Search results for "CARDIOVASCULAR DISEASE."

showing 10 items of 2331 documents

Nitrate therapy: new aspects concerning molecular action and tolerance.

2011

Although the short-term vasodilatory properties of organic nitrates are potent and well known, a number of vascular and extravascular changes have been shown to compromise their hemodynamic effects on long-term administration. Among these changes, systemic phenomena such as neurohormonal activation and intravascular volume expansion1 as well as specific vascular changes such as increased vascular superoxide (O2·−) production,2 increased sensitivity to vasoconstrictors,3 and decreased responsiveness to nitric oxide (NO) donors4,5 have long been identified as playing a role. Several hypotheses have been proposed to explain these abnormalities, and over the last 15 years, our groups have focus…

medicine.medical_specialtymedicine.disease_causeNitric oxideSuperoxide dismutasechemistry.chemical_compoundPhysiology (medical)Internal medicineMedicineHumansEndothelial dysfunctionchemistry.chemical_classificationReactive oxygen speciesNitratesbiologybusiness.industrySuperoxideDrug Tolerancemedicine.diseaseNitric oxide synthaseOxidative StressEndocrinologychemistryCardiovascular Diseasesbiology.proteinEndothelium VascularCardiology and Cardiovascular MedicinebusinessPeroxynitriteOxidative stressCirculation
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Letter by Barco et al Regarding Article, "Restarting Anticoagulant Therapy After Intracranial Hemorrhage: A Systematic Review and Meta-Analysis"

2017

We read with interest the systematic review and meta-analysis authored by Murthy et al1 that appeared in Stroke . The authors studied the efficacy and safety of anticoagulant resumption after nontraumatic intracranial hemorrhage (ICH) and showed that resumption was associated with a lower risk of arterial thromboembolism but a similar risk of recurrent ICH. We do have some comments on their interpretation of the results. First, all the included studies had a retrospective design and, therefore, are characterized by heterogeneity in treatment regimens and timing of anticoagulation restart. As the authors argue in their discussion, location matters for the risk of recurrent ICH: lobar bleedin…

medicine.medical_specialtymedicine.drug_class030204 cardiovascular system & hematologyLower risk03 medical and health sciences0302 clinical medicinemedicineHumanscardiovascular diseasesIntensive care medicineStrokeAdvanced and Specialized NursingHumans; Anticoagulants; Intracranial HemorrhagesTreatment regimenbusiness.industryAnticoagulantAnticoagulantsmedicine.diseaseCausalitynervous system diseasesSurgeryAnticoagulant therapyMeta-analysisNeurology (clinical)Cardiology and Cardiovascular MedicinebusinessIntracranial Hemorrhages030217 neurology & neurosurgeryRetrospective design
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Clinical pharmacokinetics of atenolol — A review

1982

Atenolol is a hydrophilic betareceptor blocking drug, which is predominantly eliminated via the kidneys, only about 5% of the atenolol is metabolised by the liver. After oral administration atenolol is incompletely absorbed from the intestine, so about 50% of the beta blocker are finally biovailable. In plasma only 3% of atenolol are protein-bound. There exists a linear relationship between the atenolol plasma levels and the degree of beta blocking effect measured by inhibition of the exercise-induced tachycardia. No correlation was found between plasma levels of atenolol and blood pressure lowering activity of the drug. After oral administration elimination half life of atenolol is calcula…

medicine.medical_specialtymedicine.drug_classAdministration OralBiological AvailabilityRenal functionPharmacologyKidneyIntestinal absorptionPropanolaminesPharmacokineticsRenal DialysisOral administrationInternal medicinemedicineHumansDrug InteractionsPharmacology (medical)cardiovascular diseasesBeta blockerPharmacologyChemistryLiver DiseasesKidney metabolismAtenololKineticsEndocrinologyAtenololIntestinal AbsorptionInjections IntravenousKidney DiseasesBiological half-lifecirculatory and respiratory physiologymedicine.drugEuropean Journal of Drug Metabolism and Pharmacokinetics
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Overview of Venous Thromboembolism

2010

Thrombosis occurs at sites of injury to the vessel wall, by inflammatory processes leading to activation of platelets, platelet adherence to the vessel wall and the formation of a fibrin network. A thrombus that goes on to occlude a blood vessel is known as a thromboembolism. Venous thromboembolism begins with deep vein thrombosis (DVT), which forms in the deep veins of the leg (calf) or pelvis. In some cases, the DVT becomes detached from the vein and is transported to the right-hand side of the heart, and from there to the pulmonary arteries, giving rise to a pulmonary embolism (PE). Certain factors predispose patients toward the development of venous thromboembolism (VTE), including surg…

medicine.medical_specialtymedicine.drug_classDeep veinFondaparinuxRisk FactorsmedicineHumansPharmacology (medical)cardiovascular diseasesThrombusIntensive care medicineVeinSocieties Medicalbusiness.industryAnticoagulantAnticoagulantsVenous Thromboembolismequipment and suppliesmedicine.diseaseThrombosisUnited StatesSurgeryPulmonary embolismVenous thrombosismedicine.anatomical_structurePractice Guidelines as Topicbusinessmedicine.drugDrugs
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Treatment of venous thromboembolism – effects of different therapeutic strategies on bleeding and recurrence rates and considerations for future anti…

2012

Abstract Effective treatment of venous thromboembolism (VTE) strikes a balance between prevention of recurrence and bleeding complications. The current standard of care is heparin followed by a vitamin K antagonist such as warfarin. However, this option is not without its limitations, as the anticoagulant effect of warfarin is associated with high inter- and intra-patient variability and patients must be regularly monitored to ensure that anticoagulation is within the narrow target therapeutic range. Several novel oral anticoagulant agents are in the advanced stages of development for VTE treatment, some of which are given after an initial period of heparin treatment, in line with current p…

medicine.medical_specialtymedicine.drug_classDeep veinReviewTherapeutic indexRecurrencemedicinecardiovascular diseasesIntensive care medicinebusiness.industryHeparinlcsh:RC633-647.5AnticoagulantBleedingWarfarinAnticoagulantsHeparinlcsh:Diseases of the blood and blood-forming organsHematologyVitamin K antagonistmedicine.diseaseThrombosisPulmonary embolismSurgerymedicine.anatomical_structureVitamin K antagonistsbusinessmedicine.drugVenous thromboembolismThrombosis Journal
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Increased nitrotyrosine plasma levels in relation to systemic markers of inflammation and myeloperoxidase in chronic heart failure

2009

The presence of a reciprocal link between inflammation and oxidative/nitrosative stress has been postulated in chronic heart failure (CHF). We aimed to determine signs of nitrosative stress in serum/plasma of CHF patients. ELISA tests were used for quantification of serum/plasma levels of Nitrotyrosine (NT), H(2)O(2), total NO, nitrite (NO(2)(-)), myeloperoxidase (MPO), Tumor Necrosis Factor-alpha (TNFalpha) and pro-Brain Natriuretic Peptide (proBNP) in 66 CHF patients (9 in NYHA I, 34 NYHA II, 23 NYHA III) and in 14 age-matched healthy subjects. NT levels were higher in NYHA III CHF patients compared to NYHA II (p<0.05), NYHA I (p<0.03) and controls (p<0.02), whereas NO(2)(-) and total NO …

medicine.medical_specialtymedicine.drug_classInflammationSystemic inflammationGastroenterologyNITROSATIVE STRESSchemistry.chemical_compoundInternal medicineBlood plasmamedicineNatriuretic peptidecardiovascular diseasesOXIDATIVE STRESSEndothelial dysfunctionbiologybusiness.industryNitrotyrosinemedicine.diseasehumanitiesEndocrinologychemistryMyeloperoxidaseHeart failureENDOTHELIAL DYSFUNCTIONcardiovascular systembiology.proteinmedicine.symptomCardiology and Cardiovascular Medicinebusinesscirculatory and respiratory physiology
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Blood Coagulation and Thrombosis in Patients with Ovarian Malignancy

1997

SummaryOvarian cancer cells appear to be capable of both thrombin formation and induction of fibrin degradation which may be essential prerequisites for the development of deep vein thrombosis (DVT) as well as the spread of malignancy. To study further this coagulation – cancer interaction in 60 patients with untreated ovarian cancer of FIGO stage I-IV the incidence of DVT was recorded pre-operatively, postoperatively on day 1, 3, 5, 7, 10, before each of six cycles of Cisplati- num/Epirubicin/Cyclophosphamide chemotherapy, during follow-up and in the post-operative period of second look surgery. In addition, blood coagulation tests results were determined prospectively. Two patients were e…

medicine.medical_specialtymedicine.drug_classLow molecular weight heparinGastroenterologyPostoperative ComplicationsMedian follow-upThromboembolismInternal medicinemedicineHumansProspective Studiescardiovascular diseasesBlood CoagulationAgedBlood coagulation testOvarian NeoplasmsUnivariate analysisHeparinbusiness.industryAntithrombinAnticoagulantAnticoagulantsHematologyHeparinHeparin Low-Molecular-WeightMiddle AgedSurvival AnalysisSurgeryFemaleBlood Coagulation Testsbusinessmedicine.drugEpirubicinThrombosis and Haemostasis
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The role of fibrate treatment in dyslipidemia: an overview.

2012

Dyslipidemia, and especially atherogenic dyslipidemia, a combination of small low-density lipoproteins cholesterol (LDL-C), decreased high-density lipoprotein cholesterol (HDL-C) and increased triglyceride (TG) concentrations, represents a major cardiovascular (CV) risk factor. Nuclear receptor peroxisome proliferator-activated receptors (PPARs) are involved in the regulation of lipid metabolism; PPAR ligands are used to treat dyslipidemias. Fibrates have a major impact on TG metabolism as well as on modulating LDL size and subclasses. Fibrates target atherogenic dyslipidemia by increasing plasma HDL-C concentrations and decreasing small dense LDL (sdLDL) particles and TGs, thus contributin…

medicine.medical_specialtymedicine.drug_classPeroxisome proliferator-activated receptorAdipokineFibratechemistry.chemical_compoundInternal medicineDrug DiscoverymedicineAnimalsHumansTriglyceridesDyslipidemiasHypolipidemic AgentsPharmacologychemistry.chemical_classificationTriglycerideCholesterolbusiness.industryFibric Acidsnutritional and metabolic diseasesLipid metabolismCholesterol LDLmedicine.diseaseFibrates dyslipidemia cardiovascular risk diabetes.EndocrinologychemistryCardiovascular Diseaseslipids (amino acids peptides and proteins)Metabolic syndromebusinessDyslipidemiaCurrent pharmaceutical design
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New approaches on diagnosis and treatment of venous thromboembolism

2014

Summary Pulmonary embolism (PE) and deep vein thrombosis (DVT) are two clinical presentations of venous thromboembolism (VTE) and share the same predisposing factors. In patients admitted to a hospital the rationale use of thromboprophylaxis is based on the high prevalence of VTE amongst hospitalised patients, the adverse consequences of unprevented VTE, and the efficacy of thromboprophylaxis. There is no doubt about the benefit/risk ratio of perioperative venous thromboembolism prophylaxis, but for a safety performance of regional anaesthesia, particularly neuraxial blocks, an appropriate management based on safety intervals suited to the characteristics of the drug is needed. The first st…

medicine.medical_specialtymedicine.drug_classbusiness.industryDeep veinLow molecular weight heparinPerioperativeCritical Care and Intensive Care Medicinemedicine.diseaseThrombosisPulmonary embolismAnesthesiology and Pain Medicinemedicine.anatomical_structureRelative riskmedicinecardiovascular diseasesIntensive care medicineGeneva scorebusinessVenous thromboembolismTrends in Anaesthesia and Critical Care
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Antihistamine-resistant Angioedema in Women with Negative Family History: Estrogens and F12 Gene Mutations

2013

Abstract Background In women with sporadic recurrent angioedema with an unknown cause who are unresponsive to antihistamines and have normal C1 inhibitor activity and a negative family history of angioedema, it is unclear whether they have idiopathic angioedema or hereditary angioedema with normal C1 inhibitor, and what impact exogenous estrogens have on their angioedema. Methods A cohort of 147 women was analyzed for F12 exon 9 mutations and for the influence of oral contraceptives, hormonal replacement therapy, and pregnancy on their angioedema. Results A total of 142 women had idiopathic angioedema unresponsive to antihistamines. Five women had an F12 mutation and thereby hereditary angi…

medicine.medical_specialtymedicine.drug_classmedicine.medical_treatmentGene mutationC1-inhibitorimmune system diseasesInternal medicinemedicineHereditary Angioedema Type IIIcardiovascular diseasesFamily historyskin and connective tissue diseasesbiologyAngioedemabusiness.industryfood and beveragesGeneral Medicinemedicine.diseaseDermatologyEndocrinologyEstrogenHereditary angioedemabiology.proteinAntihistaminemedicine.symptombusinessThe American Journal of Medicine
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