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Published on: February 14, 2017
Effect of heparin, platelets, activated platelets, platelet fragments, and hematocrit on activated clotting time
1Department of Pediatrics and Ludwig Boltzmann Research Institute for Pediatric Hemostasis and Thrombosis, University of Graz, Austria.
Activated clotting time (ACT) is the most commonly used laboratory test to control the heparin effect during extracorporeal techniques. The study was undertaken in order to test in vitro the influence of heparin, platelet count, hematocrit, platelet fragmentation, and platelet activation on ACT. Blood was drawn from volunteer donors into syringes containing citrate. Platelet counts and hematocrit were modified. Platelets were fragmented by sonifier or activated by collagen and adenosine diphosphate (ADP). Different heparin final concentrations were created. Increasing concentrations of heparin had a significant effect on ACT. However, it was not predictable in every case in concentrations lower than 1.0 U/ml. Platelet count generally had no significant effect on ACT. The effect of hematocrit was detectable in a group but not in single cases. Fragmented platelets significantly shortened ACT only without addition of heparin, and the effect was only partly predictable. Activation of platelets by collagen and ADP induced no significant changes. Our results show that heparin is reflected by ACT but that effect is not predictable in every specific patient. Our results also show that other variables that may be altered during extracorporeal techniques such as platelet count, hematocrit, activation, and fragmentation of platelets do not severely influence the ACT.
Activated clotting time (ACT) is the most commonly used laboratory test to control the heparin effect during extracorporeal techniques. The study was undertaken in order to test in vitro the influence of heparin, platelet count, hematocrit, platelet fragmentation, and platelet activation on ACT. Blood was drawn from volunteer donors into syringes containing citrate. Platelet counts and hematocrit were modified. Platelets were fragmented by sonifier or activated by collagen and adenosine diphosphate (ADP). Different heparin final concentrations were created. Increasing concentrations of heparin had a significant effect on ACT. However, it was not predictable in every case in concentrations lower than 1.0 U/ml. Platelet count generally had no significant effect on ACT. The effect of hematocrit was detectable in a group but not in single cases. Fragmented platelets significantly shortened ACT only without addition of heparin, and the effect was only partly predictable. Activation of platelets by collagen and ADP induced no significant changes. Our results show that heparin is reflected by ACT but that effect is not predictable in every specific patient. Our results also show that other variables that may be altered during extracorporeal techniques such as platelet count, hematocrit, activation, and fragmentation of platelets do not severely influence the ACT.
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