pcbi.1009331.g006.tif (544.76 kB)

Pro-coagulant environment quantification based on concentration of activated platelets and agonists.

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posted on 2021-09-07, 17:47 authored by Noelia Grande Gutiérrez, Mark Alber, Andrew M. Kahn, Jane C. Burns, Mathew Mathew, Brian W. McCrindle, Alison L. Marsden

a) Changes in fraction of aneurysm volume where [AP] >5, 8, 10 nM; b) fraction of aneurysm volume where [AP] >10 nM. Pro-coagulant environment quantification based on ADP and PolyP critical thresholds. c) Fraction of aneurysm volume where [ADP] > [ADP]_crit; d) fraction of aneurysm volume where [PolyP] > [PolyP]_crit. Th = confirmed thrombosis, NonTh = non confirmed thrombosis, [AP] = activated platelet concentration.

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yet fully understood suggesting predictive capabilities persistent aneurysms requires intrinsic coagulation pathway healthy coronary case diffusion equations solved coagulation pathway even clinical decisions regarding case &# 8212 thrombotic risk assessment computational simulations show computational fluid dynamics biochemical &# 8212 thrombosis prevention tailored coronary artery thrombosis activated platelet concentrations local agonist concentration track platelet activation major risk associated local concentration platelet aggregation high risk computational modeling biochemical activation confirmed thrombosis concentration levels underlying mechanisms term management reported location rate exposure potential initiation leading factors kawasaki disease including three flow stagnation findings suggest extrinsic factor coagulant environment anticoagulation therapy adenosine diphosphate activated platelets

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