The lack of augmentation by aspirin of inhibition of platelet reactivity by ticlopidine

Farrell, Timothy P.; Hayes, Kelly B; Sobel, Burton E.; Schneider, David J.

doi:10.1016/s0002-9149(98)00987-4

Cited by 16 publications

(12 citation statements)

References 18 publications

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“…The horizontal lines are medians, the boxes are the interquartile range, whiskers are the 5th and 95th percentiles, and p values were obtained by the Wilcoxon signed-rank test; *p Ͻ 0.05. aggregation. The TRAP effects were not influenced by ASA, as previously documented (20,23). Effects of clopidogrel.…”

Section: Discussionsupporting

confidence: 85%

Matching the Evaluation of the Clinical Efficacy of Clopidogrel to Platelet Function Tests Relevant to the Biological Properties of the Drug

Labarthe

Théroux

Angioı̈

et al. 2005

Journal of the American College of Cardiology

115

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The evaluation of clopidogrel responsiveness by platelet function tests is largely influenced by the choice of blood preservative and functional tests. Measures of aggregation stabilization, and of consequent secretion and activation, identified most patients as responders, contrasting with measures of peak aggregation, by likely reflecting better the interactions clopidogrel and the P2Y12 receptor.

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Section: Discussionsupporting

confidence: 85%

Matching the Evaluation of the Clinical Efficacy of Clopidogrel to Platelet Function Tests Relevant to the Biological Properties of the Drug

Labarthe

Théroux

Angioı̈

et al. 2005

Journal of the American College of Cardiology

115

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show abstract

“…No clinical endpoints were assessed, so the superior antiaggregant effects seen in the ticlopidine and combination groups are of uncertain importance clinically. These results also conflict with other reports that failed to find augmentation of antiaggregant effects with ticlopidine and aspirin in healthy subjects [40]. The use of clopidogrel in combination with aspirin in patients with coronary stents has been described and endorsed by expert opinion [41] and is supported by some animal data [42], but lacks confirmation by clinical trials.…”

Section: Combination Therapymentioning

confidence: 56%

Antiplatelet therapy in secondary stroke prevention

Worrall

Johnston

2000

Curr Atheroscler Rep

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“…Assays were performed as previously described [6,[11][12][13][14][15][16][17][18][19][20] . Surface expression of P-selectin was delineated with a phycoerythrin (PE)-conjugated monoclonal antibody (anti-CD62; Becton Dickinson).…”

Section: Assessment Of Platelet Reactivity With Flow Cytometrymentioning

confidence: 99%

Adenosine Diphosphate-Induced Platelet Aggregation Correlates with Platelet Activation Identified with the Use of Flow Cytometry

García

Schneider²

2007

Pathophysiol Haemos Thromb

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Background: Assessment of the likelihood of platelet activation (i.e. platelet reactivity) identifies patients at high and low risk of subsequent thrombotic events. Turbidometric platelet aggregation has been used to assess platelet function for more than 4 decades. We have developed a method to assess individual components of platelet activation with the use of flow cytometry that is performed in minimally altered whole blood. Aims: To compare assessment of platelet reactivity determined with the use of aggregometry and flow cytometry. Material and Methods: Twenty adult patients with atherosclerotic vascular disease were included in this study. Blood from each patient was used to determine turbidometric platelet aggregation and to assess platelet activation by flow cytometry. ADP was used as the agonist. Values are means ± SEM. Comparison was performed with the use of Student’s t test and correlation was assessed with the use of Pearson’s correlation analysis. Results: Both maximal aggregation and the slope of aggregation correlate with the percentage of platelets that bound fibrinogen in response to 0.2 μM ADP. The best correlation was seen between the slope of aggregation induced by 0.2 or 1 μM ADP and the percentage of platelets that bound fibrinogen in response to 0.2 μM ADP (for 0.2 μM r = 0.62, p = 0.038; for 1 μM r = 0.71, p = 0.025). Conclusion: The binding of fibrinogen to activated platelets assessed with the use of flow cytometry correlates best with the slope of turbidometric aggregation and appears to reflect the propensity of platelets to activate.

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The lack of augmentation by aspirin of inhibition of platelet reactivity by ticlopidine

Cited by 16 publications

References 18 publications

Matching the Evaluation of the Clinical Efficacy of Clopidogrel to Platelet Function Tests Relevant to the Biological Properties of the Drug

Matching the Evaluation of the Clinical Efficacy of Clopidogrel to Platelet Function Tests Relevant to the Biological Properties of the Drug

Antiplatelet therapy in secondary stroke prevention

Adenosine Diphosphate-Induced Platelet Aggregation Correlates with Platelet Activation Identified with the Use of Flow Cytometry

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