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  1. Article: Dental interventions in oral antithrombotic therapy.

    Deglovič, Juraj / Remková, Anna

    Vnitrni lekarstvi

    2023  Volume 69, Issue 1, Page(s) 31–36

    Abstract: Dentists commonly encounter patients taking oral antithrombotic agents who require invasive dental procedures. Although antithrombotics can cause an increase in bleeding, there is consensus that treatment regimens with antiplatelet agents, older ... ...

    Title translation Dentálne výkony pri perorálnej antitrombotickej liečbe.
    Abstract Dentists commonly encounter patients taking oral antithrombotic agents who require invasive dental procedures. Although antithrombotics can cause an increase in bleeding, there is consensus that treatment regimens with antiplatelet agents, older anticoagulants (warfarin) and direct oral anticoagulants should not be altered before routine dental procedures when the risk of bleeding is low. Thromboembolic risk of their discontinuing likely outweighs potential bleeding complications associated with surgery. Therefore, the risks of stopping or reducing these medications must be weighed against the potential consequences of prolonged bleeding, which can be controlled with local measures such as mechanical pressure, suturing, haemostatic agents or antifibrinolytics. Some patients who are taking antithrombotic medications may have additional comorbid conditions or receive other therapy that can increase the risk of prolonged bleeding after dental treatment. Where a patient is believed to be at high bleeding risk, the dentist should consider a consultation with the patient's physician to discuss temporarily discontinuing the antithrombotic therapy.
    MeSH term(s) Humans ; Fibrinolytic Agents/adverse effects ; Anticoagulants/adverse effects ; Hemorrhage/chemically induced ; Hemorrhage/prevention & control ; Platelet Aggregation Inhibitors/adverse effects ; Warfarin/therapeutic use
    Chemical Substances Fibrinolytic Agents ; Anticoagulants ; Platelet Aggregation Inhibitors ; Warfarin (5Q7ZVV76EI)
    Language English
    Publishing date 2023-02-20
    Publishing country Czech Republic
    Document type Journal Article
    ZDB-ID 138213-5
    ISSN 1801-7592 ; 0042-773X
    ISSN (online) 1801-7592
    ISSN 0042-773X
    DOI 10.36290/vnl.2023.004
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  2. Article: May warfarin prevent cancer?

    Remková, Anna / Remko, Milan

    Vnitrni lekarstvi

    2020  Volume 65, Issue 11, Page(s) 679–684

    Abstract: Animal and epidemiologic studies suggest that the use of warfarin might reduce cancer incidence. The antitumor potential of warfarin is demonstrated in different experimental cancer models. Specifically, studies in murine cancer models have shown that ... ...

    Title translation Môže warfarín zabrániť vzniku nádorov?
    Abstract Animal and epidemiologic studies suggest that the use of warfarin might reduce cancer incidence. The antitumor potential of warfarin is demonstrated in different experimental cancer models. Specifically, studies in murine cancer models have shown that warfarin blocks AXL receptor tyrosine kinase by inhibiting a vitamin K-dependent protein called GAS6, thereby may halt the spread of cancer cells. An off-target effect of the anticoagulant warfarin is inhibition of GAS6-AXL signaling, which enhances antitumor immunity and blocks tumorigenesis independently of anticoagulation. Hence, the observed association between warfarin use and lower cancer incidence is likely due to an enhanced antitumor immune surveillance of early cancer. The large observational study also showed a reduction in cancer incidence among regular warfarin users. The study data indicate that warfarin provides a possible cancer protection. Despite some limitations, the results of this study give further support for the hypothesis that warfarin use decreases cancer incidence, which warrants continued investigation. This finding may have important implications for choosing medications in patients who need anticoagulant therapy.
    MeSH term(s) Animals ; Anticoagulants/pharmacology ; Anticoagulants/therapeutic use ; Humans ; Incidence ; Intercellular Signaling Peptides and Proteins/metabolism ; Mice ; Neoplasms/immunology ; Neoplasms/prevention & control ; Proto-Oncogene Proteins/antagonists & inhibitors ; Proto-Oncogene Proteins/metabolism ; Receptor Protein-Tyrosine Kinases/antagonists & inhibitors ; Receptor Protein-Tyrosine Kinases/metabolism ; Warfarin/pharmacology ; Warfarin/therapeutic use
    Chemical Substances Anticoagulants ; Intercellular Signaling Peptides and Proteins ; Proto-Oncogene Proteins ; growth arrest-specific protein 6 ; Warfarin (5Q7ZVV76EI) ; Receptor Protein-Tyrosine Kinases (EC 2.7.10.1) ; axl receptor tyrosine kinase (EC 2.7.10.1)
    Language English
    Publishing date 2020-01-06
    Publishing country Czech Republic
    Document type Journal Article
    ZDB-ID 138213-5
    ISSN 1801-7592 ; 0042-773X
    ISSN (online) 1801-7592
    ISSN 0042-773X
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  3. Article: Máme venovať pozornosť defektu koagulačného faktora XII?

    Remková, Anna / Remko, Milan

    Vnitrni lekarstvi

    2015  Volume 61 Suppl 5, Page(s) 63–66

    Abstract: Unlabelled: Severe coagulation factor XII (FXII) deficiency is a very rare, mysterious and not well known inherited condition. Unlike other coagulation factor deficiencies, it is totally asymptomatic. Surprisingly, it does not lead to abnormal bleeding, ...

    Title translation Are we to pay attention to factor XII deficiency?.
    Abstract Unlabelled: Severe coagulation factor XII (FXII) deficiency is a very rare, mysterious and not well known inherited condition. Unlike other coagulation factor deficiencies, it is totally asymptomatic. Surprisingly, it does not lead to abnormal bleeding, even with major surgical procedures. The explanation for the lack of bleeding manifestations is unknown. It is suggested, but unproven, that patients are not sufficiently protected from thrombosis. FXII deficiency is usually discovered by accident through a routine coagulation testing done prior to surgery. Since FXII plays an important role in clot formation during in vitro measurements, its deficiency causes a marked prolongation of the activated partial thromboplastin time in the laboratory examination. The main concern related to FXII deficiency is the unnecessary testing, delay in health care and worry of surgical interventions that may be prompted by the abnormal laboratory result.
    Key words: activated partial thromboplastin time - bleeding - blood coagulation - factor XII.
    Language Czech
    Publishing date 2015
    Publishing country Czech Republic
    Document type English Abstract ; Journal Article
    ZDB-ID 138213-5
    ISSN 1801-7592 ; 0042-773X
    ISSN (online) 1801-7592
    ISSN 0042-773X
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  4. Article: Máme venovat' pozornost' defektu koagulacného faktora XII?

    Remková, Anna / Remko, Milan

    Vnitrni lekarstvi

    2015  Volume 61, Issue 12 Suppl 5, Page(s) 5S63–6

    Abstract: Severe coagulation factor XII (FXII) deficiency is a very rare, mysterious and not well known inherited condition. Unlike other coagulation factor deficiencies, it is totally asymptomatic. Surprisingly, it does not lead to abnormal bleeding, even with ... ...

    Title translation Are we to pay attention to factor XII deficiency?.
    Abstract Severe coagulation factor XII (FXII) deficiency is a very rare, mysterious and not well known inherited condition. Unlike other coagulation factor deficiencies, it is totally asymptomatic. Surprisingly, it does not lead to abnormal bleeding, even with major surgical procedures. The explanation for the lack of bleeding manifestations is unknown. It is suggested, but unproven, that patients are not sufficiently protected from thrombosis. FXII deficiency is usually discovered by accident through a routine coagulation testing done prior to surgery. Since FXII plays an important role in clot formation during in vitro measurements, its deficiency causes a marked prolongation of the activated partial thromboplastin time in the laboratory examination. The main concern related to FXII deficiency is the unnecessary testing, delay in health care and worry of surgical interventions that may be prompted by the abnormal laboratory result.
    MeSH term(s) Asymptomatic Diseases ; Factor XII Deficiency/blood ; Factor XII Deficiency/diagnosis ; Humans ; Incidental Findings ; Partial Thromboplastin Time ; Preoperative Care
    Language Slovak
    Publishing date 2015-12
    Publishing country Czech Republic
    Document type English Abstract ; Journal Article
    ZDB-ID 138213-5
    ISSN 1801-7592 ; 0042-773X
    ISSN (online) 1801-7592
    ISSN 0042-773X
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  5. Article: Máme venovať pozornosť defektu koagulačného faktora XII?

    Remková, Anna / Remko, Milan

    Vnitrni lekarstvi

    2015  Volume 61 Suppl 5, Page(s) 63–66

    Abstract: Unlabelled: Severe coagulation factor XII (FXII) deficiency is a very rare, mysterious and not well known inherited condition. Unlike other coagulation factor deficiencies, it is totally asymptomatic. Surprisingly, it does not lead to abnormal bleeding, ...

    Title translation Are we to pay attention to factor XII deficiency?.
    Abstract Unlabelled: Severe coagulation factor XII (FXII) deficiency is a very rare, mysterious and not well known inherited condition. Unlike other coagulation factor deficiencies, it is totally asymptomatic. Surprisingly, it does not lead to abnormal bleeding, even with major surgical procedures. The explanation for the lack of bleeding manifestations is unknown. It is suggested, but unproven, that patients are not sufficiently protected from thrombosis. FXII deficiency is usually discovered by accident through a routine coagulation testing done prior to surgery. Since FXII plays an important role in clot formation during in vitro measurements, its deficiency causes a marked prolongation of the activated partial thromboplastin time in the laboratory examination. The main concern related to FXII deficiency is the unnecessary testing, delay in health care and worry of surgical interventions that may be prompted by the abnormal laboratory result.
    Key words: activated partial thromboplastin time - bleeding - blood coagulation - factor XII.
    Language Czech
    Publishing date 2015
    Publishing country Czech Republic
    Document type English Abstract ; Journal Article
    ZDB-ID 138213-5
    ISSN 1801-7592 ; 0042-773X
    ISSN (online) 1801-7592
    ISSN 0042-773X
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  6. Article ; Online: Theoretical Study of Molecular Structure and Physicochemical Properties of Novel Factor Xa Inhibitors and Dual Factor Xa and Factor IIa Inhibitors.

    Remko, Milan / Remková, Anna / Broer, Ria

    Molecules (Basel, Switzerland)

    2016  Volume 21, Issue 2

    Abstract: The geometries and energies of factor Xa inhibitors edoxaban, eribaxaban, fidexaban, darexaban, letaxaban, and the dual factor Xa and thrombin inhibitors tanogitran and SAR107375 in both the gas-phase and aqueous solution were studied using the Becke3LYP/ ...

    Abstract The geometries and energies of factor Xa inhibitors edoxaban, eribaxaban, fidexaban, darexaban, letaxaban, and the dual factor Xa and thrombin inhibitors tanogitran and SAR107375 in both the gas-phase and aqueous solution were studied using the Becke3LYP/6-31++G(d,p) or Grimme's B97D/6-31++G(d,p) method. The fully optimized conformers of these anticoagulants show a characteristic l-shape structure, and the water had a remarkable effect on the equilibrium geometry. According to the calculated pKa values eribaxaban and letaxaban are in neutral undissociated form at pH 7.4, while fidexaban and tanogitran exist as zwitterionic structures. The lipophilicity of the inhibitors studied lies within a large range of log P between 1 and 4. The dual inhibitor SAR107375 represents an improvement in structural, physicochemical and pharmacokinetic characteristics over tanogitran. At blood pH, SAR107375 predominantly exists in neutral form. In contrast with tanogitran, it is better absorbed and more lipophilic and active after oral application.
    MeSH term(s) Amidines/chemistry ; Drug Stability ; Factor Xa/chemistry ; Factor Xa Inhibitors/chemistry ; Humans ; Hydrogen-Ion Concentration ; Hydrophobic and Hydrophilic Interactions ; Models, Molecular ; Molecular Structure ; Prothrombin/chemistry ; Pyridines/chemistry ; Solvents/chemistry
    Chemical Substances Amidines ; Factor Xa Inhibitors ; Pyridines ; Solvents ; Fidexaban (10NHF3008V) ; Prothrombin (9001-26-7) ; Factor IIa (9002-04-4) ; Factor Xa (EC 3.4.21.6)
    Language English
    Publishing date 2016-02-04
    Publishing country Switzerland
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1413402-0
    ISSN 1420-3049 ; 1431-5165 ; 1420-3049
    ISSN (online) 1420-3049
    ISSN 1431-5165 ; 1420-3049
    DOI 10.3390/molecules21020185
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    Zs.MO 81: Show issues

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  7. Article ; Online: A Comparative Study of Molecular Structure, pKa, Lipophilicity, Solubility, Absorption and Polar Surface Area of Some Antiplatelet Drugs.

    Remko, Milan / Remková, Anna / Broer, Ria

    International journal of molecular sciences

    2016  Volume 17, Issue 3, Page(s) 388

    Abstract: Theoretical chemistry methods have been used to study the molecular properties of antiplatelet agents (ticlopidine, clopidogrel, prasugrel, elinogrel, ticagrelor and cangrelor) and several thiol-containing active metabolites. The geometries and energies ... ...

    Abstract Theoretical chemistry methods have been used to study the molecular properties of antiplatelet agents (ticlopidine, clopidogrel, prasugrel, elinogrel, ticagrelor and cangrelor) and several thiol-containing active metabolites. The geometries and energies of most stable conformers of these drugs have been computed at the Becke3LYP/6-311++G(d,p) level of density functional theory. Computed dissociation constants show that the active metabolites of prodrugs (ticlopidine, clopidogrel and prasugrel) and drugs elinogrel and cangrelor are completely ionized at pH 7.4. Both ticagrelor and its active metabolite are present at pH = 7.4 in neutral undissociated form. The thienopyridine prodrugs ticlopidine, clopidogrel and prasugrel are lipophilic and insoluble in water. Their lipophilicity is very high (about 2.5-3.5 logP values). The polar surface area, with regard to the structurally-heterogeneous character of these antiplatelet drugs, is from very large interval of values of 3-255 Ų. Thienopyridine prodrugs, like ticlopidine, clopidogrel and prasugrel, with the lowest polar surface area (PSA) values, exhibit the largest absorption. A high value of polar surface area (PSA) of cangrelor (255 Ų) results in substantial worsening of the absorption in comparison with thienopyridine drugs.
    MeSH term(s) Absorption, Physicochemical ; Hydrophobic and Hydrophilic Interactions ; Molecular Structure ; Platelet Aggregation Inhibitors/chemistry ; Solubility ; Surface Properties
    Chemical Substances Platelet Aggregation Inhibitors
    Language English
    Publishing date 2016-03-19
    Publishing country Switzerland
    Document type Comparative Study ; Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2019364-6
    ISSN 1422-0067 ; 1422-0067 ; 1661-6596
    ISSN (online) 1422-0067
    ISSN 1422-0067 ; 1661-6596
    DOI 10.3390/ijms17030388
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  8. Article ; Online: Platelet abnormalities in adults with severe pulmonary arterial hypertension related to congenital heart defects (Eisenmenger syndrome).

    Remková, Anna / Šimková, Iveta / Valkovičová, Tatiana / Kaldarárová, Monika

    Blood coagulation & fibrinolysis : an international journal in haemostasis and thrombosis

    2016  Volume 27, Issue 8, Page(s) 925–929

    Abstract: Patients with severe pulmonary arterial hypertension suffer from life-threatening thrombotic and bleeding complications. The aim of this study was to compare selected platelet, endothelial, and coagulation parameters in healthy volunteers and patients ... ...

    Abstract Patients with severe pulmonary arterial hypertension suffer from life-threatening thrombotic and bleeding complications. The aim of this study was to compare selected platelet, endothelial, and coagulation parameters in healthy volunteers and patients with severe pulmonary arterial hypertension because of congenital heart defects. The study included healthy volunteers (n = 50) and patients with cyanotic congenital heart defects classified as Eisenmenger syndrome (n = 41). We investigated platelet count, mean platelet volume, and platelet aggregation - spontaneous and induced by various concentrations of five agonists. Von Willebrand factor (vWF), fibrinogen, factor VIII and XII, plasminogen activator inhibitor, antithrombin, D-dimer, and antiphospholipid antibodies were also investigated. We found a decreased platelet count [190 (147-225) vs. 248 (205-295) 10 l, P < 0.0001], higher mean platelet volume [10.9 (10.1-12.0) vs. 10.2 (9.4-10.4) fl, P < 0.0001], and significantly decreased platelet aggregation (induced by five agonists, in various concentrations) in patients with Eisenmenger syndrome compared with controls. These changes were accompanied by an increase of plasma vWF antigen [141.6 (108.9-179.1) vs. 117.4 (9.2-140.7) IU/dl, P = 0.022] and serum anti-β2-glycoprotein [2.07 (0.71-3.41) vs. 0.47 (0.18-0.99) U/ml, P < 0.0001]. Eisenmenger syndrome is accompanied by platelet abnormalities. Thrombocytopenia with increased platelet size is probably due to a higher platelet turnover associated with platelet activation. Impaired platelet aggregation can reflect specific platelet behaviour in patients with Eisenmenger syndrome. These changes can be related both to bleeding and to thrombotic events. A higher vWF antigen may be a consequence of endothelial damage in Eisenmenger syndrome, but the cause for an increase of anti-β2-glycoprotein is unknown.
    MeSH term(s) Adult ; Aged ; Female ; Heart Defects, Congenital/blood ; Heart Defects, Congenital/complications ; Humans ; Hypertension, Pulmonary/blood ; Male ; Mean Platelet Volume ; Middle Aged ; Platelet Aggregation ; Platelet Count
    Language English
    Publishing date 2016-12
    Publishing country England
    Document type Journal Article
    ZDB-ID 1033551-1
    ISSN 1473-5733 ; 0957-5235
    ISSN (online) 1473-5733
    ISSN 0957-5235
    DOI 10.1097/MBC.0000000000000523
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  9. Article: Platelet abnormalities in chronic thromboembolic pulmonary hypertension.

    Remková, Anna / Šimková, Iveta / Valkovičová, Tatiana

    International journal of clinical and experimental medicine

    2015  Volume 8, Issue 6, Page(s) 9700–9707

    Abstract: The reasons for non-resolving thrombosis in chronic thromboembolic pulmonary hypertension (CTEPH) have not been fully elucidated. Despite platelets being implied in its pathogenesis, they have been poorly studied. We hypothesized that platelets would be ... ...

    Abstract The reasons for non-resolving thrombosis in chronic thromboembolic pulmonary hypertension (CTEPH) have not been fully elucidated. Despite platelets being implied in its pathogenesis, they have been poorly studied. We hypothesized that platelets would be altered in CTEPH. The aim of our study was to compare selected platelet parameters in CTEPH patients with healthy subjects. The study included healthy subjects (n = 50) and patients with CTEPH (n = 47). We investigated platelet count, mean platelet volume (MPV), and platelet aggregation-spontaneous (SPA) and induced by various concentrations of five agonists. In addition, some other hemostatic parameters were also investigated to provide a comprehensive view on hemostasis. We found a decreased platelet count [212 (171-251) versus 248 (205-408) 10(9) L(-1), P<0.01], higher MPV [11.3 (10.5-11.7) versus 10.1 fL (9.4-10.4), P<0.001] and higher SPA [9.5 (7.1-12.4) versus 5 (1.3-9) %, P<0.001], but a decrease of induced platelet aggregation (only by maximal agonist concentrations) in CTEPH patients compared to controls. These changes were accompanied by a significant increase of plasma fibrinogen, factor VIII, von Willebrand factor (antigen and activity), and plasminogen activator inhibitor. Thus, we can conclude that CTEPH is accompanied by a prothrombotic state, including platelet abnormalities. They reflect a higher platelet turnover/reactivity and specific platelet behavior (impaired aggregation) in these patients. Our findings imply that platelet disorders can contribute to the pathogenesis of CTEPH. However, further research would be desirable to better understand the reason for this finding.
    Language English
    Publishing date 2015-06-15
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2418305-2
    ISSN 1940-5901
    ISSN 1940-5901
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  10. Article: Markery funkcie endotelu vo vcasných stádiách esenciálnej hypertenzie a ucinok antihypertenznej terapie.

    Remková, A / Remko, M

    Vnitrni lekarstvi

    2010  Volume 56, Issue 12, Page(s) 1210–1216

    Abstract: Objective: Endothelial abnormalities appear to play a role in the pathogenesis of atherosclerotic/atherothrombotic complications of hypertension. They may contribute to the increased risk and severity of target organ damage. The aim of the study was to ... ...

    Title translation Markers of endothelial function in the early stages of essential hypertension and the effect of antihypertensive therapy.
    Abstract Objective: Endothelial abnormalities appear to play a role in the pathogenesis of atherosclerotic/atherothrombotic complications of hypertension. They may contribute to the increased risk and severity of target organ damage. The aim of the study was to investigate the endothelial markers in patients at the early stages of mild-to-moderate untreated hypertension with low-to-moderate added risk, and the effect of antihypertensive therapy by perindopril, telmisartan or rilmenidine on endothelial function.
    Subjects and methods: The measurements were carried out in 54 previously untreated hypertensive patients before and after one month of antihypertensive therapy by perindopril-arginine (5 mg once daily, n = 20), telmisartan (40 mg once daily, n = 16), rilmenidine (1 mg once daily, n = 18) or after placebo administration (n = 23). A population of 50 healthy normotensive subjects of similar sex, age and ethnic origin was also examined. Plasma thrombomodulin (TM) and von Willebrand factor (vWF) measurements were used as indicators of endothelial dysfunction.
    Results: In untreated hypertensive patients compared with a control group of healthy subjects a significant increase of plasma vWF (86.26 +/- 26.18 IU/dl against 69.14 +/- 18.74 IU/dl, P < 0.001) and TM (35.98 +/- 12.98 ng/ml against 29.34 +/- 9.18 ng/ml, P < 0.01) was found. BP was reduced (P < 0.001) or normalized due to each therapy. No significant changes of endothelial markers after placebo administration were found. A decrease of plasma vWF antigen level after 1 month of therapy by perindopril (from 81.93 +/- 22.07 to 72.88 +/- 23.26 IU/dl, P < 0.05) or rilmenidine (from 100.6 +/- 26.09 to 86.07 +/- 27.66 IU/dl, P < 0.05) was observed. No significant changes of vWF antigen levels were found after telmisartan therapy. We failed to find any changes of plasma TM due to any therapy.
    Conclusion: Our results demonstrate that antihypertensive treatment by perindopril or rilmenidine has a favourable affect on some endothelial markers.
    MeSH term(s) Adult ; Aged ; Aged, 80 and over ; Antihypertensive Agents/therapeutic use ; Blood Pressure ; Endothelium, Vascular/physiopathology ; Female ; Humans ; Hypertension/drug therapy ; Hypertension/physiopathology ; Male ; Middle Aged ; Young Adult
    Chemical Substances Antihypertensive Agents
    Language Slovak
    Publishing date 2010-12
    Publishing country Czech Republic
    Document type English Abstract ; Journal Article
    ZDB-ID 138213-5
    ISSN 1801-7592 ; 0042-773X
    ISSN (online) 1801-7592
    ISSN 0042-773X
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