewsChemotherapyErbB2 inhibitorcancer immunotherapyvascular endothelial growth factorbusiness.industryCell BiologyCardiotoxicityMitochondriaVascular endothelial growth factoroxidative/nitrosative streErbB2 inhibitorschemistry030220 oncology & carcinogenesisGeneral Earth and Planetary SciencesbusinessOxidation-ReductionAfter treatmentoxidative/nitrosative stress
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Timely recognition of cardiovascular toxicity by anticancer agents: a common objective of the pharmacologist, oncologist and cardiologist.

2011

Both conventional and new anticancer drugs can frequently cause adverse cardiovascular effects, which can span from subclinical abnormalities to serious life-threatening and sometimes fatal events. This review examines the principal basic and clinical elements that may be of profit to identify, prevent and treat such toxicities. Clearly, the accomplishment of such objectives requires the strong commitment and cooperation of different professional figures including, but not limited to, pharmacologists, oncologists and cardiologists. The aspect of anticancer drug cardiotoxicity seems to be somehow underestimated, mainly due to inadequate reporting of adverse reactions from oncology drugs in t…

Cardiovascular toxicityTime FactorsSettore MED/06 - Oncologia MedicaPharmacology toxicologyCardiologyAntineoplastic AgentsPharmacologyToxicologyMedical OncologyCardiotoxinsCardiovascular SystemProfessional RolePharmacovigilanceMedicineAnimalsHumansPhysician's RoleMolecular BiologyPharmacologyCardiotoxicitybusiness.industryCardiovascular toxicity Anthracyclines Tyrosine kinase inhibitors TrastuzumabSettore MED/11 - Malattie Dell'Apparato CardiovascolareAnticancer drugLaboratory PersonnelCardiovascular DiseasesSettore BIO/14 - FarmacologiaCardiology and Cardiovascular MedicinebusinessOncology drugsCardiovascular toxicology
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IMPAIRMENT OF DIASTOLIC FUNCTION DURING SHORT-TERM ANTHRACYCLINE CHEMOTHERAPY

1995

International audience; Abstract: Objective-To assess the early changes in left ventricular diastolic and systolic function due to anthracycline treatment. Design-A prospective study of cardiac function by radionuclide angiography in adults before and one month after the end of anthracycline treatment. Patients-60 patients without cardiac disease treated with chemotherapy containing anthracycline. Methods-Cardiac function was assessed by radionuclide measurement throughout treatment. Ejection fraction, peak ejection rate, time to peak ejection rate, filling rate, and time to peak filling rate were measured before and after treatment, To normalise radionuclide measurements of the left ventri…

DIASTOLIC FUNCTIONanimal structures[ INFO.INFO-IM ] Computer Science [cs]/Medical ImagingRADIONUCLIDE ANGIOGRAPHY[INFO.INFO-IM] Computer Science [cs]/Medical Imaging[INFO.INFO-IM]Computer Science [cs]/Medical ImagingANTHRACYCLINE CARDIOTOXICITY
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Pathophysiology of anthracycline cardiotoxicity.

2016

Anthracyclines (ANTs) are powerful drugs that have reduced the mortality of cancer patients. However, their use is limited by the development of cardiotoxicity (CTX), which is dose dependent and may lead to left ventricular dysfunction and heart failure. Although various strategies have been suggested to reduce the negative effects of ANTs, CTX is still an important unresolved clinical issue. This may be due at least partly to the incomplete characterization of the molecular and cellular mechanisms of ANT-induced CTX. In addition, although various forms of cardiac damage have been demonstrated with the use of these drugs in experimental studies, it is not yet clear how these translate to th…

DrugAnthracyclinemedia_common.quotation_subjectLeftanthracyclines; cancer; cardiotoxicity; Cardiology and Cardiovascular MedicineDose dependenceAntineoplastic Agents030204 cardiovascular system & hematologyanthracyclineBioinformatics03 medical and health sciencesVentricular Dysfunction Left0302 clinical medicineAntibioticsNeoplasmsVentricular DysfunctionmedicinecancerHumansGenetic Predisposition to DiseaseAnthracyclinesmedia_commonHeart FailureCardiotoxicityAntibiotics AntineoplasticDose-Response Relationship Drugbusiness.industryanthracyclines cancer cardiotoxicityCancerHeartGeneral Medicinebiochemical phenomena metabolism and nutritionmedicine.diseaseAntineoplasticPathophysiologyCardiotoxicityCardiovascular Diseases030220 oncology & carcinogenesisHeart failureCardiology and Cardiovascular Medicinebusinessanthracyclines; cancer; cardiotoxicity; Anthracyclines; Antibiotics Antineoplastic; Cardiotoxicity; Heart Failure; Humans; Neoplasms; Ventricular Dysfunction LeftJournal of cardiovascular medicine (Hagerstown, Md.)
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Cardiotoxicity mechanisms of the combination of BRAF-inhibitors and MEK-inhibitors.

2018

Many new drugs have appeared in last years in the oncological treatment scenario. Each drug carries an important set of adverse events, not less, cardiovascular adverse events. This aspect is even more important considering the increasing use of combination therapies with two drugs, or three drugs as in some ongoing clinical trials. Besides it represents a growing problem for Cardiologists, that face it in every day clinical practice and that will face it probably more and more in the coming years. This work reviews the mechanism of action of BRAF-inhibitors and MEK-inhibitors used together, the pathophysiological mechanisms that lead to cardiovascular toxicity. Particularly, it focuses on …

DrugCardiovascular toxicityBRAF inhibitorProto-Oncogene Proteins B-rafmedicine.medical_specialtyCombination therapySettore MED/06 - Oncologia Medicamedia_common.quotation_subjectDecreased ejection fraction030204 cardiovascular system & hematologyCardiovascular System03 medical and health sciences0302 clinical medicineCardiovascular toxicityAntineoplastic Combined Chemotherapy ProtocolsMedicineHumansPharmacology (medical)Intensive care medicineAdverse effectBRAF inhibitor; Cardio-oncology; Cardiovascular toxicity; Decreased ejection fraction; Hypertension; MEK inhibitor; Pharmacology; Pharmacology (medical)MelanomaProtein Kinase Inhibitorsmedia_commonPharmacologyMitogen-Activated Protein Kinase KinasesCardiotoxicityMEK inhibitorClinical Trials as Topicbusiness.industryMEK inhibitorCancermedicine.diseaseCardiotoxicityClinical trialCardio-oncology030220 oncology & carcinogenesisHypertensionbusinessPharmacologytherapeutics
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The role of histamine in doxorubicin and teniposide-induced cardiotoxicity in dog and mouse.

1987

In previous studies we reported that teniposide (VM26) induced acute cardiac effects in dogs seem to be related to a release of histamine and that a prior treatment with chlorpheniramine, an H, histamine blocker, prevents the onset of this phenomenon. Since histamine and other vasoactive substances also seem to be involved in doxorubicin (DXR)-induced acute cardiac effects, experiments were undertaken in the aim to prevent, as in the case of VM26, the onset of this phenomenon by administering chlorpheniramine. Since DXR-induced chronic cardiomyopathy also seems to be related to the same mechanisms involved in the onset of acute cardiac effects induced by this drug, additional studies were …

DrugMaleCancer ResearchChlorpheniraminedoxorubicincardiotoxicity.media_common.quotation_subjectCardiomyopathyPharmacology030218 nuclear medicine & medical imaging03 medical and health scienceschemistry.chemical_compoundMice0302 clinical medicineDogsVasoactiveMedicineAnimalsDoxorubicinmedia_commonPodophyllotoxinTeniposideCardiotoxicitybusiness.industryMyocardiumHeartGeneral Medicinemedicine.diseaseOncologychemistryDoxorubicin030220 oncology & carcinogenesisInotropismFemalebusinessHistamineTeniposidemedicine.drugHistamineTumori
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