Search results for "MYOPATHY"

showing 10 items of 352 documents

Assessment of atrial diastolic function in patients with hypertrophic cardiomyopathy by cine magnetic resonance imaging

2015

Purpose: This study was conducted to assess the role of atrial function by cardiac magnetic resonance (CMR) for the evaluation of diastolic physiology in patients with hypertrophic cardiomyopathy (HCM) compared to healthy controls. Materials and methods: We enrolled 23 consecutive patients affected by HCM and 43 healthy subjects as age-matched control cases (CC). CMR was performed through acquisition of cine steady-state free precession sequences using a 1.5-T scanner. Image postprocessing was carried out using Tracking Tool software. Results: Atrial volumes were significantly higher in patients with HCM compared to CC: maximum atrial volume (p = 0.007) and minimum atrial volume (p = 0.01).…

AdultMalemedicine.medical_specialtyRadiology Nuclear Medicine and ImagingDiastolic functionCardiac magnetic resonanceDiastoleContrast MediaMagnetic Resonance Imaging CineDiastoleInternal medicineImage Interpretation Computer-AssistedmedicineOrganometallic CompoundsHumansIn patientDiastolic functioncardiovascular diseasesHeart AtriaNeuroradiologyOrganometallic Compoundmedicine.diagnostic_testbusiness.industryMedicine (all)UltrasoundAtrial functionHypertrophic cardiomyopathyMagnetic resonance imagingInterventional radiologyGeneral MedicineCardiomyopathy Hypertrophicmedicine.diseaseHypertrophic cardiomyopathyCase-Control Studiescardiovascular systemCardiologyFemalebusinessCase-Control StudieSettore MED/36 - Diagnostica Per Immagini E RadioterapiaHuman
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Therapeutic management in Sicilian patients with definite arrhythmogenic right ventricular dysplasia/cardiomyopathy and focus on the role of implanta…

2014

Arrhythmogenic Right Ventrticular Dysplasia/Cardiomyopathy(ARVD/C) is an inherited cardiomyopathy characterized by right ven-tricularmyocytelosswithfibrofattyreplacement,ahighriskofventric-ular arrhythmias (VA) and sudden cardiac death (SCD) [1]. Preventionof SCD represents the most important management strategy and theachievement of this target can be reached by different therapeuticstrategies including implantable cardioverter-defibrillator (ICD)implantation, pharmacologic therapy, catheter ablation of ventriculartachycardia (VT) and cardiac transplantation [2,3]. The aim of thisstudy is to examine the outcome of the different therapies adopted ina group of affected patients, focusing on th…

AdultMalemedicine.medical_specialtyTime FactorsCardiomyopathymedicine.medical_treatmentCardiomyopathyCatheter ablationImplantable cardioverterdefibrillatorSudden deathInternal medicinemedicineHumansMedical managementSicilySurvival rateArrhythmogenic Right Ventricular DysplasiaCardiomyopathy; Implantable cardioverterdefibrillator; Medical management; Predictors; Sudden deathSudden deathbusiness.industryPrognosisImplantable cardioverter-defibrillatormedicine.diseaseSettore MED/11 - Malattie Dell'Apparato CardiovascolareDefibrillators ImplantableArrhythmogenic right ventricular dysplasiaSurvival RateTransplantationDeath Sudden CardiacTreatment OutcomeHeart failureCardiologyFemaleMorbidityCardiology and Cardiovascular MedicinebusinessFollow-Up StudiesPredictorInternational Journal of Cardiology
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Nemaline myopathy and heart failure: role of ivabradine; a case report

2015

Background Nemaline myopathy (NM) is a rare congenital myopathy characterized by muscle weakness, hypotonia and the presence in muscle fibers of inclusions known as nemaline bodies and a wide spectrum of clinical phenotypes, ranging from severe forms with neonatal onset to asymptomatic forms. The adult-onset form is heterogeneous in terms of clinical presentation and disease progression. Cardiac involvement occurs in the minority of cases and little is known about medical management in this subgroup of NM patients. We report a rare case of heart failure (HF) in a patient with adult-onset NM in whom ivabradine proved to be able to dramatically improve the clinical picture. Case presentation …

AdultMalemedicine.medical_specialtymedicine.medical_treatmentDilated cardiomyopathyCase ReportMyopathies NemalineElectrocardiographyNemaline myopathyInternal medicinemedicineHumansIvabradineCarvedilolNemaline myopathyHeart FailureEjection fractionbusiness.industryDilated cardiomyopathyCardiovascular AgentsBenzazepinesmedicine.diseaseImplantable cardioverter-defibrillatorCongenital myopathyTreatment OutcomeEchocardiographyHeart failureCardiologybusinessCardiology and Cardiovascular MedicineIvabradinemedicine.drugBMC Cardiovascular Disorders
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Glucose insulin potassium infusion improves systolic function in patients with chronic ischemic cardiomyopathy

2002

Objective: We assessed the effects of glucose–insulin–potassium (GIK) by echocardiography in stable patients with ischemic dysfunction. Methods: Twelve male patients with stable coronary disease (SCD) and ejection fraction (EF) <45% were studied for systolic function. GIK (glucose 30%, 300 insulin units and KCl 6 g/l) was infused at 1 ml/kg per h over 20 min. Hemodynamic and echocardiographic measurements were recorded at rest (T0), at the end (20 min) of GIK infusion (T + 20), 20 and 40 min after the end of the infusion (T + 40 and T + 60). Results: At T + 20, a significant decrease in WMSI (wall motion score index) was observed compared with T0 (2.16±0.14 vs. 2.30±0.16: P<0.05). An increa…

AdultMalemedicine.medical_specialtymedicine.medical_treatmentHemodynamicsBlood PressureSystolic functionVentricular Dysfunction LeftHeart RateInternal medicinemedicineHumansInsulinIn patientInfusion PumpsAgedEjection fractionIschemic cardiomyopathyGlucose insulin potassiumbusiness.industryInsulinStroke VolumeMiddle Agedmedicine.diseaseGlucoseTreatment OutcomeEchocardiographyHeart failureChronic DiseasePotassiumCardiologyCardiomyopathiesCardiology and Cardiovascular MedicinebusinessFollow-Up StudiesEuropean Journal of Heart Failure
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Desmin-related myopathies

1997

Desmin-related myopathies are marked by accumulation of desmin, which is often familial and associated with cardiomyopathy. When multifocal this excess is characterized by inclusions such as cytoplasmic or spheroid bodies, when disseminated the excess is called granulofilamentous material. Excess of desmin might represent an abnormal type of protein metabolism.

AdultPathologymedicine.medical_specialtyGranulofilamentous materialCardiomyopathyChromosome DisordersGenes Recessivemacromolecular substancesBiologyDesminMuscular DiseasesmedicineHumansChildMuscle SkeletalGenotype-Phenotype CorrelationsGenes DominantChromosome AberrationsInclusion BodiesDESMIN-RELATED MYOPATHYMyocardiumMolecular pathogenesismusculoskeletal systemmedicine.diseaseActin CytoskeletonNeurologyCytoplasmDesminNeurology (clinical)CardiomyopathiesCurrent Opinion in Neurology
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Myo-, neuro-, gastrointestinal encephalopathy (MNGIE syndrome) due to partial deficiency of cytochrome-c-oxidase

1987

A 42-year-old woman had a 10-year history of external ophthalmoplegia, malabsorption resulting in chronic malnutrition, muscle atrophy and polyneuropathy. Computer tomography revealed hypodensity of her cerebral white matter. A metabolic disturbance consisted of lactic acidosis after moderate glucose loads with increased excretion of hydroxybutyric and fumaric acids. Post-mortem studies revealed gastrointestinal scleroderma as the morphological manifestation of her malabsorption syndrome, ocular and skeletal myopathy with ragged red fibers, peripheral neuropathy, vascular abnormalities of meningeal and peripheral nerve vessels. Biochemical examination of the liver and muscle tissues reveale…

AdultPathologymedicine.medical_specialtyMalabsorptionGastrointestinal DiseasesEncephalopathyRespiratory chainCytochrome-c Oxidase DeficiencyEyePathology and Forensic Medicine03 medical and health sciencesCellular and Molecular Neuroscience0302 clinical medicineMuscular DiseasesMitochondrial myopathymedicineHumansMuscular dystrophy030304 developmental biology2. Zero hungerBrain Diseases0303 health sciencesbusiness.industryPeripheral Nervous System DiseasesSyndromemedicine.diseaseMitochondria MusclePeripheral neuropathyLactic acidosisFemaleNeurology (clinical)businessPolyneuropathy030217 neurology & neurosurgeryActa Neuropathologica
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Maternally inherited diabetes and deafness (MIDD): unusual occult exocrine pancreatic manifestation in an affected German family

2000

The mitochondrial (mt) 3243 DNA mutation is an underlying cause of maternally inherited diabetes and deafness (MIDD) syndrome and the syndrome of mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes (MELAS). We report an affected German MIDD pedigree with maternal lineage over three generations. The index patient, her mother, her maternal aunt and her maternal grandmother all suffered from diabetes and premature hearing loss and were positive on testing for the mt 3243 DNA mutation. The 27-year-old index patient had a history of grand mal seizures. As sequela of abdominal ultrasound and confirmed by magnetic resonance cholangio-pancreaticography, she was diagnose…

AdultPathologymedicine.medical_specialtyPancreatic diseaseEndocrinology Diabetes and MetabolismEncephalopathyDeafnessMELAS syndromeDNA MitochondrialDiabetes ComplicationsEndocrinologyMitochondrial myopathyGermanyDiabetes MellitusInternal MedicineHumansMedicinePancreatic ductCommon bile ductbusiness.industryPancreatic DuctsCalcinosisPancreatic DiseasesSyndromeGeneral MedicineMiddle Agedmedicine.diseasePedigreemedicine.anatomical_structurePancreatitisLactic acidosisMutationPancreatitisFemalebusinessDilatation PathologicExperimental and Clinical Endocrinology &amp; Diabetes
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Monocyte/macrophage differentiation in dermatomyositis and polymyositis.

2004

Recent advances have revealed significant differences in the pathogenesis of inflammatory myopathies. To determine whether different patterns of macrophage differentiation are a useful tool to delineate the major groups of inflammatory myopathies, the muscle biopsies of 11 patients with dermatomyositis and 12 patients with polymyositis were studied using different macrophage markers. In polymyositis, the early-activation markers MRP14 and 27E10 stained the majority of macrophages, which were recognized by the pan-macrophage marker Ki-M1P and which were located primarily in the endomysium. In dermatomyositis, macrophages predominantly expressed the late-activation marker 25F9 and were found …

AdultPathologymedicine.medical_specialtyPhysiologyPolymyositisDermatomyositisMonocytesPathogenesisDiagnosis Differential03 medical and health sciencesCellular and Molecular Neuroscience0302 clinical medicinePhysiology (medical)medicineMacrophageCalgranulin BHumansMyopathyChildMuscle Skeletal030304 developmental biologyAgedAutoimmune disease0303 health sciencesbusiness.industryMonocyteMacrophagesCell DifferentiationDermatomyositisMiddle Agedmedicine.diseaseEndomysiumImmunohistochemistryPolymyositismedicine.anatomical_structureCase-Control StudiesChild PreschoolImmunologyNeurology (clinical)medicine.symptombusinessLeukocyte L1 Antigen Complex030217 neurology & neurosurgeryBiomarkersMusclenerve
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Ultrastructural pathology in emetine-induced myopathy

1988

Progressive myopathy developed in two women who consumed ipecac syrup containing emetine hydrochloride to induce vomiting as part of their anorexia nervosa. Muscle biopsy specimens were characterized by severe disruption of the sarcomeres. The ultrastructural spectrum extended from "Z-band streaming" to the formation of cytoplasmic bodies and also comprised abnormalities of the sarcotubular system, thus suggesting that muscle weakness may be related to both sarcomeric and sarcotubular lesions in this self-inflicted myopathy. It is tempting to suggest that muscle weakness may be correlated with or based on the pathology in sarcomeres and the sarcotubular system. As the myopathy is clinically…

AdultSarcomeresPathologymedicine.medical_specialtyAnorexia NervosaSubstance-Related DisordersEmetineEmetine HydrochlorideEmetineBiologySarcomereUltrastructural PathologyPathology and Forensic MedicineCellular and Molecular NeuroscienceMuscular DiseasesmedicineHumansMyopathyMuscle biopsymedicine.diagnostic_testMusclesMuscle weaknessMitochondriaSarcoplasmic ReticulumAnorexia nervosa (differential diagnoses)FemaleNeurology (clinical)medicine.symptommedicine.drugActa Neuropathologica
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Fetal akinesia caused by a novel actin filament aggregate myopathy skeletal muscle actin gene (ACTA1) mutation.

2010

We report a female newborn, diagnosed with fetal akinesia in utero, who died one hour after birth. Post-mortem muscle biopsy demonstrated actin-filament myopathy based on immunolabelling for sarcomeric actin, and large areas of filaments, without rod formation, ultrastructurally. Analysis of DNA extracted from the muscle disclosed a novel de novo heterozygous c.44G>A, GGC>GAC, 'p.Gly15Asp' mutation in the ACTA1 gene. Analysis of the location of the mutated amino-acid in the actin molecule suggests the mutation most likely causes abnormal nucleotide binding, and consequent pathological actin polymerization. This case emphasizes the association of fetal akinesia with actin-filament myopathy.

AdultSarcomeresmacromolecular substancesBiologymedicine.disease_causeSarcomereNemaline myopathyPregnancymedicineHumansMyopathyMuscle SkeletalGenetics (clinical)ActinMutationMuscle biopsymedicine.diagnostic_testMicrofilament ProteinsInfant NewbornSkeletal muscleDNANeuromuscular DiseasesActin cytoskeletonmedicine.diseaseMolecular biologyActin CytoskeletonFetal Diseasesmedicine.anatomical_structureNeurologyBiochemistryPediatrics Perinatology and Child HealthMutationFemaleNeurology (clinical)medicine.symptomNeuromuscular disorders : NMD
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