Search results for " cardiac"

showing 10 items of 523 documents

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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Epicardial Fat, Cardiac Geometry and Cardiac Function in Patients with Nonalcoholic Fatty Liver Disease: Association with the Severity of Liver Disea…

2015

Background & Aims Non-alcoholic fatty liver disease (NAFLD) has been associated with increased cardiovascular risk, including coronary artery disease and cardiac dysfunction. In addition, recent evidence highlighted the possible role of epicardial fat as a new cardiometabolic risk factor. We tested the correlation between epicardial fat, alterations in cardiac geometry and function, and severity of liver damage, in patients with biopsy-proven NAFLD. Methods The anthropometric, biochemical and metabolic features were recorded in 147 consecutive biopsy-proven NAFLD cases (Kleiner score). Epicardial fat thickness was measured by echocardiography. Results Epicardial fat was higher in patients w…

Cardiac function curveAdultMalemedicine.medical_specialtySettore MED/09 - Medicina InternaStatistics as TopicDiastoleEPICARDIAL FATSettore MED/08 - Anatomia PatologicaSeverity of Illness IndexCoronary artery diseaseLiver diseaseFibrosisNon-alcoholic Fatty Liver DiseaseRisk FactorsNASH; NAFLD; EPICARDIAL FAT; CARDIAC DYSFUNCTION;Internal medicineNAFLDmedicineHumansSettore MED/12 - GastroenterologiaEjection fractionHepatologybusiness.industryFatty liverNASHHeartMiddle Agedmedicine.diseaseEndocrinologyLiverCardiovascular DiseasesEchocardiographyCardiologyFemaleSteatohepatitisbusinessPericardiumCARDIAC DYSFUNCTION
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Chemotherapy cardiotoxicity: cardioprotective drugs and early identification of cardiac dysfunction.

2016

Background: Chemotherapy cardiotoxicity is an emerging problem and it is very important to prevent cardiac dysfunction caused by anticancer drugs. The aim of this study was to assess the alterations of the cardiac function induced by chemotherapy in a follow-up of 2 years and to evaluate the cardioprotective role of angiotensin-converting enzyme inhibitors (ACEIs) in the prevention of cardiac dysfunction. Methods: A prospective study was carried out using patients with breast cancer (85 women; median age 57W12years) and other inclusion and exclusion criteria. On the basis of treatment, patients were divided into six groups: fluorouracil-epirubicincyclophosphamide, FEC (group A); FEC and tra…

Cardiac function curveAdultmedicine.medical_specialtyCardiotonic Agentsmedicine.medical_treatmentAngiotensin-Converting Enzyme InhibitorsBreast Neoplasms030204 cardiovascular system & hematologyBioinformaticsCardiac dysfunctionAngiotensin-converting enzyme inhibitor; Cardiotoxicity; Chemotherapy; Prevention; Tissue Doppler imaging; Adult; Aged; Aged 80 and over; Angiotensin-Converting Enzyme Inhibitors; Antineoplastic Combined Chemotherapy Protocols; Breast Neoplasms; Cardiotonic Agents; Cardiotoxicity; Early Diagnosis; Echocardiography Doppler; Female; Follow-Up Studies; Humans; Middle Aged; Prospective Studies03 medical and health sciencesTissue Doppler imaging0302 clinical medicinecardiac toxicity anti cancer drugs cardiac dysfunctionInternal medicineAntineoplastic Combined Chemotherapy Protocols80 and overMedicineChemotherapyHumansProspective StudiesAgedAged 80 and overCardiotoxicityChemotherapybusiness.industryPreventionFollow up studiesDopplerGeneral MedicineMiddle AgedCardiotoxicityEchocardiography DopplerClinical trialEarly DiagnosisAngiotensin-converting enzyme inhibitorEchocardiography030220 oncology & carcinogenesiscardiovascular systemCardiologyFemaleCardiology and Cardiovascular MedicinebusinessFollow-Up StudiesJournal of cardiovascular medicine (Hagerstown, Md.)
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miR-133a Enhances the Protective Capacity of Cardiac Progenitors Cells after Myocardial Infarction

2014

Summary miR-133a and miR-1 are known as muscle-specific microRNAs that are involved in cardiac development and pathophysiology. We have shown that both miR-1 and miR-133a are early and progressively upregulated during in vitro cardiac differentiation of adult cardiac progenitor cells (CPCs), but only miR-133a expression was enhanced under in vitro oxidative stress. miR-1 was demonstrated to favor differentiation of CPCs, whereas miR-133a overexpression protected CPCs against cell death, targeting, among others, the proapoptotic genes Bim and Bmf. miR-133a-CPCs clearly improved cardiac function in a rat myocardial infarction model by reducing fibrosis and hypertrophy and increasing vasculari…

Cardiac function curveProgrammed cell deathMyocardial InfarctionGene ExpressionCardiomegalyBiologyBiochemistryArticleMuscle hypertrophyParacrine signallingDownregulation and upregulationmiR-133a; Cardiac Progenitors Cells; Myocardial InfarctionFibrosisREGENERATIONmicroRNAGeneticsmedicineMyocyteAnimalsRNA MessengerOXIDATIVE STRESSlcsh:QH301-705.5ENGINEERED HEART-TISSUElcsh:R5-920Gene Expression ProfilingMICRORNAComputational BiologyCell BiologyMUSCLEmedicine.disease3. Good healthCell biologyRatsAPOPTOSISHYPERTROPHYMicroRNAsDIFFERENTIATIONlcsh:Biology (General)ImmunologyGROWTHRNA Interferencelcsh:Medicine (General)EMBRYONIC STEM-CELLSMyoblasts CardiacDevelopmental BiologyStem Cell Reports
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Down-regulation of OPA1 alters mouse mitochondrial morphology, PTP function, and cardiac adaptation to pressure overload

2012

AIMS: The optic atrophy 1 (OPA1) protein is an essential protein involved in the fusion of the mitochondrial inner membrane. Despite its high level of expression, the role of OPA1 in the heart is largely unknown. We investigated the role of this protein in Opa1(+/-) mice, having a 50% reduction in OPA1 protein expression in cardiac tissue. METHODS AND RESULTS: In mutant mice, cardiac function assessed by echocardiography was not significantly different from that of the Opa1(+/+). Electron and fluorescence microscopy revealed altered morphology of the Opa1(+/-) mice mitochondrial network; unexpectedly, mitochondria were larger with the presence of clusters of fused mitochondria and altered c…

Cardiac function curveendocrine systemPhysiologyAdaptation BiologicalDown-RegulationBiologyMitochondrionMitochondrial Membrane Transport ProteinsPermeabilityGTP PhosphohydrolasesMitochondrial ProteinsMice03 medical and health sciencesMitochondrial membrane transport protein0302 clinical medicinePhysiology (medical)Optic Atrophy Autosomal DominantPressuremedicineAnimalsMyocyteMyocytes CardiacInner mitochondrial membrane030304 developmental biologyMice KnockoutPressure overload0303 health sciencesMitochondrial Permeability Transition Poremedicine.diseaseeye diseasesMitochondriaCell biologyBiochemistryMitochondrial permeability transition poreMitochondrial Membranesbiology.proteinOptic Atrophy 1Cardiology and Cardiovascular Medicine030217 neurology & neurosurgeryCardiovascular Research
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Inhibition of class I histone deacetylase with an apicidin derivative prevents cardiac hypertrophy and failure

2008

AIMS: Recent studies have demonstrated the importance of chromatin remodelling via histone acetylation/deacetylation for the control of cardiac gene expression. Specific histone deacetylases (HDACs) can, in fact, play a positive or negative role in determining cardiac myocyte (CM) size. Here, we report on the effect on hypertrophy development of three inhibitors (HDACi) of class I HDACs. METHODS AND RESULTS: The compounds were first analysed in vitro by scoring hypertrophy, expression of foetal genes, and apoptosis of neonatal rat CMs stimulated with phenylephrine, an alpha1-adrenergic agonist. This initial screening indicated that a truncated derivative of apicidin with class I HDAC specif…

Cardiac function curvemedicine.medical_specialtyHypertrophy Heart failurePhysiologymedicine.drug_classBiologyPeptides CyclicHistone DeacetylasesCell LineMuscle hypertrophychemistry.chemical_compoundPhysiology (medical)Internal medicinemedicineAnimalsHumansMyocytes CardiacEnzyme InhibitorsRats WistarCells CulturedHeart FailurePressure overloadHistone deacetylase inhibitorHypertrophic cardiomyopathyHypertrophymedicine.diseaseRatsHistone Deacetylase InhibitorsDisease Models AnimalEndocrinologychemistryEchocardiographyHeart failureHypertrophy Left VentricularHistone deacetylaseCardiology and Cardiovascular MedicineApicidinCardiovascular Research
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Genistein supplementation and cardiac function in postmenopausal women with metabolic syndrome: Results from a pilot strain-echo study

2017

Genistein, a soy-derived isoflavone, may improve cardiovascular risk profile in postmenopausal women with metabolic syndrome (MetS), but few literature data on its cardiac effects in humans are available. The aim of this sub-study of a randomized double-blind case-control study was to analyze the effect on cardiac function of one-year genistein dietary supplementation in 22 post-menopausal patients with MetS. Participants received 54 mg/day of genistein (n = 11) or placebo (n = 11) in combination with a Mediterranean-style diet and regular exercise. Left ventricular (LV) systolic function was assessed as the primary endpoint, according to conventional and strain-echocardiography measurement…

Cardiac function curvemedicine.medical_specialtycardiac function; echocardiography; genistein; menopause; metabolic syndromegenistein; metabolic syndrome; menopause; cardiac function; echocardiographyGenisteinlcsh:TX341-641030204 cardiovascular system & hematologyPlaceboArticle03 medical and health scienceschemistry.chemical_compound0302 clinical medicineDouble-Blind MethodInterquartile rangeInternal medicinemedicineHumans030212 general & internal medicineEnd-systolic volumeBody surface areaNutrition and DieteticsEjection fractionbusiness.industryCardiac functionHeartMiddle Agedmedicine.diseaseGenisteinMetabolic syndromePostmenopauseEndocrinologychemistryEchocardiographyDietary SupplementsCardiologyCardiac function; Echocardiography; Genistein; Menopause; Metabolic syndrome; Food ScienceFemaleMetabolic syndromeMenopausebusinesslcsh:Nutrition. Foods and food supplyFood Science
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Comparison between doppler-echocardiography and uncalibrated pulse contour method for cardiac output measurement. a multicenter observational study

2016

Objectives: Echocardiography and pulse contour methods allow, respectively, noninvasive and less invasive cardiac output estimation. The aim of the present study was to compare Doppler echocardiography with the pulse contour method MostCare for cardiac output estimation in a large and nonselected critically ill population. Design: A prospective multicenter observational comparison study. Setting: The study was conducted in 15 European medicosurgical ICUs. Patients: We assessed cardiac output in 400 patients in whom an echocardiographic evaluation was performed as a routine need or for cardiocirculatory assessment. Interventions: None. Measurements and Main Results: One echocardiographic car…

Cardiac outputgenetic structuresintensive care unitsBlood PressureDoppler echocardiographyCritical Care and Intensive Care Medicinearterial waveform analysis; cardiac output; Doppler echocardiography; echocardiography; hemodynamic monitoring; pulse contour method; Critical Care and Intensive Care Medicinehemodynamic monitoring0302 clinical medicine030202 anesthesiologyechocardiographyhumansarterial waveform analysisarterial waveform analysis; cardiac output; doppler echocardiography; echocardiography; hemodynamic monitoring; pulse contour method; heart; humans; intensive care units; linear models; monitoring; physiologic; prospective studies; blood pressure; cardiac output; echocardiography; doppler; pulse; critical care and intensive care medicinemedicine.diagnostic_testPulse (signal processing)physiologicblood pressureHeartEchocardiography Dopplercardiovascular systemCardiologysymbolsLinear ModelDoppler effectHumandoppler echocardiographymedicine.medical_specialtyIntensive Care UnitLess invasiveheartpulse contour methoddoppler03 medical and health sciencesCardiac output measurementsymbols.namesakeInternal medicinemedicinePulsearterial waveform analysiMonitoring Physiologicbusiness.industrycardiac output030208 emergency & critical care medicineDoppler echocardiographyprospective studiesProspective StudiemonitoringMulticenter studycritical care and intensive care medicineObservational studylinear modelsbusinesspulse
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Masse cardiache e paracardiache

2010

CardioTC masse cardiacheSettore MED/36 - Diagnostica Per Immagini E Radioterapia
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Deleting Full Length Titin Versus the Titin M-Band Region Leads to Differential Mechanosignaling and Cardiac Phenotypes

2019

Background: Titin is a giant elastic protein that spans the half-sarcomere from Z-disk to M-band. It acts as a molecular spring and mechanosensor and has been linked to striated muscle disease. The pathways that govern titin-dependent cardiac growth and contribute to disease are diverse and difficult to dissect. Methods: To study titin deficiency versus dysfunction, the authors generated and compared striated muscle specific knockouts (KOs) with progressive postnatal loss of the complete titin protein by removing exon 2 (E2-KO) or an M-band truncation that eliminates proper sarcomeric integration, but retains all other functional domains (M-band exon 1/2 [M1/2]-KO). The authors evaluated c…

Cardiomyopathy DilatedMaleSarcomeresanimal structuresVentricular Dysfunction Rightmacromolecular substances030204 cardiovascular system & hematologyMechanotransduction CellularVentricular Function LeftArticleMuscle hypertrophyVentricular Dysfunction Left03 medical and health sciences0302 clinical medicinePhysiology (medical)AnimalsMedicineMyocytes CardiacMuscle Skeletal030304 developmental biologyMice Knockout0303 health sciencesbiologybusiness.industryMolecular springmusculoskeletal systemPhenotypeCell biologyMuscular AtrophyPhenotypeMuscle diseasecardiovascular systemVentricular Function Rightbiology.proteinTitinCardiology and Cardiovascular MedicinebusinessProtein KinasesGene DeletionDifferential (mathematics)Circulation
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