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Simon Panzer - One of the best experts on this subject based on the ideXlab platform.
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preserved thrombin inducible Platelet Activation in thienopyridine treated patients
European Journal of Clinical Investigation, 2013Co-Authors: Thomas Gremmel, Christoph W Kopp, Daniela Seidinger, Renate Koppensteiner, Sabine Steiner, Simon PanzerAbstract:BACKGROUND: Abundant thrombin generation may be a major reason for subsequent thromboembolic events in patients with cardiovascular disease receiving dual antiPlatelet therapy. We therefore investigated the susceptibility of thienopyridine responders and nonresponders to thrombin receptor-activating peptide (TRAP)-6- and adenosine diphosphate (ADP)-inducible Platelet Activation. MATERIALS AND METHODS: Response to clopidogrel or prasugrel was determined by the vasodilator-stimulated phosphoprotein (VASP) phosphorylation assay and multiple electrode aggregometry (MEA) in 317 patients undergoing angioplasty and stenting for cardiovascular disease. Baseline, TRAP-6-, and ADP-inducible P-selectin expression, activated glycoprotein IIb/IIIa (GPIIb/IIIa) and monocyte-Platelet aggregate (MPA) formation were measured as sensitive parameters of Platelet Activation. RESULTS: In patients with high on-treatment residual ADP-inducible Platelet reactivity (HRPR), baseline P-selectin expression, GPIIb/IIIa and MPA formation were similar to those in patients without HRPR (all P > 0.05). After Platelet Activation with TRAP-6 or ADP, patients with HRPR by both assays exhibited significantly higher levels of P-selectin expression, GPIIb/IIIa and MPA formation than patients with an adequate thienopyridine-mediated Platelet inhibition (all P ≤ 0.02). However, high levels of TRAP-6-inducible P-selectin, GPIIb/IIIa and MPA formation also occurred in 20.4%, 19.1% and 20.1% of the good responders by the VASP assay, and in 19.6%, 16.6% and 20.6% of the good responders by MEA, respectively. CONCLUSIONS: Thienopyridine nonresponders are more susceptible to thrombin- and ADP-inducible Platelet Activation than patients with good Platelet inhibition. However, even patients with adequate thienopyridine-mediated Platelet inhibition often show a preserved responsiveness to thrombin. These patients may benefit from additional thrombin receptor blockage or inhibition of thrombin generation.
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Preserved thrombin-inducible Platelet Activation in thienopyridine-treated patients.
European Journal of Clinical Investigation, 2013Co-Authors: Thomas Gremmel, Christoph W Kopp, Daniela Seidinger, Renate Koppensteiner, Sabine Steiner, Simon PanzerAbstract:Background Abundant thrombin generation may be a major reason for subsequent thromboembolic events in patients with cardiovascular disease receiving dual antiPlatelet therapy. We therefore investigated the susceptibility of thienopyridine responders and nonresponders to thrombin receptor–activating peptide (TRAP)-6- and adenosine diphosphate (ADP)-inducible Platelet Activation. Materials and methods Response to clopidogrel or prasugrel was determined by the vasodilator-stimulated phosphoprotein (VASP) phosphorylation assay and multiple electrode aggregometry (MEA) in 317 patients undergoing angioplasty and stenting for cardiovascular disease. Baseline, TRAP-6-, and ADP-inducible P-selectin expression, activated glycoprotein IIb/IIIa (GPIIb/IIIa) and monocyte–Platelet aggregate (MPA) formation were measured as sensitive parameters of Platelet Activation. Results In patients with high on-treatment residual ADP-inducible Platelet reactivity (HRPR), baseline P-selectin expression, GPIIb/IIIa and MPA formation were similar to those in patients without HRPR (all P > 0·05). After Platelet Activation with TRAP-6 or ADP, patients with HRPR by both assays exhibited significantly higher levels of P-selectin expression, GPIIb/IIIa and MPA formation than patients with an adequate thienopyridine-mediated Platelet inhibition (all P ≤ 0·02). However, high levels of TRAP-6-inducible P-selectin, GPIIb/IIIa and MPA formation also occurred in 20·4%, 19·1% and 20·1% of the good responders by the VASP assay, and in 19·6%, 16·6% and 20·6% of the good responders by MEA, respectively. Conclusions Thienopyridine nonresponders are more susceptible to thrombin- and ADP-inducible Platelet Activation than patients with good Platelet inhibition. However, even patients with adequate thienopyridine-mediated Platelet inhibition often show a preserved responsiveness to thrombin. These patients may benefit from additional thrombin receptor blockage or inhibition of thrombin generation.
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Platelet Activation and function during eltrombopag treatment in immune thrombocytopenia
Annals of Hematology, 2012Co-Authors: Johanna Haselboeck, Ingrid Pabinger, Cihan Ay, Silvia Koder, Simon PanzerAbstract:We monitored Platelet Activation by means of P-selectin and Platelet monocyte aggregates (PMA) and Platelet function by whole blood multiple electrode aggregometry and Platelet adhesion under high shear in chronic immune thrombocytopenia patients to define changes in Platelet Activation during treatment with eltrombopag. Overall, Platelet Activation and function normalized with increasing Platelet counts. However, P-selectin, which was already elevated before treatment, and PMA increased further transiently during the first weeks. The increases in P-selectin and in PMA indicate ongoing Platelet Activation during the early period of treatment.
John R. Owen - One of the best experts on this subject based on the ideXlab platform.
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Platelet Activation and fibrinopeptide formation in pulmonary hypertension
Chest, 1993Co-Authors: Larry L Schulman, John R. Owen, Betty GrossmanAbstract:Intravascular thrombosis is postulated to cause or to contribute to the development of uncharacterized (“primary”) pulmonary hypertension (PPH). To assess whether there is ongoing Platelet-fibrin thrombosis in patients with PPH, we measured specific markers of Platelet Activation: Platelet factor 4 (PF4) and s-thromboglobulin (BTC); of fibrin formation: fibrinopeptide A (FPA); and of fibrin dissolution: fibrinopeptide BB1-42 (FPBB1-42) in peripheral venous blood from 10 patients with PPH (group 2). Results were compared with those of normal volunteers (group 1, n = 9) and with results from patients with pulmonary hypertension secondary to congenital heart disease (group 3, n = 7). Both groups 2 and 3 exhibited severe pulmonary hypertension (mean pulmonary arterial pressure = 62 ±20 mm Hg and 70 ±13 mm Hg, respectively). Mean levels of PF4, BTC, FPA, and FPBB1-42 in patients with pulmonary hypertension, either primary or secondary to congenital heart disease, did not differ from levels in normal subjects. Within group 2, levels of Platelet proteins and fibrinopeptides did not differ between patients who were classified clinically as having plexogenic arteriopathy vs thromboembolic disease. These observations suggest that a sustained state of abnormal Platelet Activation and fibrin formation or dissolution is not present in patients with established pulmonary hypertension.
Thomas Gremmel - One of the best experts on this subject based on the ideXlab platform.
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preserved thrombin inducible Platelet Activation in thienopyridine treated patients
European Journal of Clinical Investigation, 2013Co-Authors: Thomas Gremmel, Christoph W Kopp, Daniela Seidinger, Renate Koppensteiner, Sabine Steiner, Simon PanzerAbstract:BACKGROUND: Abundant thrombin generation may be a major reason for subsequent thromboembolic events in patients with cardiovascular disease receiving dual antiPlatelet therapy. We therefore investigated the susceptibility of thienopyridine responders and nonresponders to thrombin receptor-activating peptide (TRAP)-6- and adenosine diphosphate (ADP)-inducible Platelet Activation. MATERIALS AND METHODS: Response to clopidogrel or prasugrel was determined by the vasodilator-stimulated phosphoprotein (VASP) phosphorylation assay and multiple electrode aggregometry (MEA) in 317 patients undergoing angioplasty and stenting for cardiovascular disease. Baseline, TRAP-6-, and ADP-inducible P-selectin expression, activated glycoprotein IIb/IIIa (GPIIb/IIIa) and monocyte-Platelet aggregate (MPA) formation were measured as sensitive parameters of Platelet Activation. RESULTS: In patients with high on-treatment residual ADP-inducible Platelet reactivity (HRPR), baseline P-selectin expression, GPIIb/IIIa and MPA formation were similar to those in patients without HRPR (all P > 0.05). After Platelet Activation with TRAP-6 or ADP, patients with HRPR by both assays exhibited significantly higher levels of P-selectin expression, GPIIb/IIIa and MPA formation than patients with an adequate thienopyridine-mediated Platelet inhibition (all P ≤ 0.02). However, high levels of TRAP-6-inducible P-selectin, GPIIb/IIIa and MPA formation also occurred in 20.4%, 19.1% and 20.1% of the good responders by the VASP assay, and in 19.6%, 16.6% and 20.6% of the good responders by MEA, respectively. CONCLUSIONS: Thienopyridine nonresponders are more susceptible to thrombin- and ADP-inducible Platelet Activation than patients with good Platelet inhibition. However, even patients with adequate thienopyridine-mediated Platelet inhibition often show a preserved responsiveness to thrombin. These patients may benefit from additional thrombin receptor blockage or inhibition of thrombin generation.
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Preserved thrombin-inducible Platelet Activation in thienopyridine-treated patients.
European Journal of Clinical Investigation, 2013Co-Authors: Thomas Gremmel, Christoph W Kopp, Daniela Seidinger, Renate Koppensteiner, Sabine Steiner, Simon PanzerAbstract:Background Abundant thrombin generation may be a major reason for subsequent thromboembolic events in patients with cardiovascular disease receiving dual antiPlatelet therapy. We therefore investigated the susceptibility of thienopyridine responders and nonresponders to thrombin receptor–activating peptide (TRAP)-6- and adenosine diphosphate (ADP)-inducible Platelet Activation. Materials and methods Response to clopidogrel or prasugrel was determined by the vasodilator-stimulated phosphoprotein (VASP) phosphorylation assay and multiple electrode aggregometry (MEA) in 317 patients undergoing angioplasty and stenting for cardiovascular disease. Baseline, TRAP-6-, and ADP-inducible P-selectin expression, activated glycoprotein IIb/IIIa (GPIIb/IIIa) and monocyte–Platelet aggregate (MPA) formation were measured as sensitive parameters of Platelet Activation. Results In patients with high on-treatment residual ADP-inducible Platelet reactivity (HRPR), baseline P-selectin expression, GPIIb/IIIa and MPA formation were similar to those in patients without HRPR (all P > 0·05). After Platelet Activation with TRAP-6 or ADP, patients with HRPR by both assays exhibited significantly higher levels of P-selectin expression, GPIIb/IIIa and MPA formation than patients with an adequate thienopyridine-mediated Platelet inhibition (all P ≤ 0·02). However, high levels of TRAP-6-inducible P-selectin, GPIIb/IIIa and MPA formation also occurred in 20·4%, 19·1% and 20·1% of the good responders by the VASP assay, and in 19·6%, 16·6% and 20·6% of the good responders by MEA, respectively. Conclusions Thienopyridine nonresponders are more susceptible to thrombin- and ADP-inducible Platelet Activation than patients with good Platelet inhibition. However, even patients with adequate thienopyridine-mediated Platelet inhibition often show a preserved responsiveness to thrombin. These patients may benefit from additional thrombin receptor blockage or inhibition of thrombin generation.
Barbara C Furie - One of the best experts on this subject based on the ideXlab platform.
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thrombin initiated Platelet Activation in vivo is vwf independent during thrombus formation in a laser injury model
Journal of Clinical Investigation, 2007Co-Authors: Christophe Dubois, Laurence Panicotdubois, Justin F Gainor, Barbara C FurieAbstract:Adhesion of Platelets to an injured vessel wall and Platelet Activation are critical events in the formation of a thrombus. Of the agonists involved in Platelet Activation, thrombin, collagen, and vWF are known to induce in vitro calcium mobilization in Platelets. Using a calcium-sensitive fluorochrome and digital multichannel intravital microscopy to image unstimulated and stimulated Platelets, calcium mobilization was monitored as a reporter of Platelet Activation (as distinct from Platelet accumulation) during thrombus formation in live mice. In the absence of vWF, Platelet Activation was normal, but Platelet adherence and aggregation were attenuated during thrombus formation following laser-induced injury in the cremaster muscle microcirculation. In WT mice treated with lepirudin, Platelet Activation was blocked, and Platelet adherence and aggregation were inhibited. The kinetics of Platelet Activation and Platelet accumulation were similar in FcRγ–/– mice lacking glycoprotein VI (GPVI), GPVI-depleted mice, and WT mice. Our results indicate that the tissue factor–mediated pathway of thrombin generation, but not the collagen-induced GPVI-mediated pathway, is the major pathway leading to Platelet Activation after laser-induced injury under the conditions employed. In the tissue factor–mediated pathway, vWF plays a role in Platelet accumulation during thrombus formation but is not required for Platelet Activation in vivo.
Andrew D. Blann - One of the best experts on this subject based on the ideXlab platform.
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Platelet Activation assessment and quantification
European Heart Journal, 2001Co-Authors: Sunil Kamath, Andrew D. BlannAbstract:.Whilst there is increasing realization that inappropri-ate Platelet Activation plays a prime role in the increas-ing heart disease burden of society, there is still nogenerally accepted ideal measure of Platelet Activationthat would indicate a state of ‘high risk’. There is also aneed for the objective assessment of the relative effec-tiveness and safety of antiPlatelet agents. Furthermore,despite the great success of aspirin, it is clearly far fromperfect
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Platelet Activation: Assessment and quantification
European Heart Journal, 2001Co-Authors: Sunil Kamath, Andrew D. Blann, Gregory Y H LipAbstract:The Platelet is one of the key elements of human blood. Platelets play a central role in the process ofthrombus formation (thrombogenesis)[1] , as well as animportant role in atherogenesis[2] and the progression of atherosclerotic lesions. The interaction of the Platelet with the vessel wall and its subsequent contribution to atheroma formation and thrombosis is of pivotal importance in the aetiology and pathogenesis of peripheral, coronary, cerebrovascu-lar and other vascular diseases[3,4] . Acknowledgement of the fact that Platelets have a central role to play in these disease states has led to a considerable amount of research into its pathophysiology. Indeed, inappropriatePlatelet Activation is common in atherosclerosis[5,6 ] and many of its risk factors, such as smoking anddiabetes[7,8] . The role of antiPlatelet therapy (such as aspirin) in reducing the risk of many cardiovascular andcerebrovascular disorders is also well established[9] . Whilst there is increasing realization that inappropri-ate Platelet Activation plays a prime role in the increas-ing heart disease burden of society, there is still no generally accepted ideal measure of Platelet Activation that would indicate a state of ‘high risk’. There is also a need for the objective assessment of the relative eff ec-tiveness and safety of antiPlatelet agents. Furthermore, despite the great success of aspirin, it is clearly far fromperfect[10] . Greater attention directed to the understand-ing and appreciation of Platelet pathophysiology and its quantification should yield valuable information that may translate into improved means to counter inappro-priate Platelet Activation. The objective of this review is to provide a comprehensive overview of the literature that would provide a guide to a better understanding of the pathophysiology and quantification of Platelet Activation.
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Evidence of Platelet Activation in hypertension
Journal of Human Hypertension, 1997Co-Authors: Andrew D. Blann, I. F. Islim, D. G. BeeversAbstract:To test the hypothesis that Platelet Activation is present in hypertension, we measured plasma markers beta thromboglobulin and soluble P-selectin in hypertensive patients and normotensive controls. Both markers were raised in the patients (P < 0.05), and in a subgroup of patients, beta thromboglobulin was reduced with successful treatment of hypertension with the ACE inhibitor quinapril. We suggest that reversible Platelet Activation is present in hypertension. This may be a contributing factor to the link between this risk factor and the development of thrombotic disease such as stroke.