The Experts below are selected from a list of 114 Experts worldwide ranked by ideXlab platform

Willibald Hochholzer - One of the best experts on this subject based on the ideXlab platform.

  • validation of a p2y12 receptor specific whole blood Platelet Aggregation Assay
    Platelets, 2016
    Co-Authors: Michael Amann, Miroslaw Ferenc, Christian M Valina, Timo Bomicke, Christian Stratz, Stefan Leggewie, Dietmar Trenk, Franzjosef Neumann, Willibald Hochholzer
    Abstract:

    Testing of P2Y12-receptor antagonist effects can support clinical decision-making. However, most Platelet function Assays use only ADP as agonist which is not P2Y12-receptor specific. For this reason P2Y12-receptor specific Assays have been developed by adding prostaglandin E1 (PGE1) to reduce ADP-induced Platelet activation via the P2Y1-receptor. The present study sought to evaluate a P2Y12-receptor specific Assay for determination of pharmacodynamic and clinical outcomes. This study enrolled 400 patients undergoing coronary stenting after loading with clopidogrel or prasugrel. ADP-induced Platelet reactivity was assessed by whole blood aggregometry at multiple time points with a standard ADP Assay (ADPtest) and a P2Y12-receptor specific Assay (ADPtest HS, both run on Multiplate Analyzer, Roche Diagnostics). Patients were clinically followed for 1 month and all events adjudicated by an independent committee. In total, 2084 pairs of test results of ADPtest and ADPtest HS were available showing a strong correlation between results of both Assays (r = 0.96, p < 0.001). These findings prevailed in multiple prespecified subgroups (e.g., age; body mass index; diabetes). Calculated cutoffs for ADPtest HS and the established cutoffs of ADPtest showed a substantial agreement for prediction of ischemic and hemorrhagic events with a Cohen's κ of 0.66 and 0.66, respectively. The P2Y12-receptor specific ADPtest HS Assay appears similarly predictive for pharmacodynamic and clinical outcomes as compared to the established ADPtest Assay indicating its applicability for clinical use. Further evaluation in large cohorts is needed to determine if P2Y12-receptor specific testing offers any advantage for prediction of clinical outcome.

  • PHARMACODYNAMIC AND CLINICAL VALIDATION OF A P2Y12 RECEPTOR SPECIFIC WHOLE BLOOD Platelet Aggregation Assay
    Journal of the American College of Cardiology, 2016
    Co-Authors: Willibald Hochholzer, Michael Amann, Christian M Valina, Christian Stratz, Dietmar Trenk, Timo Boemicke, Franzjosef Neumann
    Abstract:

    Testing of P2Y12-receptor antagonist effects can support clinical decision making. However, most Platelet function Assays use only ADP as agonist which is not P2Y12 receptor specific. For this reason P2Y12 receptor specific Assays have been developed by adding prostaglandin E1 (PGE1) to reduce ADP-

Naglaa F Elorabi - One of the best experts on this subject based on the ideXlab platform.

  • effect of evening primrose oil and omega 3 polyunsaturated fatty acids on the cardiovascular risk of celecoxib in rats
    Journal of Cardiovascular Pharmacology, 2011
    Co-Authors: Sawsan A Zaitone, Yasser M Moustafa, Sarah M Mosaad, Naglaa F Elorabi
    Abstract:

    Abstract Experimental data raised the specter of increased cardiovascular risk with selective cyclooxygenase-2 inhibitors. The study aimed to investigate the cardiovascular risk caused by celecoxib by studying its effect on blood pressure (BP) and thrombogenesis in rats. We tested the possible protective effects of evening primrose oil (EPO) or ω-3 polyunsaturated fatty acids (n-3 PUFAs). Male Wistar rats were assigned to the following groups: vehicle, celecoxib, celecoxib/n-3 PUFAs, celecoxib/EPO, n-3 PUFAs, and EPO. The rats were treated with celecoxib (20 mg·kg(-1)·d(-1)) by gastric gavage for 6 weeks. The mean BP was recorded, and blood samples were collected for testing prothrombin time and activated partial thromboplastin time. Platelet Aggregation Assay and collagen-induced Platelet consumption test were used as models of thrombogenesis. Celecoxib increased the BP without affecting coagulation parameters and accelerated thrombogenesis by increasing Platelet Aggregation and collagen-induced thrombocytopenia. EPO and n-3 PUFAs decreased the celecoxib-induced elevation in BP. Although EPO significantly decreased Platelet Aggregation and collagen-induced thrombocytopenia, n-3 PUFAs did not. Celecoxib elevated BP and increased the risk of thrombogenesis in rats. A combination of celecoxib and the selected natural supplements is suggested as a novel approach to minimize cardiovascular risk caused by celecoxib.

  • effect of evening primrose oil and ω 3 polyunsaturated fatty acids on the cardiovascular risk of celecoxib in rats
    Journal of Cardiovascular Pharmacology, 2011
    Co-Authors: Sawsan A Zaitone, Yasser M Moustafa, Sarah M Mosaad, Naglaa F Elorabi
    Abstract:

    Experimental data raised the specter of increased cardiovascular risk with selective cyclooxygenase-2 inhibitors. The study aimed to investigate the cardiovascular risk caused by celecoxib by studying its effect on blood pressure (BP) and thrombogenesis in rats. We tested the possible protective effects of evening primrose oil (EPO) or ω-3 polyunsaturated fatty acids (n-3 PUFAs). Male Wistar rats were assigned to the following groups: vehicle, celecoxib, celecoxib/n-3 PUFAs, celecoxib/EPO, n-3 PUFAs, and EPO. The rats were treated with celecoxib (20 mg·kg(-1)·d(-1)) by gastric gavage for 6 weeks. The mean BP was recorded, and blood samples were collected for testing prothrombin time and activated partial thromboplastin time. Platelet Aggregation Assay and collagen-induced Platelet consumption test were used as models of thrombogenesis. Celecoxib increased the BP without affecting coagulation parameters and accelerated thrombogenesis by increasing Platelet Aggregation and collagen-induced thrombocytopenia. EPO and n-3 PUFAs decreased the celecoxib-induced elevation in BP. Although EPO significantly decreased Platelet Aggregation and collagen-induced thrombocytopenia, n-3 PUFAs did not. Celecoxib elevated BP and increased the risk of thrombogenesis in rats. A combination of celecoxib and the selected natural supplements is suggested as a novel approach to minimize cardiovascular risk caused by celecoxib.

Franzjosef Neumann - One of the best experts on this subject based on the ideXlab platform.

  • validation of a p2y12 receptor specific whole blood Platelet Aggregation Assay
    Platelets, 2016
    Co-Authors: Michael Amann, Miroslaw Ferenc, Christian M Valina, Timo Bomicke, Christian Stratz, Stefan Leggewie, Dietmar Trenk, Franzjosef Neumann, Willibald Hochholzer
    Abstract:

    Testing of P2Y12-receptor antagonist effects can support clinical decision-making. However, most Platelet function Assays use only ADP as agonist which is not P2Y12-receptor specific. For this reason P2Y12-receptor specific Assays have been developed by adding prostaglandin E1 (PGE1) to reduce ADP-induced Platelet activation via the P2Y1-receptor. The present study sought to evaluate a P2Y12-receptor specific Assay for determination of pharmacodynamic and clinical outcomes. This study enrolled 400 patients undergoing coronary stenting after loading with clopidogrel or prasugrel. ADP-induced Platelet reactivity was assessed by whole blood aggregometry at multiple time points with a standard ADP Assay (ADPtest) and a P2Y12-receptor specific Assay (ADPtest HS, both run on Multiplate Analyzer, Roche Diagnostics). Patients were clinically followed for 1 month and all events adjudicated by an independent committee. In total, 2084 pairs of test results of ADPtest and ADPtest HS were available showing a strong correlation between results of both Assays (r = 0.96, p < 0.001). These findings prevailed in multiple prespecified subgroups (e.g., age; body mass index; diabetes). Calculated cutoffs for ADPtest HS and the established cutoffs of ADPtest showed a substantial agreement for prediction of ischemic and hemorrhagic events with a Cohen's κ of 0.66 and 0.66, respectively. The P2Y12-receptor specific ADPtest HS Assay appears similarly predictive for pharmacodynamic and clinical outcomes as compared to the established ADPtest Assay indicating its applicability for clinical use. Further evaluation in large cohorts is needed to determine if P2Y12-receptor specific testing offers any advantage for prediction of clinical outcome.

  • PHARMACODYNAMIC AND CLINICAL VALIDATION OF A P2Y12 RECEPTOR SPECIFIC WHOLE BLOOD Platelet Aggregation Assay
    Journal of the American College of Cardiology, 2016
    Co-Authors: Willibald Hochholzer, Michael Amann, Christian M Valina, Christian Stratz, Dietmar Trenk, Timo Boemicke, Franzjosef Neumann
    Abstract:

    Testing of P2Y12-receptor antagonist effects can support clinical decision making. However, most Platelet function Assays use only ADP as agonist which is not P2Y12 receptor specific. For this reason P2Y12 receptor specific Assays have been developed by adding prostaglandin E1 (PGE1) to reduce ADP-

Michael Amann - One of the best experts on this subject based on the ideXlab platform.

  • validation of a p2y12 receptor specific whole blood Platelet Aggregation Assay
    Platelets, 2016
    Co-Authors: Michael Amann, Miroslaw Ferenc, Christian M Valina, Timo Bomicke, Christian Stratz, Stefan Leggewie, Dietmar Trenk, Franzjosef Neumann, Willibald Hochholzer
    Abstract:

    Testing of P2Y12-receptor antagonist effects can support clinical decision-making. However, most Platelet function Assays use only ADP as agonist which is not P2Y12-receptor specific. For this reason P2Y12-receptor specific Assays have been developed by adding prostaglandin E1 (PGE1) to reduce ADP-induced Platelet activation via the P2Y1-receptor. The present study sought to evaluate a P2Y12-receptor specific Assay for determination of pharmacodynamic and clinical outcomes. This study enrolled 400 patients undergoing coronary stenting after loading with clopidogrel or prasugrel. ADP-induced Platelet reactivity was assessed by whole blood aggregometry at multiple time points with a standard ADP Assay (ADPtest) and a P2Y12-receptor specific Assay (ADPtest HS, both run on Multiplate Analyzer, Roche Diagnostics). Patients were clinically followed for 1 month and all events adjudicated by an independent committee. In total, 2084 pairs of test results of ADPtest and ADPtest HS were available showing a strong correlation between results of both Assays (r = 0.96, p < 0.001). These findings prevailed in multiple prespecified subgroups (e.g., age; body mass index; diabetes). Calculated cutoffs for ADPtest HS and the established cutoffs of ADPtest showed a substantial agreement for prediction of ischemic and hemorrhagic events with a Cohen's κ of 0.66 and 0.66, respectively. The P2Y12-receptor specific ADPtest HS Assay appears similarly predictive for pharmacodynamic and clinical outcomes as compared to the established ADPtest Assay indicating its applicability for clinical use. Further evaluation in large cohorts is needed to determine if P2Y12-receptor specific testing offers any advantage for prediction of clinical outcome.

  • PHARMACODYNAMIC AND CLINICAL VALIDATION OF A P2Y12 RECEPTOR SPECIFIC WHOLE BLOOD Platelet Aggregation Assay
    Journal of the American College of Cardiology, 2016
    Co-Authors: Willibald Hochholzer, Michael Amann, Christian M Valina, Christian Stratz, Dietmar Trenk, Timo Boemicke, Franzjosef Neumann
    Abstract:

    Testing of P2Y12-receptor antagonist effects can support clinical decision making. However, most Platelet function Assays use only ADP as agonist which is not P2Y12 receptor specific. For this reason P2Y12 receptor specific Assays have been developed by adding prostaglandin E1 (PGE1) to reduce ADP-

Sawsan A Zaitone - One of the best experts on this subject based on the ideXlab platform.

  • effect of evening primrose oil and omega 3 polyunsaturated fatty acids on the cardiovascular risk of celecoxib in rats
    Journal of Cardiovascular Pharmacology, 2011
    Co-Authors: Sawsan A Zaitone, Yasser M Moustafa, Sarah M Mosaad, Naglaa F Elorabi
    Abstract:

    Abstract Experimental data raised the specter of increased cardiovascular risk with selective cyclooxygenase-2 inhibitors. The study aimed to investigate the cardiovascular risk caused by celecoxib by studying its effect on blood pressure (BP) and thrombogenesis in rats. We tested the possible protective effects of evening primrose oil (EPO) or ω-3 polyunsaturated fatty acids (n-3 PUFAs). Male Wistar rats were assigned to the following groups: vehicle, celecoxib, celecoxib/n-3 PUFAs, celecoxib/EPO, n-3 PUFAs, and EPO. The rats were treated with celecoxib (20 mg·kg(-1)·d(-1)) by gastric gavage for 6 weeks. The mean BP was recorded, and blood samples were collected for testing prothrombin time and activated partial thromboplastin time. Platelet Aggregation Assay and collagen-induced Platelet consumption test were used as models of thrombogenesis. Celecoxib increased the BP without affecting coagulation parameters and accelerated thrombogenesis by increasing Platelet Aggregation and collagen-induced thrombocytopenia. EPO and n-3 PUFAs decreased the celecoxib-induced elevation in BP. Although EPO significantly decreased Platelet Aggregation and collagen-induced thrombocytopenia, n-3 PUFAs did not. Celecoxib elevated BP and increased the risk of thrombogenesis in rats. A combination of celecoxib and the selected natural supplements is suggested as a novel approach to minimize cardiovascular risk caused by celecoxib.

  • effect of evening primrose oil and ω 3 polyunsaturated fatty acids on the cardiovascular risk of celecoxib in rats
    Journal of Cardiovascular Pharmacology, 2011
    Co-Authors: Sawsan A Zaitone, Yasser M Moustafa, Sarah M Mosaad, Naglaa F Elorabi
    Abstract:

    Experimental data raised the specter of increased cardiovascular risk with selective cyclooxygenase-2 inhibitors. The study aimed to investigate the cardiovascular risk caused by celecoxib by studying its effect on blood pressure (BP) and thrombogenesis in rats. We tested the possible protective effects of evening primrose oil (EPO) or ω-3 polyunsaturated fatty acids (n-3 PUFAs). Male Wistar rats were assigned to the following groups: vehicle, celecoxib, celecoxib/n-3 PUFAs, celecoxib/EPO, n-3 PUFAs, and EPO. The rats were treated with celecoxib (20 mg·kg(-1)·d(-1)) by gastric gavage for 6 weeks. The mean BP was recorded, and blood samples were collected for testing prothrombin time and activated partial thromboplastin time. Platelet Aggregation Assay and collagen-induced Platelet consumption test were used as models of thrombogenesis. Celecoxib increased the BP without affecting coagulation parameters and accelerated thrombogenesis by increasing Platelet Aggregation and collagen-induced thrombocytopenia. EPO and n-3 PUFAs decreased the celecoxib-induced elevation in BP. Although EPO significantly decreased Platelet Aggregation and collagen-induced thrombocytopenia, n-3 PUFAs did not. Celecoxib elevated BP and increased the risk of thrombogenesis in rats. A combination of celecoxib and the selected natural supplements is suggested as a novel approach to minimize cardiovascular risk caused by celecoxib.