ORIGINAL ARTICLESAn ex-vivo model of shear-rate-based activation of blood coagulationRanucci, Marco; Ranucci, Matteo; Baryshnikova, EkaterinaAuthor Information Department of Cardiothoracic – Vascular Anesthesia and Intensive Care, IRCCS Policlinico San Donato, Milan, Italy Correspondence to Marco Ranucci, MD, FESC, Director of Clinical Research, Department of Anesthesia and Intensive Care, IRCCS Policlinico San Donato, Via Morandi 30, San Donato Milanese, 20097 Milan, Italy Tel: +39 02 52774320; fax: +39 02 55602262; e-mail: firstname.lastname@example.org Received 14 September, 2017 Revised 22 October, 2017 Accepted 27 November, 2017 Blood Coagulation & Fibrinolysis: March 2018 - Volume 29 - Issue 2 - p 172-177 doi: 10.1097/MBC.0000000000000688 Buy Metrics Abstract The study presents a model of shear-stress-based platelet activation. Twenty-eight patients (22 free from anticoagulants and major antiplatelet agents, and six under the effects of P2Y12 platelet inhibitors) participated. The main purpose was to verify the hypothesis that a model of shear-dependent blood activation does not require artificial activators to trigger clot formation. Whole blood collected from the patients received platelet function tests [ADPtest and thrombin receptor-activating peptide (TRAP)test] and was tested with a cone-on-plate viscosimeter at a shear rate of 100 s−1. Changes in blood viscosity were characterized by a time-to-gel point (TGP), a maximum clot viscosity and a steady clot viscosity (SCV). In patients free from major antiplatelet effects, the TGP was 180 s (interquartile range 148–290 s), while in patients under double antiplatelet therapy the TGP was significantly (P = 0.039) longer (345 s, interquartile range 250–452 s). The SCV was 16 centipoise (cP) (interquartile range 11–47 cP) in the patients free from major antiplatelet agents, significantly (P = 0.012) higher than in patients under double antiplatelet therapy (10 cP, interquartile range 6–11 cP). There was a significant (P = 0.011) association between platelet function at the TRAPtest and the maximum clot viscosity, and between TRAPtest and the SCV (P = 0.021). A shear rate of 100 s−1 triggers clot formation through a primary role of platelet activation in this model of blood activation. Copyright © 2018 YEAR Wolters Kluwer Health, Inc. All rights reserved.