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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

Kander, Thomas LU orcid ; Dankiewicz, Josef LU orcid ; Friberg, Hans LU and Schött, Ulf LU (2014) In Critical Care 18(5).
Abstract
Introduction: We 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). Methods: Comatose 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 degrees C) and were compared to blood samples collected 12-28 hours after reaching normothermia (37 degrees C) (T2) within each group. All... (More)
Introduction: We 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). Methods: Comatose 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 degrees C) and were compared to blood samples collected 12-28 hours after reaching normothermia (37 degrees C) (T2) within each group. All samples were analysed by Sonoclot viscoelasticity, flow cytometry based VASP and with multiple electrode aggregometry, Multiplate (R); adenosine diphosphate (ADP), collagen (COL), thrombin receptor agonist peptide (TRAP) and arachidonic acid (ASPI). Sonoclot and Multiplate (R) 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. Results: In total, 23 patients were included. In patients with dual platelet inhibition (n = 14) Multiplate (R)-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 +/- 28(T1) to 24 +/- 22(T2), (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. Conclusions: We 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. (Less)
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author
; ; and
organization
publishing date
type
Contribution to journal
publication status
published
subject
in
Critical Care
volume
18
issue
5
article number
495
publisher
BioMed Central (BMC)
external identifiers
  • wos:000351850600015
  • scopus:84908087110
  • pmid:25292183
ISSN
1364-8535
DOI
10.1186/s13054-014-0495-z
project
Koagulation vid kirurgi och kritisk sjukdom
language
English
LU publication?
yes
id
c80da7c2-64b8-4d29-a3d1-00b8f0ee4d5e (old id 5281700)
date added to LUP
2016-04-01 10:52:38
date last changed
2022-04-28 02:13:28
@article{c80da7c2-64b8-4d29-a3d1-00b8f0ee4d5e,
  abstract     = {{Introduction: We 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). Methods: Comatose 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 degrees C) and were compared to blood samples collected 12-28 hours after reaching normothermia (37 degrees C) (T2) within each group. All samples were analysed by Sonoclot viscoelasticity, flow cytometry based VASP and with multiple electrode aggregometry, Multiplate (R); adenosine diphosphate (ADP), collagen (COL), thrombin receptor agonist peptide (TRAP) and arachidonic acid (ASPI). Sonoclot and Multiplate (R) 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 &lt; 0.01. Results: In total, 23 patients were included. In patients with dual platelet inhibition (n = 14) Multiplate (R)-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 +/- 28(T1) to 24 +/- 22(T2), (P &lt; 0.001). The average volume of gastric secretion aspirated before T1 correlated well with VASP (T1), r = 0.81 (P &lt; 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. Conclusions: We 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.}},
  author       = {{Kander, Thomas and Dankiewicz, Josef and Friberg, Hans and Schött, Ulf}},
  issn         = {{1364-8535}},
  language     = {{eng}},
  number       = {{5}},
  publisher    = {{BioMed Central (BMC)}},
  series       = {{Critical Care}},
  title        = {{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}},
  url          = {{https://lup.lub.lu.se/search/files/2204091/8161018}},
  doi          = {{10.1186/s13054-014-0495-z}},
  volume       = {{18}},
  year         = {{2014}},
}