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David J. Schneider - One of the best experts on this subject based on the ideXlab platform.
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Effect of exercise training and weight loss on Platelet Reactivity in overweight patients with coronary artery disease.
Journal of Cardiopulmonary Rehabilitation and Prevention, 2013Co-Authors: Friederike K. Keating, David J. Schneider, Patrick D. Savage, Janice Y. Bunn, Jean Harvey-berino, Maryann Ludlow, Michael J. Toth, Philip A. AdesAbstract:PURPOSE: Obesity is associated with increased Platelet Reactivity. Greater Platelet Reactivity presages adverse events in patients with coronary artery disease (CAD). We investigated whether exercise training and weight loss reduce Platelet Reactivity in overweight subjects with CAD. METHODS: Study subjects (N = 46) were enrolled in a prospective randomized study of exercise training and behavioral weight loss, which contrasted the amount of exercise performed (750 vs >3000 kcal/week). Platelet Reactivity was assessed with the use of flow cytometry as the percentage of Platelets expressing P-selectin or capable of binding fibrinogen in response to 1 [mu]M adenosine diphosphate in blood before and after a 4-month program of exercise and behavioral weight loss. Markers of inflammation (high-sensitivity C-reactive protein), procoagulant activity (tissue plasminogen activator, plasminogen activator inhibitor 1), insulin sensitivity, body composition, physical activity, and fitness were also recorded. RESULTS: Platelet Reactivity as assessed by P-selectin expression was decreased after exercise training and weight loss in study participants (from 34 +/- 17% to 29 +/- 17%; P = .01). The decrease was more pronounced in women (by 13% vs 2% in men; P < .01). The change in Platelet Reactivity was not independently associated with measures of body composition or fitness. After controlling for exercise group and gender, the change in Platelet Reactivity was associated with changes in high-sensitivity C-reactive protein (r = 0.46) and insulin sensitivity (r = 0.46). CONCLUSIONS: In overweight patients with CAD, exercise training and weight loss are associated with a decrease in Platelet Reactivity that may predict an improved prognosis.
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Factors Contributing to Increased Platelet Reactivity in People With Diabetes
Diabetes Care, 2009Co-Authors: David J. SchneiderAbstract:People with diabetes, particularly those with type 2 diabetes, exhibit increased Platelet Reactivity. Hyperglycemia contributes to greater Platelet Reactivity through direct effects and by promoting glycation of Platelet proteins. Hypertriglyceridemia increases Platelet Reactivity. Both insulin resistance and insulin deficiency increase Platelet Reactivity. Insulin antagonizes activation of Platelets. Thus, relative or absolute deficiency of insulin would be expected to increase Platelet Reactivity. Diabetes is associated with oxidative stress and inflammation. Resultant endothelial dysfunction promotes activation of Platelets by decreasing production of nitric oxide (NO) that attenuates Platelet Reactivity. Oxidative stress accentuates this effect by attenuating activity of NO and promoting Platelet activation. Inflammation and Platelet activation are reciprocally related. Inflammation promotes Platelet activation that, in turn, promotes inflammation. Accordingly, improved metabolic control achieved with regimens that improve insulin sensitivity and preserve pancreatic β-cell function is likely to decrease Platelet Reactivity and enhance effects of antiPlatelet agents. Platelets from subjects with diabetes exhibit increased Reactivity (i.e., increased propensity to activate in response to a stimulus) (1). This review highlights factors that contribute to increased Platelet Reactivity. Type 2 diabetes is more prevalent than type 1 diabetes and is associated with a substantially increased risk of macrovascular complications. Accordingly, this review focuses on Platelet Reactivity in subjects with type 2 diabetes. Key aspects of type 2 diabetes are insulin resistance, metabolic abnormalities including hyperglycemia, and systemic abnormalities including oxidative stress and inflammation. The influence of each of these abnormalities on Platelet function is addressed. ### Metabolic abnormalities and Platelet function Induction of hyperglycemia and hyperinsulinemia in healthy subjects without diabetes increases Platelet Reactivity (2). Consistent with this observation, improved glycemic control has been associated with decreased Platelet …
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Attenuation of Platelet Reactivity by enoxaparin compared with unfractionated heparin in patients undergoing haemodialysis
Nephrology Dialysis Transplantation, 2004Co-Authors: Atul Aggarwal, Burton E Sobel, Deborah A. Whitaker, Jeffrey M. Rimmer, Richard Solomon, F. John Gennari, David J. SchneiderAbstract:Background. Increased Platelet Reactivity presages adverse cardiac events. Because both haemodialysis and unfractionated heparin (UFH) can increase Platelet Reactivity, we compared Platelet Reactivity during haemodialysis when patients were anticoagulated with UFH or enoxaparin. Methods. Patients (n ¼ 20) underwent consecutive haemodialysis sessions with either UFH or enoxaparin in a random order. Blood was taken from the arterial end of the haemodialysis circuit at the initiation of haemodialysis before anticoagulation. Subsequently, blood was taken during dialysis from the venous end of the circuit 10 min after treatment with UFH or enoxaparin. Platelet Reactivity was assessed with the use of flow cytometry by determining the capacity of Platelets to bind fibrinogen and the surface expression of P-selectin in response to adenosine diphosphate (ADP, 0 and 0.2mM). Results were compared with the use of two-way repeated measure ANOVA. Results. Platelet Reactivity in arterial blood obtained at the beginning of dialysis prior to patients being treated with either UFH [0.2mM ADP-induced capacity to bind fibrinogen ¼ 28±15% (SD)] or enoxaparin (30±18%) was similar (P ¼ 0.15). In contrast, Platelet Reactivity was less after treatment with enoxaparin compared with UFH (P ¼ 0.006). The 0.2mM ADPinduced capacity to bind fibrinogen in venous blood obtained 10 min after anticoagulation was 34±11% after treatment with UFH and 22±11% after treatment with enoxaparin. Conclusions. Anticoagulation with enoxaparin during haemodialysis is associated with less Platelet Reactivity compared with UFH. Accordingly, enoxaparin use may contribute to a lesser risk of cardiac events in patients with end-stage renal disease treated with haemodialysis.
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Relation of augmented Platelet Reactivity to the magnitude of distribution of atherosclerosis
The American Journal of Cardiology, 2004Co-Authors: Friederike K. Keating, Burton E Sobel, Deborah A. Whitaker, Samer S. Kabbani, Michael A. Ricci, David J. SchneiderAbstract:The extent of luminal involvement of atherosclerotic vascular disease and Platelet Reactivity portend subsequent cardiovascular events. This study was designed to determine whether Platelet Reactivity correlates with the extent of the territorial distribution of vascular disease. Blood was obtained from 130 patients who had known atherosclerotic vascular disease categorized as being in ≥1 of the following territories: coronary artery disease (CAD; n = 89), cerebrovascular disease (n = 36), and peripheral arterial disease (n = 61). Platelet Reactivity, i.e., the activation of Platelets in response to a low concentration of adenosine diphosphate (0.2 μmol/L), was measured using flow cytometry. Patients with vascular disease in >1 territory compared with those with disease in only 1 territory had greater Platelet Reactivity with respect to P-selectin expression (p = 0.01). The percentages of Platelets expressing P-selectin (mean ± SD) were 6.4 ± 4.2 in patients who had involvement of 1 territory (n = 88), 10.0 ± 6.8 in those who had involvement of 2 territories (n = 28), and 10.1 ± 9.9 in those who had involvement of 3 territories (n = 14). Patients who had CAD and diabetes mellitus had greater P-selectin expression than did those who had CAD without diabetes (p
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Decreased Platelet Reactivity in blood anticoagulated with bivalirudin or enoxaparin compared with unfractionated heparin: implications for coronary intervention.
Journal of Thrombosis and Thrombolysis, 2002Co-Authors: Atul Aggarwal, Burton E Sobel, David J. SchneiderAbstract:Background: Platelet Reactivity predicts complications after percutaneous coronary intervention (PCI). Accordingly, agents that suppress Platelet Reactivity should decrease adverse events after PCI. This study was designed to determine the effects of therapeutic concentrations of unfractionated heparin (UFH), bivalirudin, or enoxaparin alone or in combination with tirofiban on Platelet Reactivity.
Antonio Castro - One of the best experts on this subject based on the ideXlab platform.
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assessment of Platelet Reactivity after transcatheter aortic valve replacement the reac tavi trial
Jacc-cardiovascular Interventions, 2019Co-Authors: Victor Alfonso Jimenez Diaz, Antonio Tellomontoliu, Raul Moreno, Ignacio Cruz Gonzalez, Jose Antonio Baz Alonso, Rafael Romaguera, Eduardo Molina Navarro, Pablo Juan Salvadores, E Galan, Antonio CastroAbstract:Abstract Objectives The REAC-TAVI (Assessment of Platelet Reactivity after Transcatheter Aortic Valve Implantation) trial enrolled patients with aortic stenosis (AS) undergoing transcatheter aortic valve replacement (TAVR) pre-treated with aspirin + clopidogrel, aimed to compare the efficacy of clopidogrel and ticagrelor in suppressing high Platelet Reactivity (HPR) after TAVI. Background Current recommendations support short-term use of aspirin + clopidogrel for patients with severe AS undergoing TAVR despite the lack of compelling evidence. Methods This was a prospective, randomized, multicenter investigation. Platelet Reactivity was measured at 6 different time points with the VerifyNow assay (Accriva Diagnostics, San Diego, California). HPR was defined as (P2Y12 reaction units (PRU) ≥208. Patients with HPR before TAVR were randomized to either aspirin + ticagrelor or aspirin + clopidogrel for 3 months. Patients without HPR continued with aspirin + clopidogrel (registry cohort). The primary endpoint was non-HPR status (PRU Results A total of 68 patients were included. Of these, 48 (71%) had HPR (PRU 273 ± 09) and were randomized to aspirin + ticagrelor (n = 24, PRU 277 ± 08) or continued with aspirin + clopidogrel (n = 24, PRU 269 ± 49). The remaining 20 patients (29%) without HPR (PRU 133 ± 12) were included in the registry. Overall, Platelet Reactivity across all the study time points after TAVR was lower in patients randomized to ticagrelor compared with those treated with clopidogrel, including those enrolled in the registry (p Conclusions HPR to clopidogrel is present in a considerable number of patients with AS undergoing TAVR. Ticagrelor achieves a better and faster effect, providing sustained suppression of HPR to these patients. (Platelet Reactivity After TAVI: A Multicenter Pilot Study [REAC-TAVI]; NCT02224066)
Victor Alfonso Jimenez Diaz - One of the best experts on this subject based on the ideXlab platform.
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assessment of Platelet Reactivity after transcatheter aortic valve replacement the reac tavi trial
Jacc-cardiovascular Interventions, 2019Co-Authors: Victor Alfonso Jimenez Diaz, Antonio Tellomontoliu, Raul Moreno, Ignacio Cruz Gonzalez, Jose Antonio Baz Alonso, Rafael Romaguera, Eduardo Molina Navarro, Pablo Juan Salvadores, E Galan, Antonio CastroAbstract:Abstract Objectives The REAC-TAVI (Assessment of Platelet Reactivity after Transcatheter Aortic Valve Implantation) trial enrolled patients with aortic stenosis (AS) undergoing transcatheter aortic valve replacement (TAVR) pre-treated with aspirin + clopidogrel, aimed to compare the efficacy of clopidogrel and ticagrelor in suppressing high Platelet Reactivity (HPR) after TAVI. Background Current recommendations support short-term use of aspirin + clopidogrel for patients with severe AS undergoing TAVR despite the lack of compelling evidence. Methods This was a prospective, randomized, multicenter investigation. Platelet Reactivity was measured at 6 different time points with the VerifyNow assay (Accriva Diagnostics, San Diego, California). HPR was defined as (P2Y12 reaction units (PRU) ≥208. Patients with HPR before TAVR were randomized to either aspirin + ticagrelor or aspirin + clopidogrel for 3 months. Patients without HPR continued with aspirin + clopidogrel (registry cohort). The primary endpoint was non-HPR status (PRU Results A total of 68 patients were included. Of these, 48 (71%) had HPR (PRU 273 ± 09) and were randomized to aspirin + ticagrelor (n = 24, PRU 277 ± 08) or continued with aspirin + clopidogrel (n = 24, PRU 269 ± 49). The remaining 20 patients (29%) without HPR (PRU 133 ± 12) were included in the registry. Overall, Platelet Reactivity across all the study time points after TAVR was lower in patients randomized to ticagrelor compared with those treated with clopidogrel, including those enrolled in the registry (p Conclusions HPR to clopidogrel is present in a considerable number of patients with AS undergoing TAVR. Ticagrelor achieves a better and faster effect, providing sustained suppression of HPR to these patients. (Platelet Reactivity After TAVI: A Multicenter Pilot Study [REAC-TAVI]; NCT02224066)
Paul A. Gurbel - One of the best experts on this subject based on the ideXlab platform.
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Peri-Procedural Platelet Reactivity in Percutaneous Coronary Intervention.
Thrombosis and Haemostasis, 2018Co-Authors: Dimitrios Alexopoulos, Iosif Xenogiannis, Panagiotis Vlachakis, Udaya S. Tantry, Paul A. GurbelAbstract:Platelet activation and aggregation play a pivotal role in thrombotic complications occurring during percutaneous coronary intervention (PCI), and peri-PCI anti-Platelet therapy represents a standard of care. High Platelet Reactivity prior to PCI has been correlated with an increased incidence of peri-procedural myonecrosis. Pre-PCI Platelet Reactivity predicts post-PCI Platelet Reactivity and has a prognostic impact on subsequent ischaemic and bleeding events, so as the Platelet inhibition measured post-PCI. Many anti-Platelet treatment strategies, including aspirin, glycoprotein IIb/IIIa inhibitors, P2Y12 receptor blockers and vorapaxar, are being used in the routine clinical practice to modify Platelet Reactivity at each stage, e.g. pre-, during and post-PCI. Anti-Platelet strategies with a ‘stronger and faster’ pharmacodynamic effect than clopidogrel have been mostly adopted in patients with acute coronary syndromes. However, several issues regarding the anti-Platelet treatment such as benefits/risks of anti-Platelet therapy pre-treatment and duration, and definite association between speed and potency of various anti-Platelet agents and clinical outcomes remain controversial. We believe that a better understanding of peri-PCI Platelet Reactivity and its relations to outcomes may lead to the development of more effective and safe treatment strategies.
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clopidogrel effect on Platelet Reactivity in patients with stent thrombosis results of the crest study
Journal of the American College of Cardiology, 2005Co-Authors: Paul A. Gurbel, Waiel M Samara, Kevin P Bliden, Jason A Yoho, Kevin Hayes, Mulugeta Fissha, Udaya S. TantryAbstract:Objectives We investigated whether patients who suffered subacute stent thrombosis (SAT) have higher post-treatment Reactivity than those who do not encounter stent thrombosis. Background High post-treatment Platelet Reactivity has been reported after coronary stenting after clopidogrel therapy and may be an important factor in the occurrence of SAT. Methods We identified patients with SAT treated at two tertiary care centers over a 1.5-year period. Light transmittance aggregation induced by adenosine diphosphate (ADP) and arachidonic acid, total and activated glycoprotein (GP) IIb/IIIa after stimulation with ADP, and vasodilator-stimulated phosphoprotein phosphorylation levels to measure P2Y12receptor inhibition were determined (n = 20) and compared with an age-matched group of patients without SAT (n = 100). High post-treatment Platelet Reactivity was defined as >75th percentile ADP-induced aggregation in the group without SAT. Results The SAT patients had higher mean Platelet Reactivity than those without SAT by all measurements (p Conclusions High post-treatment Platelet Reactivity and incomplete P2Y12receptor inhibition are risk factors for SAT. Measures to uniformly determine Platelet Reactivity after coronary stenting and treatment strategies to improve P2Y12receptor inhibition in patients with high post-treatment Platelet Reactivity should be further investigated.
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The difference between clopidogrel responsiveness and posttreatment Platelet Reactivity.
Thrombosis Research, 2005Co-Authors: Waiel M Samara, Udaya S. Tantry, Kevin P Bliden, Paul A. GurbelAbstract:Aggregation is the most common measure of Platelet Reactivity. The relative inhibition of Platelet aggregation between pretreatment and posttreatment is the most common estimate of clopidogrel responsiveness. However, patients responsive to clopidogrel may remain with highly reactive Platelets and thus have increased thrombotic risk. Platelet Reactivity was determined by ADP-induced aggregation (%) in 62 patients undergoing elective coronary stenting at pretreatment and 5 days postprocedure. All patients were on aspirin (325 mg) and received 300 mg of clopidogrel immediately poststenting and 75 mg qd. Pretreatment Reactivity was divided into tertiles. Based on clopidogrel drug responsiveness, nonresponders were defined as <10% relative inhibition of pretreatment aggregation, semiresponders as 10-30%, and responders as >30%. We determined the relation between clopidogrel responsiveness and Platelet Reactivity. Pretreatment Reactivity tertiles by 5 microM ADP were: low (47+/-9%), moderate (64+/-4%), and high (78+/-6%). Eight patients were nonresponders, 18 were semiresponders, and 36 were responders. Clopidogrel responsiveness directly correlated with pretreatment Reactivity, 86% of responders had moderate or high pretreatment Reactivity, whereas 75% of nonresponders had low pretreatment Reactivity. Despite being more responsive, 16% of patients with high pretreatment Reactivity and 17% with moderate pretreatment Reactivity remained with moderate posttreatment Reactivity. Measuring clopidogrel responsiveness may overestimate the risk of stent thrombosis in nonresponders with low pretreatment Reactivity and underestimate risk in those responders who remain with high posttreatment Platelet Reactivity. Posttreatment Platelet Reactivity is a better measure of thrombotic risk than responsiveness to clopidogrel.
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The difference between clopidogrel responsiveness and posttreatment Platelet Reactivity.
Thrombosis Research, 2004Co-Authors: Waiel M Samara, Udaya S. Tantry, Kevin P Bliden, Paul A. GurbelAbstract:Abstract Background Aggregation is the most common measure of Platelet Reactivity. The relative inhibition of Platelet aggregation between pretreatment and posttreatment is the most common estimate of clopidogrel responsiveness. However, patients responsive to clopidogrel may remain with highly reactive Platelets and thus have increased thrombotic risk. Methods Platelet Reactivity was determined by ADP-induced aggregation (%) in 62 patients undergoing elective coronary stenting at pretreatment and 5 days postprocedure. All patients were on aspirin (325 mg) and received 300 mg of clopidogrel immediately poststenting and 75 mg qd. Pretreatment Reactivity was divided into tertiles. Based on clopidogrel drug responsiveness, nonresponders were defined as 30%. We determined the relation between clopidogrel responsiveness and Platelet Reactivity. Results Pretreatment Reactivity tertiles by 5 μM ADP were: low (47±9%), moderate (64±4%), and high (78±6%). Eight patients were nonresponders, 18 were semiresponders, and 36 were responders. Clopidogrel responsiveness directly correlated with pretreatment Reactivity, 86% of responders had moderate or high pretreatment Reactivity, whereas 75% of nonresponders had low pretreatment Reactivity. Despite being more responsive, 16% of patients with high pretreatment Reactivity and 17% with moderate pretreatment Reactivity remained with moderate posttreatment Reactivity. Conclusion Measuring clopidogrel responsiveness may overestimate the risk of stent thrombosis in nonresponders with low pretreatment Reactivity and underestimate risk in those responders who remain with high posttreatment Platelet Reactivity. Posttreatment Platelet Reactivity is a better measure of thrombotic risk than responsiveness to clopidogrel.
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The stratification of Platelet Reactivity and activation in patients with stable coronary artery disease on aspirin therapy
Thrombosis Research, 2003Co-Authors: Paul A. Gurbel, Kevin P BlidenAbstract:Abstract Condensed abstract : Heightened Platelet Reactivity may affect the occurrence of ischemic events in patients with coronary artery disease on aspirin therapy. However, a definition to stratify Platelet Reactivity in this group of patients has not been previously reported. We studied Platelet Reactivity and activation by measuring Platelet aggregation and the expression of p-selectin, total GP IIb/IIIa and active GP IIb/IIIa ( n =96). Patients were divided into quartiles by each of the markers; correlations were made between the markers; and a definition of heightened Platelet Reactivity was proposed. Marked variability in activation and Reactivity were observed despite aspirin therapy. Background : Heightened Platelet Reactivity and activation may affect the occurrence of ischemic events in patients with coronary artery disease on aspirin therapy. However, a definition to stratify Platelet Reactivity has not been previously reported. Methods and results : Platelet aggregation (5 and 20 μmol/l ADP), total GP IIb/IIIa, active GP IIb/IIIa and the expression of maximally stimulated p-selectin were measured in patients about to undergo elective coronary stenting ( n =96). All patients had received aspirin (325 mg). There was marked variability in Platelet Reactivity and activation as measured by all markers. The highest quartile was defined by 77±1% and 98±1% aggregation by 5 and 20 μmol/l ADP, respectively; 65±2% p-selectin positivity; 508±15 MFI for total GP IIb/IIIa; and 23.0±1.8 MFI for active GP IIb/IIIa. Conclusions : There is a wide range in Platelet Reactivity and activation as measured by multiple markers in stable coronary disease patients on aspirin therapy. From these indices, we can define those patients at the extremes of Reactivity and activation and thus, the greatest potential risk of thrombosis and bleeding. These indices will serve as a guide to future studies investigating the relationships of Platelet Reactivity, activation, drug-induced inhibition and clinical outcomes.
Kevin P Bliden - One of the best experts on this subject based on the ideXlab platform.
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clopidogrel effect on Platelet Reactivity in patients with stent thrombosis results of the crest study
Journal of the American College of Cardiology, 2005Co-Authors: Paul A. Gurbel, Waiel M Samara, Kevin P Bliden, Jason A Yoho, Kevin Hayes, Mulugeta Fissha, Udaya S. TantryAbstract:Objectives We investigated whether patients who suffered subacute stent thrombosis (SAT) have higher post-treatment Reactivity than those who do not encounter stent thrombosis. Background High post-treatment Platelet Reactivity has been reported after coronary stenting after clopidogrel therapy and may be an important factor in the occurrence of SAT. Methods We identified patients with SAT treated at two tertiary care centers over a 1.5-year period. Light transmittance aggregation induced by adenosine diphosphate (ADP) and arachidonic acid, total and activated glycoprotein (GP) IIb/IIIa after stimulation with ADP, and vasodilator-stimulated phosphoprotein phosphorylation levels to measure P2Y12receptor inhibition were determined (n = 20) and compared with an age-matched group of patients without SAT (n = 100). High post-treatment Platelet Reactivity was defined as >75th percentile ADP-induced aggregation in the group without SAT. Results The SAT patients had higher mean Platelet Reactivity than those without SAT by all measurements (p Conclusions High post-treatment Platelet Reactivity and incomplete P2Y12receptor inhibition are risk factors for SAT. Measures to uniformly determine Platelet Reactivity after coronary stenting and treatment strategies to improve P2Y12receptor inhibition in patients with high post-treatment Platelet Reactivity should be further investigated.
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The difference between clopidogrel responsiveness and posttreatment Platelet Reactivity.
Thrombosis Research, 2005Co-Authors: Waiel M Samara, Udaya S. Tantry, Kevin P Bliden, Paul A. GurbelAbstract:Aggregation is the most common measure of Platelet Reactivity. The relative inhibition of Platelet aggregation between pretreatment and posttreatment is the most common estimate of clopidogrel responsiveness. However, patients responsive to clopidogrel may remain with highly reactive Platelets and thus have increased thrombotic risk. Platelet Reactivity was determined by ADP-induced aggregation (%) in 62 patients undergoing elective coronary stenting at pretreatment and 5 days postprocedure. All patients were on aspirin (325 mg) and received 300 mg of clopidogrel immediately poststenting and 75 mg qd. Pretreatment Reactivity was divided into tertiles. Based on clopidogrel drug responsiveness, nonresponders were defined as <10% relative inhibition of pretreatment aggregation, semiresponders as 10-30%, and responders as >30%. We determined the relation between clopidogrel responsiveness and Platelet Reactivity. Pretreatment Reactivity tertiles by 5 microM ADP were: low (47+/-9%), moderate (64+/-4%), and high (78+/-6%). Eight patients were nonresponders, 18 were semiresponders, and 36 were responders. Clopidogrel responsiveness directly correlated with pretreatment Reactivity, 86% of responders had moderate or high pretreatment Reactivity, whereas 75% of nonresponders had low pretreatment Reactivity. Despite being more responsive, 16% of patients with high pretreatment Reactivity and 17% with moderate pretreatment Reactivity remained with moderate posttreatment Reactivity. Measuring clopidogrel responsiveness may overestimate the risk of stent thrombosis in nonresponders with low pretreatment Reactivity and underestimate risk in those responders who remain with high posttreatment Platelet Reactivity. Posttreatment Platelet Reactivity is a better measure of thrombotic risk than responsiveness to clopidogrel.
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The difference between clopidogrel responsiveness and posttreatment Platelet Reactivity.
Thrombosis Research, 2004Co-Authors: Waiel M Samara, Udaya S. Tantry, Kevin P Bliden, Paul A. GurbelAbstract:Abstract Background Aggregation is the most common measure of Platelet Reactivity. The relative inhibition of Platelet aggregation between pretreatment and posttreatment is the most common estimate of clopidogrel responsiveness. However, patients responsive to clopidogrel may remain with highly reactive Platelets and thus have increased thrombotic risk. Methods Platelet Reactivity was determined by ADP-induced aggregation (%) in 62 patients undergoing elective coronary stenting at pretreatment and 5 days postprocedure. All patients were on aspirin (325 mg) and received 300 mg of clopidogrel immediately poststenting and 75 mg qd. Pretreatment Reactivity was divided into tertiles. Based on clopidogrel drug responsiveness, nonresponders were defined as 30%. We determined the relation between clopidogrel responsiveness and Platelet Reactivity. Results Pretreatment Reactivity tertiles by 5 μM ADP were: low (47±9%), moderate (64±4%), and high (78±6%). Eight patients were nonresponders, 18 were semiresponders, and 36 were responders. Clopidogrel responsiveness directly correlated with pretreatment Reactivity, 86% of responders had moderate or high pretreatment Reactivity, whereas 75% of nonresponders had low pretreatment Reactivity. Despite being more responsive, 16% of patients with high pretreatment Reactivity and 17% with moderate pretreatment Reactivity remained with moderate posttreatment Reactivity. Conclusion Measuring clopidogrel responsiveness may overestimate the risk of stent thrombosis in nonresponders with low pretreatment Reactivity and underestimate risk in those responders who remain with high posttreatment Platelet Reactivity. Posttreatment Platelet Reactivity is a better measure of thrombotic risk than responsiveness to clopidogrel.
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The stratification of Platelet Reactivity and activation in patients with stable coronary artery disease on aspirin therapy
Thrombosis Research, 2003Co-Authors: Paul A. Gurbel, Kevin P BlidenAbstract:Abstract Condensed abstract : Heightened Platelet Reactivity may affect the occurrence of ischemic events in patients with coronary artery disease on aspirin therapy. However, a definition to stratify Platelet Reactivity in this group of patients has not been previously reported. We studied Platelet Reactivity and activation by measuring Platelet aggregation and the expression of p-selectin, total GP IIb/IIIa and active GP IIb/IIIa ( n =96). Patients were divided into quartiles by each of the markers; correlations were made between the markers; and a definition of heightened Platelet Reactivity was proposed. Marked variability in activation and Reactivity were observed despite aspirin therapy. Background : Heightened Platelet Reactivity and activation may affect the occurrence of ischemic events in patients with coronary artery disease on aspirin therapy. However, a definition to stratify Platelet Reactivity has not been previously reported. Methods and results : Platelet aggregation (5 and 20 μmol/l ADP), total GP IIb/IIIa, active GP IIb/IIIa and the expression of maximally stimulated p-selectin were measured in patients about to undergo elective coronary stenting ( n =96). All patients had received aspirin (325 mg). There was marked variability in Platelet Reactivity and activation as measured by all markers. The highest quartile was defined by 77±1% and 98±1% aggregation by 5 and 20 μmol/l ADP, respectively; 65±2% p-selectin positivity; 508±15 MFI for total GP IIb/IIIa; and 23.0±1.8 MFI for active GP IIb/IIIa. Conclusions : There is a wide range in Platelet Reactivity and activation as measured by multiple markers in stable coronary disease patients on aspirin therapy. From these indices, we can define those patients at the extremes of Reactivity and activation and thus, the greatest potential risk of thrombosis and bleeding. These indices will serve as a guide to future studies investigating the relationships of Platelet Reactivity, activation, drug-induced inhibition and clinical outcomes.
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The stratification of Platelet Reactivity and activation in patients with stable coronary artery disease on aspirin therapy.
Thrombosis Research, 2003Co-Authors: Paul A. Gurbel, Kevin P BlidenAbstract:Heightened Platelet Reactivity may affect the occurrence of ischemic events in patients with coronary artery disease on aspirin therapy. However, a definition to stratify Platelet Reactivity in this group of patients has not been previously reported. We studied Platelet Reactivity and activation by measuring Platelet aggregation and the expression of p-selectin, total GP IIb/IIIa and active GP IIb/IIIa (n=96). Patients were divided into quartiles by each of the markers; correlations were made between the markers; and a definition of heightened Platelet Reactivity was proposed. Marked variability in activation and Reactivity were observed despite aspirin therapy. Heightened Platelet Reactivity and activation may affect the occurrence of ischemic events in patients with coronary artery disease on aspirin therapy. However, a definition to stratify Platelet Reactivity has not been previously reported. Platelet aggregation (5 and 20 micromol/l ADP), total GP IIb/IIIa, active GP IIb/IIIa and the expression of maximally stimulated p-selectin were measured in patients about to undergo elective coronary stenting (n=96). All patients had received aspirin (325 mg). There was marked variability in Platelet Reactivity and activation as measured by all markers. The highest quartile was defined by 77+/-1% and 98+/-1% aggregation by 5 and 20 micromol/l ADP, respectively; 65+/-2% p-selectin positivity; 508+/-15 MFI for total GP IIb/IIIa; and 23.0+/-1.8 MFI for active GP IIb/IIIa. There is a wide range in Platelet Reactivity and activation as measured by multiple markers in stable coronary disease patients on aspirin therapy. From these indices, we can define those patients at the extremes of Reactivity and activation and thus, the greatest potential risk of thrombosis and bleeding. These indices will serve as a guide to future studies investigating the relationships of Platelet Reactivity, activation, drug-induced inhibition and clinical outcomes.