Search results for "Myocardial ischemia"

showing 10 items of 106 documents

Intracoronary application of C1 esterase inhibitor improves cardiac function and reduces myocardial necrosis in an experimental model of ischemia and…

1997

Background Myocardial injury from ischemia can be aggravated by reperfusion of the jeopardized area. The precise underlying mechanisms have not been clearly defined, but proinflammatory events, including complement activation, leukocyte adhesion, and infiltration and release of diverse mediators, probably play important roles. The present study addresses the possibility of reducing reperfusion damage by the application of C1 esterase inhibitor (C1-INH). Methods and Results Cardioprotection by C1-INH 20 IU/kg IC was examined in a pig model with 60 minutes of coronary occlusion, followed by 120 minutes of reperfusion. C1-INH was administered during the first 5 minutes of coronary reperfusion…

Cardiac function curveMalemedicine.medical_specialtyAnaphylatoxinsNecrosisSwinePartial PressureIschemiaMyocardial IschemiaMyocardial ReperfusionComplement C1 Inactivator ProteinsCreatineInjectionschemistry.chemical_compoundNecrosisTroponin TPhysiology (medical)Internal medicinemedicineAnimalsMyocardial infarctionLactic AcidCreatine KinaseCardioprotectionTroponin Tbusiness.industryMyocardiumHemodynamicsHeartmedicine.diseaseCoronary VesselsTroponinOxygenchemistryCoronary occlusionAnesthesiaCardiologyFemalemedicine.symptomCardiology and Cardiovascular MedicinebusinessCirculation
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Recombinant growth hormone therapy in patients with ischemic cardiomyopathy : effects on hemodynamics, left ventricular function, and cardiopulmonary…

1999

Background —We studied the effects of recombinant growth hormone (rhGH) on exercise capacity and cardiac function in patients with ischemic cardiomyopathy. Methods and Results —Seven patients (aged 55±9 years) with mild to moderate congestive heart failure (ejection fraction 31±4%) who were on standard therapy were included. The patients were studied at baseline, after 3 months of rhGH treatment, and 3 months after rhGH discontinuation. Cardiac function was assessed by exercise capacity, right heart catheterization at rest and after submaximal exercise, MRI, echocardiography, and Holter monitoring. When administered at a dose of 2 IU/d, rhGH doubled the serum concentration of insulin-like …

Cardiac function curveMalemedicine.medical_specialtyCardiac outputCardiomyopathyMyocardial IschemiaHemodynamicsVentricular Function LeftPhysiology (medical)Internal medicinemedicineHumansVentricular remodelingIschemic cardiomyopathyEjection fractionExercise Tolerancebusiness.industryHuman Growth HormoneHemodynamicsMiddle Agedmedicine.diseaseCombined Modality TherapySurgeryHeart failureCardiologyCardiology and Cardiovascular MedicinebusinessCirculation
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Local transient myocardial liposomal gene transfer of inducible nitric oxide synthase does not aggravate myocardial function and fibrosis and leads t…

2010

Microcirculation (2010) 17, 69–78. doi: 10.1111/j.1549-8719.2010.00002.x Abstract Background:  This study was designed to explore the effect of transient inducible nitric oxide synthase (iNOS) overexpression via cationic liposome-mediated gene transfer on cardiac function, fibrosis, and microvascular perfusion in a porcine model of chronic ischemia. Methods and Results:  Chronic myocardial ischemia was induced using a minimally invasive model in 23 landrace pigs. Upon demonstration of heart failure, 10 animals were treated with liposome-mediated iNOS-gene-transfer by local intramyocardial injection and 13 animals received a sham procedure to serve as control. The efficacy of this iNOS-gene-…

Cardiac function curveMalemedicine.medical_specialtyPhysiologySus scrofaIschemiaMyocardial IschemiaGene ExpressionNitric Oxide Synthase Type IINitric OxideVentricular Function LeftNeovascularizationFibrosisPhysiology (medical)Internal medicinemedicineAnimalsHumansMolecular BiologyEjection fractionbiologyNeovascularization Pathologicbusiness.industryMyocardiumGene Transfer Techniquesmedicine.diseaseFibrosisMagnetic Resonance ImagingRecombinant ProteinsNitric oxide synthaseArteriolesHeart failureLiposomesCardiologybiology.proteinDobutamineFemalemedicine.symptomCardiology and Cardiovascular Medicinebusinessmedicine.drugMicrocirculation (New York, N.Y. : 1994)
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Ischemic stroke increases heart vulnerability to ischemia-reperfusion and alters myocardial cardioprotective pathways

2018

Background and Purpose— For years, the relationship between cardiac and neurological ischemic events has been limited to overlapping pathophysiological mechanisms and common risk factors. However, acute stroke may induce dramatic changes in cardiovascular function. The aim of this study was to evaluate how prior cerebrovascular lesions affect myocardial function and signaling in vivo and ex vivo and how they influence cardiac vulnerability to ischemia-reperfusion injury. Methods— Cerebral embolization was performed in adult Wistar male rats through the injection of microspheres into the left or right internal carotid artery. Stroke lesions were evaluated by microsphere counting, tissue sta…

Cardiac function curveMalemedicine.medical_specialtySympathetic nervous systemGrowth Differentiation Factor 15Myocardial ischemiaNitro-oxidative stressHeart VentriclesIschemiaMyocardial Infarction030204 cardiovascular system & hematologyContractility03 medical and health sciences0302 clinical medicine[SDV.MHEP.CSC]Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular systemIn vivoInternal medicinemedicineAnimalsRats WistarStrokeIschemic StrokeAdvanced and Specialized Nursingbusiness.industryMyocardiumBrainIsolated Heart PreparationHeartmedicine.diseaseRatsStrokeAutonomic nervous systemOxidative Stressmedicine.anatomical_structureEchocardiographyNitrosative StressReperfusion InjuryCardiologyNeurology (clinical)Disease SusceptibilityReceptors Adrenergic beta-1Cardiology and Cardiovascular Medicinebusiness030217 neurology & neurosurgeryEx vivoAutonomic nervous system Subject terms: Ischemia
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Differential contribution of dead space ventilation and low arterial pCO2 to exercise hyperpnea in patients with chronic heart failure secondary to i…

2003

In chronic heart failure (CHF), the abnormally large ventilatory response to exercise (VE/VCO(2) slope) has 2 conceptual elements: the requirement of restraining arterial partial pressure of carbon dioxide (pCO(2)) from increasing (because of an increased ratio between increased physiologic dead space and tidal volume [VD/VT]) and the depression of arterial pCO(2) by further increased ventilation, which necessarily implies an important non-carbon dioxide stimulus to ventilation. We aimed to assess the contribution of these 2 factors in determining the elevated VE/VCO(2) slope in CHF. Thirty patients with CHF underwent cardiopulmonary exercise testing (age 65 +/- 11 years, left ventricular e…

Cardiomyopathy DilatedMalemedicine.medical_specialtyPartial PressureMyocardial IschemiaHyperpneaHypercapniaInternal medicineIdiopathic dilated cardiomyopathymedicineHumansTidal volumeAgedEjection fractionbusiness.industryVO2 maxRespiratory Dead SpaceCarbon DioxideMiddle Agedmedicine.diseasePulmonary AlveoliHeart failureExercise TestCardiologyBreathingFemaleAcidosis RespiratoryBlood Gas Analysismedicine.symptomPulmonary VentilationCardiology and Cardiovascular Medicinebusinesshuman activitiesHypercapniaThe American Journal of Cardiology
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Increased exercise ejection fraction and reversed remodeling after long-term treatment with metoprolol in congestive heart failure: a randomized, str…

2003

Background: the effects of long-term administration of β-blockers on left ventricular (LV) function during exercise in patients with ischemic heart disease (IHD) and idiopathic dilated cardiomyopathy (DCM) are controversial. Patients and methods: patients with stable congestive heart failure (CHF) (New York heart association [NYHA] class II and III) and ejection fraction (EF) ≤0.40 were randomized to metoprolol, 50 mg t.i.d. or placebo for 6 months. Patients were divided into two groups: ischemic heart disease (IHD) and idiopathic dilated cardiomyopathy (DCM). The mean EF was 0.29 in both groups and 92% were taking angiotensin-converting enzyme (ACE) inhibitors. In the IHD group, 84% had su…

Cardiomyopathy DilatedMalemedicine.medical_specialtyTime FactorsAdrenergic beta-AntagonistsMyocardial IschemiaCardiomyopathyRadionuclide angiographyDouble-Blind MethodInternal medicineIdiopathic dilated cardiomyopathymedicineHumanscardiovascular diseasesMyocardial infarctionExerciseMetoprololEjection fractionVentricular Remodelingmedicine.diagnostic_testbusiness.industryMitral Valve InsufficiencyGated Blood-Pool ImagingHeartStroke VolumeAtrial fibrillationMiddle Agedmedicine.diseaseHeart failureExercise TestCardiologyFemaleCardiology and Cardiovascular MedicinebusinessMetoprololmedicine.drugEuropean Journal of Heart Failure
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C1-esterase inhibitor in ischemia and reperfusion.

2002

Summary Myocardial injury from ischemia can be aggravated by reperfusion of the jeopardized area. The precise underlying mechanisms have not been clearly defined, but proinflammatory events including complement activation play important roles. Cardioprotection by complement inhibition inter alia C1-esterase-inhibitor (C1-INH) was examined in several experimental models and under clinical conditions with ischemia and reperfusion. C1-INH reduced local anaphylatoxin release revealing the importance of the classical complement pathway. Inhibition of local complement activation was accompanied by improvement of myocardial function and perfusion of the previously ischemic myocardium. Leukocyte en…

Cardiotonic AgentsImmunologyIschemiaMyocardial IschemiaMyocardial Reperfusion InjuryPharmacologyComplement C1 Inactivator ProteinsProinflammatory cytokineClassical complement pathwayIschemiamedicineImmunology and AllergyAnimalsHumansAnaphylatoxinComplement Pathway ClassicalCardioprotectionbusiness.industryHeartHematologymedicine.diseaseC1 esteraseComplement systemAnesthesiaModels AnimalbusinessPerfusionComplement C1 Inhibitor ProteinImmunobiology
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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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Preclinical atherosclerosis and metabolic syndrome increase cardio- and cerebrovascular events rate: a 20-year follow up

2013

BACKGROUND: Intima-media thickness (IMT) is a validated marker of preclinical atherosclerosis and a predictor of cardiovascular events. PATIENTS: We studied a population of 529 asymptomatic patients (age 62 ± 12.8 years), divided into two groups of subjects with and without Metabolic Syndrome (MetS). METHODS: All patients, at baseline, have had a carotid ultrasound evaluation and classified in two subgroups: the first one without atherosclerotic lesions and the second one with preclinical atherosclerosis (increased IMT or asymptomatic carotid plaque). Cardiovascular endpoints were investigated in a 20-years follow-up. RESULTS: There were 242 cardiovascular events: 144 among patients with Me…

Carotid Artery DiseasesMaleAsymptomatic carotid plaqueIntima-media thicknessEndocrinology Diabetes and MetabolismMyocardial InfarctionMyocardial IschemiaMetabolic syndrome Preclinical atherosclerosis Intima-media thickness Asymptomatic carotid plaque Cardiac event Cerebrovascular eventsCarotid Intima-Media ThicknessBody Mass IndexAortic aneurysmRisk FactorsPreclinical atherosclerosisLongitudinal StudiesUltrasonography Doppler ColorOriginal InvestigationAged 80 and overMetabolic Syndromeeducation.field_of_studySmokingMiddle AgedPlaque AtheroscleroticStrokeIschemic Attack TransientHypertensionCardiologyFemalemedicine.symptomCardiology and Cardiovascular MedicineAdultmedicine.medical_specialtyCardiac eventPopulationEndarterectomyRisk AssessmentAsymptomaticAngina PectorisDiabetes mellitusInternal medicinemedicineHumansObesityeducationAgedDyslipidemiasAngiologyCerebrovascular eventsAortic Aneurysm Thoracicbusiness.industrymedicine.diseaseSettore MED/11 - Malattie Dell'Apparato CardiovascolareCerebrovascular DisordersIntima-media thicknessAsymptomatic DiseasesMetabolic syndromebusinessBody mass index
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Apple Watch detecting coronary ischaemia during chest pain episodes or an apple a day may keep myocardial infarction away

2020

Chest Painmedicine.medical_specialtybusiness.industryMyocardial InfarctionMyocardial IschemiaMEDLINEIschemiaCardiovascular Flashlightsmedicine.diseaseChest painInternal medicineCardiologyHumansMedicineMyocardial infarction diagnosisMyocardial infarctionmedicine.symptomCardiology and Cardiovascular MedicinebusinessEuropean Heart Journal
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