Search results for "myocardial infarction."

showing 10 items of 1011 documents

Gender-specific diagnosis of acute myocardial infarction using high-sensitivity assayed cardiac troponin I

2013

Brachial Plexus Neuritismedicine.medical_specialtyCardiac troponinPositive pressure ventilatorsbusiness.industryInternal medicineCardiologyMedicineMyocardial infarctionCardiology and Cardiovascular Medicinebusinessmedicine.diseaseEuropean Heart Journal
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Revascularisation of a Giant Coronary Artery Aneurysm in Suspected Incomplete Kawasaki-Disease

2006

Kawasaki disease leads to typical vascular complications in up to 20 % of untreated cases. We describe a 47-year-old patient with coronary vessel disease, involving the right coronary artery with a huge aneurysmatic dilatation, suspicious for an incomplete form of Kawasaki disease. We found little information about the surgical treatment and postoperative course of this disease in adults. Typically, these infrequent patients present with acute myocardial infarction and require interdisciplinary decision-making.

Brain InfarctionPulmonary and Respiratory Medicinemedicine.medical_specialtyMyocardial InfarctionDiseaseMucocutaneous Lymph Node SyndromeCoronary AngiographyPostoperative ComplicationsAneurysmInternal medicinemedicine.arterymedicineHumanscardiovascular diseasesMyocardial infarctionCoronary Artery BypassSurgical treatmentCoronary artery aneurysmbusiness.industryCoronary ThrombosisCoronary AneurysmMiddle Agedmedicine.diseaseAortic DissectionIntracranial EmbolismRight coronary arteryCoronary vesselCardiologySurgeryKawasaki diseaseCardiology and Cardiovascular MedicinebusinessThe Thoracic and Cardiovascular Surgeon
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PECAM-1/CD31 in infarction and longevity.

2007

: Inflammation has recently proven to be associated with the pathogenesis of atherosclerosis and inflammatory genes are good candidates for the risk of developing atherosclerosis. The early phase of atherosclerosis involves the recruitment of inflammatory cells from the circulation and their transendothelial migration. This process is mainly mediated by cellular adhesion molecules, which are expressed by the vascular endothelium and by circulating leukocytes in response to several inflammatory stimuli. Adhesion of circulating cells to the arterial surface is among the first detectable events in atherogenesis. Cellular adhesion molecules, expressed by the vascular endothelium and by circulat…

CD31MaleGenotypePopulationLongevityMyocardial InfarctionSingle-nucleotide polymorphismInflammationCoronary DiseaseBiologyPolymorphism Single NucleotideGeneral Biochemistry Genetics and Molecular BiologypolymorphismSex FactorsHistory and Philosophy of ScienceKEYWORDS: centenarianmedicineCell AdhesionSNPHumansGenetic Predisposition to DiseaseCell adhesioneducationSettore MED/04 - Patologia GeneraleAged 80 and overInflammationeducation.field_of_studyPolymorphism GeneticCell adhesion moleculeGeneral NeurosciencePlatelet Endothelial Cell Adhesion Molecule-1ItalyCase-Control StudiesImmunologycardiovascular systemCentenarianmedicine.symptomAnnals of the New York Academy of Sciences
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Triglyceride-rich lipoproteins and their remnants: metabolic insights, role in atherosclerotic cardiovascular disease, and emerging therapeutic strat…

2021

Abstract Recent advances in human genetics, together with a large body of epidemiologic, preclinical, and clinical trial results, provide strong support for a causal association between triglycerides (TG), TG-rich lipoproteins (TRL), and TRL remnants, and increased risk of myocardial infarction, ischaemic stroke, and aortic valve stenosis. These data also indicate that TRL and their remnants may contribute significantly to residual cardiovascular risk in patients on optimized low-density lipoprotein (LDL)-lowering therapy. This statement critically appraises current understanding of the structure, function, and metabolism of TRL, and their pathophysiological role in atherosclerotic cardiova…

CHOLESTERYL ESTER TRANSFERTO-MODERATE HYPERTRIGLYCERIDEMIALipoprotein remnants030204 cardiovascular system & hematologyBioinformaticsResidual riskBrain Ischemiachemistry.chemical_compoundVoeding Metabolisme en Genomica0302 clinical medicineIschaemic strokeAcademicSubjects/MED00200Myocardial infarctionLOW-GRADE INFLAMMATIONALL-CAUSE MORTALITY[SDV.MHEP.EM] Life Sciences [q-bio]/Human health and pathology/Endocrinology and metabolism0303 health sciencesAtherosclerotic cardiovascular diseasedigestive oral and skin physiology[SDV.MHEP.EM]Life Sciences [q-bio]/Human health and pathology/Endocrinology and metabolismCardiovascular diseaseMetabolism and Genomics3. Good healthStrokeLOW-DENSITY LIPOPROTEINSCardiovascular DiseasesMetabolisme en GenomicaCORONARY-ARTERY-DISEASENutrition Metabolism and GenomicsCardiology and Cardiovascular MedicineB-CONTAINING LIPOPROTEINSLipoproteinsTriglyceride-rich lipoproteinsHEART-DISEASE03 medical and health sciencesSpecial ArticleVoedingmedicineHumansHOMOZYGOUS FAMILIAL HYPERCHOLESTEROLEMIATriglycerides030304 developmental biologyNutritionVLAGTriglyceridebusiness.industryAPO-Bmedicine.diseaseAtherosclerosisResidual riskIncreased riskchemistry3121 General medicine internal medicine and other clinical medicineEuropean atherosclerosis societybusinessLipoprotein
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Pharmacogenomics: a tool to prevent and cure coronary heart disease.

2007

Inflammation and genetics play an important role in the pathogenesis of coronary heart disease (CHD). This is supported by epidemiological studies which have thoroughly investigated the association between CHD and gene polymorphisms of the inflammatory molecules. Moreover, efforts to find elective therapy have not been rewarding and, despite the increasing appreciation of the role of genetics in CHD and myocardial infarction (MI) pathogenesis, pharmacogenomic approaches to uncover drug target have not been extensively explored. A critical search of published literature has suggested few inflammatory genes directly involved in the risk to develop CHD and MI. The selected genes are, the pro- …

Candidate genepharmacogenomicLipoxygenaseLipopolysaccharide ReceptorsMyocardial InfarctionCoronary DiseaseDiseaseBioinformaticsRisk AssessmentPathogenesisRisk FactorsDrug DiscoverymedicinecytokineHumansGenetic Predisposition to DiseaseMyocardial infarctionTLR4PharmacologyInflammationPolymorphism Geneticbusiness.industryPatient SelectionCase-control studyCOXLOXmedicine.diseaseAtherosclerosisToll-Like Receptor 4Treatment OutcomePharmacogeneticsProstaglandin-Endoperoxide SynthasesPharmacogenomicsCase-Control StudiesImmunologyCytokinesReceptors ChemokineChemokinesbusinessRisk assessmentCD14CCR5PharmacogeneticsCurrent pharmaceutical design
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Association of Global Longitudinal Strain With Clinical Status and Mortality in Patients With Chronic Heart Failure.

2021

IMPORTANCE: Global longitudinal strain (GLS) is an emerging echocardiographic biomarker of cardiac function in heart failure (HF). Evidence from large-scale studies comprehensively investigating GLS for its association with clinical phenotypes and mortality in asymptomatic and symptomatic chronic HF is limited. OBJECTIVE: To assess the factors associated with GLS and its prognostic value in patients with chronic HF. DESIGN, SETTING, AND PARTICIPANTS: The observational, prospective MyoVasc cohort study enrolled 3289 individuals with asymptomatic to symptomatic HF between January 17, 2013, and April 27, 2018. The median follow-up was 3.2 years (interquartile range, 2.0-4.0 years). Participant…

Cardiac function curveMalemedicine.medical_specialty030204 cardiovascular system & hematologyAsymptomatic03 medical and health sciences0302 clinical medicineInterquartile rangeInternal medicinemedicineHumans030212 general & internal medicineMyocardial infarctionProspective StudiesAgedOriginal InvestigationHeart Failurebusiness.industryHazard ratioPatient AcuityAtrial fibrillationHeartMiddle Agedmedicine.diseasePrognosisEchocardiographyHeart failureFemalemedicine.symptomCardiology and Cardiovascular MedicinebusinessBiomarkersCohort studyJAMA cardiology
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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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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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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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P863Morphometric analysis of the dynamic changes of the interstitium after reperfused myocardial infarction

2019

Abstract Background The interstitial space is mainly composed by cells, fibers and gels of polysaccharides, which act as a compression buffer against the stress placed on the extracellular matrix (ECM). After myocardial infarction (MI), heart has to withstand higher mechanical stress due to injured cardiomyocytes. ECM composition notably influences the mechanical properties of the myocardium and participates in left ventricular remodeling. Purpose To characterize the myocardial ECM changes from ischemia onset until late phases after coronary reperfusion in a swine model of reperfused MI. Methods MI was induced in swine by transient 90-min coronary occlusion using angioplasty balloons. One c…

Cardiac function curvemedicine.medical_specialtyReperfused myocardial infarctionbusiness.industryIschemiamedicine.diseaseReperfusion therapyInterstitial spaceCoronary occlusionInternal medicinemedicineCardiologyMyocardial infarctionCardiology and Cardiovascular MedicinebusinessReperfusion injuryEuropean Heart Journal
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