2011
DOI: 10.1097/eja.0b013e32834050ab
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Tranexamic acid partially improves platelet function in patients treated with dual antiplatelet therapy

Abstract: The results of this study indicate that tranexamic acid potentially corrects defects in arachidonic acid-induced and ADP-induced platelet aggregation imposed by dual antiplatelet therapy. However, platelet aggregation in response to arachidonic acid or ADP in the blood of patients who have not received aspirin and clopidogrel is unaffected by tranexamic acid. These results support the use of tranexamic acid to partially reverse platelet aggregation dysfunction due to antiplatelet therapy.

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Cited by 86 publications
(46 citation statements)
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“…In the past five years, MEA has become an important and widely used diagnostic tool for coagulation monitoring with respect to hereditary [8] and acquired [7,[9][10][11][12][13] platelet dysfunction, as well as surveillance of platelet inhibitor effects [14][15][16][17][18][19], as shown by many studies. Taking less than 10 minutes, MEA allows conclusions to be drawn about the patient's platelet function from standardized test procedures that are easy to perform.…”
Section: Introductionmentioning
confidence: 99%
“…In the past five years, MEA has become an important and widely used diagnostic tool for coagulation monitoring with respect to hereditary [8] and acquired [7,[9][10][11][12][13] platelet dysfunction, as well as surveillance of platelet inhibitor effects [14][15][16][17][18][19], as shown by many studies. Taking less than 10 minutes, MEA allows conclusions to be drawn about the patient's platelet function from standardized test procedures that are easy to perform.…”
Section: Introductionmentioning
confidence: 99%
“…It has been reported that fibrinogen supplementation is associated with recovery of platelet aggregation in antiplatelet-treated samples13 and reduces bleeding in thrombocytopenic pigs 14. TXA, the lysine analogue antifibrinolytic drug, also restores in part whole blood (WB) platelet aggregation in patients receiving aspirin and clopidogrel 15. Finally, administration of FXIII, the fibrin clot-stabilizing agent, increases clot firmness,16 in particular in Glanzmann thrombasthenia17 and partly overturns antithrombotic-induced impairment in clot structure.…”
Section: Introductionmentioning
confidence: 99%
“…What is the minimal effective concentration of TXA require to inhibit this fibrinolysis? Does TXA mechanism of action only work by fibrinolysis inhibition or by a combination with inflammatory pathway inhibition, and/or platelet function improvement [4]?…”
Section: Abstract Tranexamic Acid á Pediatric Cardiac Surgery á Transmentioning
confidence: 99%