0000000000160742

AUTHOR

Paolo Spallarossa

showing 10 related works from this author

Cardioprotection by gene therapy

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…

Cardioprotectionmedicine.medical_specialtybiologybusiness.industryGene targetingSphingosine kinase 1Heat shock proteinInternal medicineGene expressionmedicinebiology.proteinCardiologyHepatocyte growth factorSignal transductionCardiology and Cardiovascular MedicinebusinessTranscription factormedicine.drugInternational Journal of Cardiology
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Redox imbalances in ageing and metabolic alterations: Implications in cancer and cardiac diseases. An overview from the working group of cardiotoxici…

2020

Metabolic syndrome (MetS) is a well established risk factor for cardiovascular (CV) diseases. In addition, several studies indicate that MetS correlates with the increased risk of cancer in adults. The mechanisms linking MetS and cancer are not fully understood. Several risk factors involved in MetS are also cancer risk factors, such as the consumption of high calorie-food or high fat intake, low fibre intake, and sedentary lifestyle. Other common aspects of both cancer and MetS are oxidative stress and inflammation. In addition, some anticancer treatments can induce cardiotoxicity, including, for instance, left ventricular (LV) dysfunction and heart failure (HF), endothelial dysfunction an…

Oncologymedicine.medical_specialtyPhysiologyClinical BiochemistryReview030204 cardiovascular system & hematologymedicine.disease_causeBiochemistry03 medical and health sciences0302 clinical medicineInternal medicineAgeing; Cancer; Cardiovascular disease; Cardiovascular toxicity from anticancer drugs; Metabolic syndromemedicineEndothelial dysfunctionRisk factorMolecular BiologySedentary lifestyleCancerCardiotoxicitybusiness.industrylcsh:RM1-950CancerCell Biologymedicine.diseaseCardiovascular diseaseMetabolic syndromeAgeingCardiovascular toxicity from anticancer drugslcsh:Therapeutics. PharmacologyCardiovascular toxicity from anticancer drug030220 oncology & carcinogenesisHeart failureMetabolic syndromebusinessOxidative stress
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A recommended practical approach to the management of target therapy and angiogenesis inhibitors cardiotoxicity: an opinion paper of the working grou…

2016

The US National Cancer Institute estimates that cardiotoxicity (CTX) from target therapy refers mostly to four groups of drugs: epidermal growth factor receptor 2 inhibitors, angiogenic inhibitors, directed Abelson murine leukemia viral oncogene homolog inhibitors, and proteasome inhibitors. The main cardiotoxic side-effects related to antiepidermal growth factor receptor 2 therapy are left ventricular systolic dysfunction and heart failure. Angiogenesis inhibitors are associated with hypertension, left ventricular dysfunction/heart failure, myocardial ischemia, QT prolongation, and thrombosis. Moreover, other agents may be related to CTX induced by treatment. In this study, we review the g…

AngiogenesisLeftAngiogenesis Inhibitors030204 cardiovascular system & hematologyVentricular Dysfunction Left0302 clinical medicinetyrosine kinase inhibitorNeoplasmstyrosine kinase inhibitorsVentricular DysfunctionMolecular Targeted TherapyEpidermal growth factor receptorSocieties Medicalangiogenesis inhibitors; HER2/epidermal growth factor receptor 2; tyrosine kinase inhibitorABLbiologyDisease ManagementGeneral MedicineItalyCardiovascular DiseasesSupplement Submission030220 oncology & carcinogenesisangiogenesis inhibitors; HER2/epidermal growth factor receptor 2; tyrosine kinase inhibitors; Angiogenesis Inhibitors; Antineoplastic Agents; Cardiology; Cardiomyopathies; Cardiotoxicity; Heart Failure; Humans; Italy; Neoplasms; Practice Guidelines as Topic; Societies Medical; Ventricular Dysfunction Left; Disease ManagementPractice Guidelines as TopicCardiologyCardiology and Cardiovascular MedicineCardiomyopathiesmedicine.medical_specialtyCardiologyAntineoplastic AgentsRisk AssessmentQT interval03 medical and health sciencesGrowth factor receptorInternal medicineMedicalmedicineHumansMonitoring PhysiologicHeart FailureCardiotoxicitybusiness.industryCancerHER2/epidermal growth factor receptor 2medicine.diseaseangiogenesis inhibitors; HER2/epidermal growth factor receptor 2; tyrosine kinase inhibitors; Cardiology and Cardiovascular MedicineCardiotoxicityangiogenesis inhibitorHeart failurebiology.proteinbusinessSocietiesJournal of cardiovascular medicine (Hagerstown, Md.)
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A recommended practical approach to the management of anthracycline-based chemotherapy cardiotoxicity: an opinion paper of the working group on drug …

2016

Anthracyclines are the mainstay of treatment of a variety of haematological malignancies and solid tumours. Unfortunately, the clinical use of these drugs is limited by cumulative, dose-related cardiotoxicity which may ultimately lead to a severe and irreversible form of cardiomyopathy. Thus, there is an increasing need for close cooperation among cardiologists, oncologists and haemato-oncologists. As anthracyclines save lives, the logical goal of this cooperation, besides preventing or mitigating cardiotoxicity, is to promote an acceptable balance between the potential cardiac side effects and the vital benefit of anticancer treatment. This manuscript, which is specifically addressed to th…

cardio-oncologymedicine.medical_treatmentCardiomyopathyheart failure030204 cardiovascular system & hematologyanthracyclines; cardio-oncology; cardiology consult; cardiotoxicity; heart failure; Anthracyclines; Antibiotics Antineoplastic; Cardiology; Cardiomyopathies; Cardiotoxicity; Humans; Italy; Neoplasms; Practice Guidelines as Topic; Societies Medical; Disease Managementanthracyclines; cardiotoxicity; heart failurecardiology consult0302 clinical medicineCardiologistsAntibioticsNeoplasmsDisease management (health)Societies Medicalmedia_commonanthracyclinesAntibiotics AntineoplasticDisease ManagementGeneral MedicineAntineoplasticItalyCardiovascular Diseases030220 oncology & carcinogenesisSupplement SubmissionPractice Guidelines as TopicCardiologyCardiomyopathiesRisk assessmentCardiology and Cardiovascular MedicineDrugmedicine.medical_specialtyAnthracyclinemedia_common.quotation_subjectCardiologycardiotoxicityanthracyclines; cardio-oncology; cardiology consult; cardiotoxicity; heart failure; Cardiology and Cardiovascular MedicineAntineoplastic AgentsanthracyclineRisk Assessment03 medical and health sciencesMedicalInternal medicinemedicineHumansIntensive care medicineCardiotoxicityChemotherapybusiness.industrymedicine.diseaseHeart failureSocietiesbusinessJournal of cardiovascular medicine (Hagerstown, Md.)
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Improving the preclinical models for the study of chemotherapy-induced cardiotoxicity: a Position Paper of the Italian Working Group on Drug Cardioto…

2015

Although treatment for heart failure induced by cancer therapy has improved in recent years, the prevalence of cardiomyopathy due to antineoplastic therapy remains significant worldwide. In addition to traditional mediators of myocardial damage, such as reactive oxygen species, new pathways and target cells should be considered responsible for the impairment of cardiac function during anticancer treatment. Accordingly, there is a need to develop novel therapeutic strategies to protect the heart from pharmacologic injury, and improve clinical outcomes in cancer patients. The development of novel protective therapies requires testing putative therapeutic strategies in appropriate animal model…

Cardiac function curveACE inhibitorsCardiotonic AgentsNeuregulin-1CardiomyopathyAntineoplastic AgentsPreclinical modelsCardioprotectionCardiotonic AgentsPharmacologyBioinformaticsmedicine.disease_causeCancer therapy-induced cardiac injury ;Preclinical modelsMitochondria HeartBeta-blockersNeoplasmsCancer therapy-induced cardiac injuryMedicineAnimalsHumansCardiac stem cellsCardioprotectionCardiotoxicityACE inhibitors; Beta-blockers; Cancer therapy-induced cardiac injury; Cardiac stem cells; Cardioprotection; Mitochondria; Neuregulin-1; Oxidative stress; Preclinical models; Statinsbusiness.industryStatinsCancermedicine.diseaseCardiotoxicityMitochondriaCancer therapy-induced cardiac injury Preclinical models Cardioprotection Mitochondria Neuregulin-1 Oxidative stress Statins Beta-blockers ACE inhibitors Cardiac stem cellsDisease Models AnimalOxidative StressHeart failureCardiology and Cardiovascular MedicinebusinessOxidative stress
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Anthracyclines and regional myocardial damage in breast cancer patients. A multicentre study from the Working Group on Drug Cardiotoxicity and Cardio…

2021

Abstract Aims In breast cancer (BC) patients treated with anthracyclines-based therapies, we aim at assessing whether adjuvant drugs impact cardiac function differently and whether their cardiotoxicity has a regional pattern. Methods and results In a multicentre study, 146 BC patients (56 ± 11 years) were prospectively enrolled and divided into three groups according to the received treatments: AC/EC-Group (doxorubicin or epirubicin + cyclophosphamide), AC/EC/Tax-Group (AC/EC + taxanes), FEC/Tax-Group (fluorouracil + EC + taxanes). Fifty-six patients of the total cohort also received trastuzumab. Left ventricular ejection fraction (LVEF) and global longitudinal strain (GLS) were calculated …

medicine.medical_specialtymedicine.medical_treatmentPopulationCardiologyBreast NeoplasmsAnthracyclineAnthracyclines; Breast cancer; Cardiotoxicity; Myocardial strain030204 cardiovascular system & hematologyAnthracyclines Breast cancer Breast Neoplasms Cardiology Cardiotoxicity Echocardiography Female Humans italy Myocardial strain Pharmaceutical Preparations Stroke Volume Trastuzumab Ventricular Function Left Ventricular Dysfunction LeftVentricular Function LeftVentricular Dysfunction Left03 medical and health sciencesBreast cancer0302 clinical medicineTrastuzumabInternal medicineHumansMedicineAnthracyclinesRadiology Nuclear Medicine and imagingeducationeducation.field_of_studyChemotherapyCardiotoxicityEjection fractionbusiness.industryStroke VolumeGeneral MedicineTrastuzumabMyocardial strainChemotherapy regimenCardiotoxicityItalyPharmaceutical PreparationsEchocardiographyFluorouracil030220 oncology & carcinogenesisCardiologyFemaleCardiology and Cardiovascular Medicinebusinessmedicine.drugEpirubicinEuropean Heart Journal - Cardiovascular Imaging
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Arterial hypertension in cancer: The elephant in the room

2019

The great therapeutical success achieved by oncology is counterbalanced by growing evidences of cardiovascular (CV) toxicity due to many antineoplastic treatments. Cardiac adverse events may cause premature discontinuation of effective oncologic treatments or occur as late events undermining the oncologic success. Arterial hypertension is both the most common comorbidity in cancer patients and a frequent adverse effect of anticancer therapies. A pre-existing hypertension is known to increase the risk of other cardiac adverse events due to oncologic treatments, in particular heart failure. Moreover, as a strict association between cancer and CV diseases has emerged over the recent years, var…

Arterial hypertensionVascular Endothelial Growth Factor AAnthracyclines Anti VEGF agents Anti-hypertensive therapy Arterial hypertension Cancer Cardiotoxicitymedicine.medical_specialtyAnti VEGF agentmedicine.medical_treatmentAntineoplastic AgentsBlood PressureAnthracycline030204 cardiovascular system & hematologyAnthracyclines; Anti VEGF agents; Anti-hypertensive therapy; Arterial hypertension; Cancer; Cardiotoxicity; Antihypertensive Agents; Antineoplastic Agents; Blood Pressure; Humans; Hypertension; Neoplasms; Vascular Endothelial Growth Factor A03 medical and health sciences0302 clinical medicineNeoplasmsmedicineHumansAnthracyclines030212 general & internal medicineAnti-hypertensive therapyAdverse effectIntensive care medicineAntihypertensive AgentsCancerChemotherapyCardiotoxicitybusiness.industryAnti VEGF agentsCancermedicine.diseaseComorbidityCardiotoxicityDiscontinuationBlood pressureHeart failureHypertensionCardiology and Cardiovascular MedicinebusinessInternational Journal of Cardiology
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Antineoplastic Drug-Induced Cardiotoxicity: A Redox Perspective

2018

Antineoplastic drugs can be associated with several side effects, including cardiovascular toxicity (CTX). Biochemical studies have identified multiple mechanisms of CTX. Chemoterapeutic agents can alter redox homeostasis by increasing the production of reactive oxygen species (ROS) and reactive nitrogen species RNS. Cellular sources of ROS/RNS are cardiomyocytes, endothelial cells, stromal and inflammatory cells in the heart. Mitochondria, peroxisomes and other subcellular components are central hubs that control redox homeostasis. Mitochondria are central targets for antineoplastic drug-induced CTX. Understanding the mechanisms of CTX is fundamental for effective cardioprotection, without…

Stromal cellPhysiologymedicine.medical_treatmentTyrosine kinase inhibitorChemotherapy; HER-2 inhibitors; Oxidative/nitrosative stress; Tyrosine kinase inhibitors; Vascular endothelial growth factorReviewOxidative phosphorylation030204 cardiovascular system & hematologyMitochondrionPharmacologyChemotherapy; HER-2 inhibitors; Oxidative/nitrosative stress; Tyrosine kinase inhibitors; Vascular endothelial growth factor; Physiology; Physiology (medical)chemotherapyHER-2 inhibitorlcsh:Physiology03 medical and health scienceschemistry.chemical_compound0302 clinical medicinePhysiology (medical)tyrosine kinase inhibitorsMedicinechemotherapy HER-2 inhibitors oxidative/nitrosative stress vascular endothelial growth factor tyrosine kinase inhibitorsReactive nitrogen specieschemistry.chemical_classificationCardioprotectionReactive oxygen speciesChemotherapyCardiotoxicitylcsh:QP1-981vascular endothelial growth factorbusiness.industryOxidative/nitrosative strechemistry030220 oncology & carcinogenesisbusinessHER-2 inhibitorsoxidative/nitrosative stress
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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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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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