Platelet aggregation and clot formation in comatose survivors of cardiac arrest treated with induced hypothermia and dual platelet inhibition with aspirin and ticagrelor; a prospective observational studyReport as inadecuate




Platelet aggregation and clot formation in comatose survivors of cardiac arrest treated with induced hypothermia and dual platelet inhibition with aspirin and ticagrelor; a prospective observational study - Download this document for free, or read online. Document in PDF available to download.

Critical Care

, 18:495

First Online: 30 September 2014Received: 31 January 2014Accepted: 05 August 2014

Abstract

IntroductionWe conducted a prospective observational study in cardiac arrest survivors treated with mild induced hypothermia, evaluating different platelet function tests at hypo- and normothermia. We also investigated the relation between gastric emptying and vasodilator stimulated phosphoprotein VASP.

MethodsComatose survivors of out of hospital cardiac arrest were included and divided into two groups, depending on whether dual platelet inhibition with peroral ticagrelor and aspirin was given or not. The first blood samples T1 were collected 12–24 hours after reaching target temperature 33°C and were compared to blood samples collected 12–28 hours after reaching normothermia 37°C T2 within each group. All samples were analysed by Sonoclot viscoelasticity, flow cytometry based VASP and with multiple electrode aggregometry, Multiplate®; adenosine diphosphate ADP, collagen COL, thrombin receptor agonist peptide TRAP and arachidonic acid ASPI. Sonoclot and Multiplate® instruments were set on in vivo temperatures. Gastric secretion from the nasogastric tube was measured to assess absorption of per orally administered antiplatelet drugs. Differences between T1 and T2 within each group were calculated using Wilcoxon matched pairs signed test. Significance levels were set at P <0.01.

ResultsIn total, 23 patients were included. In patients with dual platelet inhibition n =14 Multiplate®-analyses showed no changes in ADP stimulated platelets. COL, TRAP and ASPI aggregations were higher at T2 compared to T1. Sonoclot-analyses showed that activated clotting time ACT was unchanged but both clot rate CR and platelet function PF were higher at T2 compared to T1. VASP decreased from 53 ± 28T1 to 24 ± 22T2, P <0.001. The average volume of gastric secretion aspirated before T1 correlated well with VASP T1, r =0.81 P <0.001. In patients with no platelet inhibition, n =9 similar changes between T1 and T2 were seen as in patients with dual platelet inhibition while VASP was unchanged.

ConclusionsWe have demonstrated increased platelet aggregation and strengthened clot formation over time in out of hospital cardiac arrest patients treated with hypothermia. In patients on oral dual platelet inhibition, the effect of ticagrelor was delayed, probably due to slow gastric emptying.

AbbreviationsACTactivated clotting time

ADPadenosine-5′-diphosphate agonist

aPTTactivated partial thromboplastin time

ASPIarachidonic acid agonist

COLcollagen agonist

CRclot rate

CRPC-reactive protein

GCSGlasgow coma scale

LMWHlow-molecular-weight heparin

MIHmild induced hypothermia

nPInon-platelet inhibition

OHCAout-of-hospital cardiac arrest

PCIpercutaneous coronary intervention

PFplatelet function

PIplatelet inhibition

PRIplatelet reactivity index

PT-INRprothrombin time international normalized ratio

ROSCreturn of spontaneous circulation

SAPS3simplified acute physiology score 3

SIRSsystemic inflammatory response syndrome

TRAPthrombin receptor agonist peptide

VASPvasodilator-stimulated phosphoprotein

Electronic supplementary materialThe online version of this article doi:10.1186-s13054-014-0495-z contains supplementary material, which is available to authorized users.

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Author: Thomas Kander - Josef Dankiewicz - Hans Friberg - Ulf Schött

Source: https://link.springer.com/







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