Search results for "Hydroxymethyl"

showing 10 items of 313 documents

Anaesthetic techniques to prevent perioperative stroke.

2013

Different techniques and interventions that can be used by an anaesthesiologist to minimize the perioperative stroke risk are summarized.The most important risk factors for perioperative stoke are not modifiable, for example previous stroke or renal failure, but they can be used to identify patients with a high risk for perioperative stroke. The antiplatelet therapy should be continued in patients with a high risk for cardiovascular thrombosis. This might be true even for operations in which bleeding should be strictly avoided such as eye surgery. One of the most recent neuroprotective approaches is the remote ischaemic preconditioning.Perioperative stroke increases morbidity and mortality …

Adrenergic beta-AntagonistsPsychological interventionMEDLINEPerioperative CareAdrenergic beta-AntagonistsPostoperative ComplicationsRisk FactorsMonitoring IntraoperativemedicineAnimalsHumansAnesthesiacardiovascular diseasesIntraoperative ComplicationsIschemic PreconditioningStrokePerioperative strokeAnestheticsbusiness.industryAnticoagulantsPerioperativemedicine.diseaseCerebrovascular CirculationStrokeAnesthesiology and Pain MedicineAnesthesiaCerebrovascular CirculationIschemic preconditioningHydroxymethylglutaryl-CoA Reductase InhibitorsbusinessCurrent opinion in anaesthesiology
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Lomitapide affects HDL composition and function

2016

Abstract Background Lomitapide reduces low-density lipoprotein-cholesterol (LDL-C) but also high-density lipoprotein-cholesterol (HDL-C) levels. The latter may reduce the clinical efficacy of lomitapide. We investigated the effect of lomitapide on HDL-C levels and on cholesterol efflux capacity (CEC) of HDL in patients with homozygous familial hypercholesterolemia (HoFH). Methods and results Four HoFH patients were treated with increasing dosages of lomitapide. Lomitapide decreased LDL-C (range −34 to −89%). Total HDL-C levels decreased (range −16 to −34%) with a shift to buoyant HDL. ABCA1-mediated CEC decreased in all patients (range −39 to −99%). The changes of total, ABCG1- and SR-BI-me…

AdultMale0301 basic medicinemedicine.medical_specialtySettore MED/09 - Medicina InternaHDLHomozygous familial hypercholesterolemiaFamilial hypercholesterolemia030204 cardiovascular system & hematologyHyperlipoproteinemia Type IIYoung Adult03 medical and health scienceschemistry.chemical_compound0302 clinical medicineInternal medicineHumansMedicineIn patientClinical efficacyHyperlipoproteinemia Type IICholesterolbusiness.industryCholesterol HDLHomozygotenutritional and metabolic diseasesCholesterol LDLCholesterol efflux capacityAtherosclerosismedicine.diseaseCholesterol lowering drugsLomitapideLomitapideCholesterolPhenotypeTreatment Outcome030104 developmental biologyEndocrinologychemistryBenzimidazolesFemalelipids (amino acids peptides and proteins)Composition (visual arts)Cholesterol lowering drugHydroxymethylglutaryl-CoA Reductase InhibitorsLipoproteins HDLCardiology and Cardiovascular MedicinebusinessATP Binding Cassette Transporter 1Atherosclerosis
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Acute Myocardial Infarction and Proinflammatory Gene Variants

2007

We identified four genetic risk sets for acute myocardial infarction (AMI) from information on functional gene variants that favor inflammation or modulate cholesterol metabolism: IL6 -174 G/C, TNF -308 G/A, IL10 -1082 G/A, SERPINA3 -51 G/T, IFNG +874 T/A, HMGCR -911 C/A, and APOE ε2/3/4; 316 patients and 461 healthy subjects, all Italian. Putative risk alleles are shown underlined. The sets were identified using grade-of-membership analysis. Membership scores in the sets are automatically generated for individuals. The ''low intrinsic risk'' set had alleles that downregulate inflammation and cholesterol synthesis (IL6, TNF, ILl0, HMGCR). ''AMI across a broad age range'' carried multiple pr…

AdultMaleApolipoprotein EAdolescentMyocardial InfarctionGeneral Biochemistry Genetics and Molecular BiologyProinflammatory cytokinePathogenesischemistry.chemical_compoundApolipoproteins EHistory and Philosophy of SciencemedicineHumansGenetic Predisposition to DiseaseMyocardial infarctionAge of OnsetAlleleAllelesSerpinsAgedAged 80 and overbusiness.industryCholesterolGeneral NeuroscienceMiddle Agedmedicine.diseaseMiddle ageInterleukin 10CholesterolchemistryAMI Grade of Membership Genetic profile IL6 -174 G/C TNF -308 G/A IL10 -1082 G/A SERPINA3 -51 G/T IFNG +874 T/A HMGCR -911 C/A APOE ε2/3/4Acute DiseaseImmunologyCytokinesFemaleHydroxymethylglutaryl CoA Reductaseslipids (amino acids peptides and proteins)businessAnnals of the New York Academy of Sciences
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Rosuvastatin Prevents Conduit Artery Endothelial Dysfunction Induced by Ischemia and Reperfusion by a Cyclooxygenase-2–Dependent Mechanism

2010

ObjectivesThe purpose of this study was to determine whether single-dose rosuvastatin (40 mg) protects against ischemia and reperfusion (IR)–induced endothelial dysfunction in humans and whether this effect is cyclooxygenase (COX)-2 dependent.BackgroundAnimal studies have demonstrated that rosuvastatin can limit damage and improve recovery after IR.MethodsIn a double-blind, parallel design, 20 volunteers were randomized to a single dose of oral rosuvastatin (40 mg) or placebo. Twenty-four hours later, endothelium-dependent, flow-mediated dilation (FMD) of the radial artery was measured before and after IR (15 min of upper arm ischemia followed by 15 min of reperfusion). In a separate protoc…

AdultMaleEndotheliumendotheliumAdolescentPremedicationIschemiaMyocardial Reperfusion InjuryPharmacologyPlaceboYoung AdultDouble-Blind Methodmedicineischemia reperfusionHumansRosuvastatinEndothelial dysfunctionRosuvastatin CalciumSulfonamidesCyclooxygenase 2 Inhibitorsbusiness.industryModels Cardiovascularnutritional and metabolic diseases3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitormedicine.diseaseFluorobenzenesVasodilationRosuvastatin Calciummedicine.anatomical_structurePyrimidinesCelecoxibCyclooxygenase 2AnesthesiaIschemic Preconditioning MyocardialRadial ArteryCelecoxibIschemic preconditioningPyrazolesFemaleEndothelium VascularHydroxymethylglutaryl-CoA Reductase InhibitorsbusinessCardiology and Cardiovascular Medicinerosuvastatinmedicine.drugJournal of the American College of Cardiology
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Editor's Note: Relates to: ‘Familial hypercholesterolaemia is underdiagnosed and undertreated in the general population: guidance for clinicians to p…

2020

Aims The first aim was to critically evaluate the extent to which familial hypercholesterolaemia (FH) is underdiagnosed and undertreated. The second aim was to provide guidance for screening and treatment of FH, in order to prevent coronary heart disease (CHD). Methods and results Of the theoretical estimated prevalence of 1/500 for heterozygous FH, <1% are diagnosed in most countries. Recently, direct screening in a Northern European general population diagnosed approximately 1/200 with heterozygous FH. All reported studies document failure to achieve recommended LDL cholesterol targets in a large proportion of individuals with FH, and up to 13-fold increased risk of CHD. Based on prevalen…

AdultMaleHeterozygoteConsensusCost-Benefit AnalysisCoronary DiseaseRisk AssessmentHyperlipoproteinemia Type IIHumansAcademicSubjects/MED00200ChildAnticholesteremic AgentsLow-density lipoproteinHomozygoteCholesterol LDLMiddle AgedCardiovascular diseaseAtherosclerosisCorrigendaPedigreeCoronary heart diseaseCholesterolEarly DiagnosisTreatment OutcomeCurrent OpinionChild PreschoolMutationFemaleHydroxymethylglutaryl-CoA Reductase InhibitorsDelivery of Health CareForecastingEuropean Heart Journal
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Statin use and non-alcoholic steatohepatitis in at risk individuals.

2015

Background &amp; Aims Excess hepatic free cholesterol contributes to the pathogenesis of non-alcoholic steatohepatitis, and statins reduce cholesterol synthesis. Aim of this study was to assess whether statin use is associated with histological liver damage related to steatohepatitis. Methods The relationship between statin use, genetic risk factors, and liver damage was assessed in a multi-center cohort of 1201 European individuals, who underwent liver biopsy for suspected non-alcoholic steatohepatitis. Results Statin use was recorded in 107 subjects, and was associated with protection from steatosis, NASH, and fibrosis stage F2-F4, in a dose-dependent manner (adjusted p &lt;0.05 for all).…

AdultMaleRiskmedicine.medical_specialtyStatinmedicine.drug_classBiopsyGastroenterologyNon-alcoholic Fatty Liver DiseaseInternal medicinemedicineHumansSteatosiPNPLA3AgedHepatologymedicine.diagnostic_testbusiness.industryNASHStatinMembrane ProteinsLipaseHepatologyMiddle AgedImpaired fasting glucosemedicine.diseaseCholesterolEndocrinologyLogistic ModelsLiverLiver biopsyCohortFemaleSteatosisSteatohepatitisHydroxymethylglutaryl-CoA Reductase InhibitorsbusinessNon-alcoholic steatohepatitiTM6SF2Journal of hepatology
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Ezetimibe/Simvastatin 10/20 mg versus Rosuvastatin 10 mg in high-risk hypercholesterolemic patients stratified by prior statin treatment potency

2010

Abstract Objective This post-hoc analysis compared the lipid-altering efficacy of Ezetimibe/Simvastatin 10/20 mg (EZ/Simva) versus Rosuvastatin 10 mg (Rosuva) in patients stratified by statin potency/dose prior to randomization. Methods Patients with elevated low-density lipoprotein cholesterol (LDL-C) despite prior statin treatment (n = 618) were randomized 1:1 to EZ/Simva 10/20 mg or Rosuva 10 mg for 6 weeks. Percent change from baseline in lipids and attainment of lipid targets were assessed within each subgroup (low potency n = 369, high potency n = 249). Consistency of the treatment effect across subgroups was evaluated by testing for treatment-by-subgroup interaction. No multiplicity …

AdultMaleSimvastatinmedicine.medical_specialtySettore MED/09 - Medicina InternaStatinRandomizationAdolescentmedicine.drug_classEndocrinology Diabetes and MetabolismHypercholesterolemiaClinical BiochemistryUrologyPharmacologyYoung AdultEndocrinologyEzetimibemedicineHumansPotencyRosuvastatinRosuvastatin Calciumlcsh:RC620-627AgedBiochemistry medicalAged 80 and overSulfonamidesSimvastatin; Ezetimibe;hypercholesterolemic;ChemistryhypercholesterolemicResearchAnticholesteremic AgentsBiochemistry (medical)nutritional and metabolic diseasesMiddle AgedEzetimibeFluorobenzeneslcsh:Nutritional diseases. Deficiency diseasesRosuvastatin CalciumPyrimidinesTreatment OutcomeSimvastatinAzetidinesFemalelipids (amino acids peptides and proteins)Ezetimibe/simvastatinHydroxymethylglutaryl-CoA Reductase Inhibitorsmedicine.drugLipids in Health and Disease
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Lipid-altering efficacy of ezetimibe/simvastatin 10/20 mg compared with rosuvastatin 10 mg in high-risk hypercholesterolaemic patients inadequately c…

2009

SUMMARY Aims: To evaluate the efficacy of switching from a previous statin monotherapy to ezetimibe ⁄simvastatin (EZE ⁄SIMVA) 10 ⁄20 mg vs. rosuvastatin (ROSUVA) 10 mg. Methods: In this randomised, double-blind study, 618 patients with documented hypercholesterolaemia [low-density lipoprotein cholesterol (LDL-C) ‡ 2.59 and £ 4.92 mmol ⁄l] and with high cardiovascular risk who were taking a stable daily dose of one of several statin medications for ‡ 6 weeks prior to the study randomisation visit entered a 6-week open-label stabilisation ⁄screening period during which they continued to receive their prestudy statin dose. Following stratification by study site and statin dose ⁄potency, patien…

AdultMaleSimvastatinmedicine.medical_specialtyimvastatinStatinmedicine.drug_classHypercholesterolemiaCoronary Artery DiseaseGastroenterologyhypercholesterolaemicchemistry.chemical_compoundDouble-Blind MethodEzetimibeRisk FactorsInternal medicinemedicineHumansRosuvastatinRosuvastatin CalciumAgedAged 80 and overSulfonamidesbiologybusiness.industryCholesterolCholesterol LDLGeneral MedicineMiddle AgedFluorobenzenesRosuvastatin CalciumPyrimidinesTreatment OutcomeEndocrinologychemistrySimvastatinHMG-CoA reductasebiology.proteinAzetidinesDrug Therapy CombinationFemalelipids (amino acids peptides and proteins)Ezetimibe/simvastatinHydroxymethylglutaryl-CoA Reductase Inhibitorsbusinessezetimibemedicine.drugInternational Journal of Clinical Practice
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Loss of the preconditioning effect of rosuvastatin during sustained therapy: a human in vivo study

2011

Studies have demonstrated that the acute administration of 3-hydroxy-3 methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors has protective effects in the setting of ischemia-reperfusion (IR). Previously, we demonstrated that a single dose of rosuvastatin prevented IR-induced endothelial dysfunction in humans through a cyclooxygenase-2-dependent mechanism. Whether the chronic administration of HMG-CoA reductase inhibitors provides similar protection remains controversial and is unknown in humans. Eighteen male volunteers were randomized to receive a single dose of rosuvastatin (20 mg) or placebo. Twenty-four hours later, endothelium-dependent, radial artery flow-mediated dilation (FMD) w…

AdultMaleTime FactorsAdolescentEndotheliumPhysiologyCoenzyme AHyperemiaPharmacologyReductaseDrug Administration ScheduleYoung Adultchemistry.chemical_compoundDouble-Blind MethodIschemiaIn vivoPhysiology (medical)medicineHumansRosuvastatinRosuvastatin CalciumOntarioAnalysis of VarianceSulfonamidesCyclooxygenase 2 Inhibitorsbiologybusiness.industryFluorobenzenesVasodilationRosuvastatin CalciumPyrimidinesmedicine.anatomical_structurechemistryCelecoxibRegional Blood FlowReperfusion InjuryRadial ArteryHMG-CoA reductasebiology.proteinCelecoxibPyrazolesHydroxymethylglutaryl-CoA Reductase InhibitorsCardiology and Cardiovascular MedicinebusinessBlood Flow Velocitymedicine.drugAmerican Journal of Physiology-Heart and Circulatory Physiology
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Coadministration of atorvastatin prevents nitroglycerin-induced endothelial dysfunction and nitrate tolerance in healthy humans.

2010

Objectives We aimed to assess whether concurrent administration of atorvastatin would modify the development of tolerance and endothelial dysfunction associated with sustained nitroglycerin (GTN) therapy in humans. Background Animal studies have demonstrated that administration of 3-hydroxy-3 methylglutaryl coenzyme A reductase inhibitors can protect against GTN-induced endothelial dysfunction and tolerance, likely through an antioxidant mechanism. Methods Thirty-six healthy male volunteers were randomized to receive continuous transdermal GTN (0.6 mg/h) and placebo, atorvastatin (80 mg/day) alone, or continuous transdermal GTN (0.6 mg/h) with concurrent atorvastatin (80 mg/day), all for 7 …

AdultMalemedicine.medical_specialtyEndotheliumendotheliumAdolescentBrachial Arterymedicine.medical_treatmentAtorvastatinVasodilator AgentsBlood PressurePlaceboNitroglycerinYoung AdultDouble-Blind MethodHeart RateReference ValuesInternal medicinemedicineAtorvastatinHumansPyrrolesEndothelial dysfunctionSalinetolerancebiologybusiness.industryDrug Administration RoutesDrug Tolerancemedicine.diseaseVasodilationOxidative StressBlood pressuremedicine.anatomical_structureEndocrinologyHeptanoic AcidsCirculatory systemHMG-CoA reductasebiology.proteincardiovascular systemlipids (amino acids peptides and proteins)Endothelium VascularHydroxymethylglutaryl-CoA Reductase InhibitorsCardiology and Cardiovascular Medicinebusinessmedicine.drugcirculatory and respiratory physiologyJournal of the American College of Cardiology
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