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The Inflammatory Marker suPAR After Cardiac Arrest.

Rundgren, Malin LU ; Lyngbaek, Stig; Fisker, Helle and Friberg, Hans LU (2015) In Therapeutic hypothermia and temperature management 5(2). p.89-94
Abstract
Background: Soluble urokinase plasminogen activator receptor (suPAR) is released in response to inflammatory stimuli, and plasma levels are associated with long-term outcomes. The ischemia/reperfusion injury caused by cardiac arrest (CA) and resuscitation triggers an inflammatory response. This pilot study aimed at investigating suPAR levels in relation to outcome after CA and mild induced hypothermia. Methods: suPAR levels were measured at 6, 36, and 72 hours in patients treated with hypothermia after CA. suPAR levels were analyzed in relation to survival after 6 months. Receiver operating characteristic curve (ROC)-analyses were performed, and area under the curve (AUC) was calculated. Time to return of spontaneous circulation (ROSC) was... (More)
Background: Soluble urokinase plasminogen activator receptor (suPAR) is released in response to inflammatory stimuli, and plasma levels are associated with long-term outcomes. The ischemia/reperfusion injury caused by cardiac arrest (CA) and resuscitation triggers an inflammatory response. This pilot study aimed at investigating suPAR levels in relation to outcome after CA and mild induced hypothermia. Methods: suPAR levels were measured at 6, 36, and 72 hours in patients treated with hypothermia after CA. suPAR levels were analyzed in relation to survival after 6 months. Receiver operating characteristic curve (ROC)-analyses were performed, and area under the curve (AUC) was calculated. Time to return of spontaneous circulation (ROSC) was correlated to suPAR levels. Results: Fifty-five patients (40 male, median 65 years) were included, and 33 (60%) were alive after 6 months. The suPAR levels were significantly higher in nonsurviving patients compared with survivors at 6 and 36 hours (p=0.006 and 0.034 respectively), but not at 72 hours. The suPAR levels increased from 6 to 72 hours (p<0.0001). Time to ROSC correlated positively with suPAR levels at 6 hours (p=0.003) but not at 36 and 72 hours. ROC analysis shoved an AUC of 0.76 at 6 hours. In the subgroup of CA of cardiac cause, the AUC was 0.84. Conclusion: suPAR levels at 6 and 36 hours after CA were significantly higher in nonsurviving patients compared with survivors; however, the overlap in suPAR levels between the outcome groups was substantial, reducing the prognostic value. There was a significant increase in suPAR levels during the first 72 hours after CA. (Less)
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author
organization
publishing date
type
Contribution to journal
publication status
published
subject
in
Therapeutic hypothermia and temperature management
volume
5
issue
2
pages
89 - 94
publisher
Mary Ann Liebert, Inc.
external identifiers
  • pmid:25695339
  • wos:000368519800007
  • scopus:84938485281
ISSN
2153-7933
DOI
10.1089/ther.2014.0027
language
English
LU publication?
yes
id
ba3d9aa2-af38-42e5-b44f-cbc191ce9078 (old id 5143347)
alternative location
http://www.ncbi.nlm.nih.gov/pubmed/25695339?dopt=Abstract
date added to LUP
2015-03-08 19:51:31
date last changed
2017-03-26 03:06:43
@article{ba3d9aa2-af38-42e5-b44f-cbc191ce9078,
  abstract     = {Background: Soluble urokinase plasminogen activator receptor (suPAR) is released in response to inflammatory stimuli, and plasma levels are associated with long-term outcomes. The ischemia/reperfusion injury caused by cardiac arrest (CA) and resuscitation triggers an inflammatory response. This pilot study aimed at investigating suPAR levels in relation to outcome after CA and mild induced hypothermia. Methods: suPAR levels were measured at 6, 36, and 72 hours in patients treated with hypothermia after CA. suPAR levels were analyzed in relation to survival after 6 months. Receiver operating characteristic curve (ROC)-analyses were performed, and area under the curve (AUC) was calculated. Time to return of spontaneous circulation (ROSC) was correlated to suPAR levels. Results: Fifty-five patients (40 male, median 65 years) were included, and 33 (60%) were alive after 6 months. The suPAR levels were significantly higher in nonsurviving patients compared with survivors at 6 and 36 hours (p=0.006 and 0.034 respectively), but not at 72 hours. The suPAR levels increased from 6 to 72 hours (p&lt;0.0001). Time to ROSC correlated positively with suPAR levels at 6 hours (p=0.003) but not at 36 and 72 hours. ROC analysis shoved an AUC of 0.76 at 6 hours. In the subgroup of CA of cardiac cause, the AUC was 0.84. Conclusion: suPAR levels at 6 and 36 hours after CA were significantly higher in nonsurviving patients compared with survivors; however, the overlap in suPAR levels between the outcome groups was substantial, reducing the prognostic value. There was a significant increase in suPAR levels during the first 72 hours after CA.},
  author       = {Rundgren, Malin and Lyngbaek, Stig and Fisker, Helle and Friberg, Hans},
  issn         = {2153-7933},
  language     = {eng},
  number       = {2},
  pages        = {89--94},
  publisher    = {Mary Ann Liebert, Inc.},
  series       = {Therapeutic hypothermia and temperature management},
  title        = {The Inflammatory Marker suPAR After Cardiac Arrest.},
  url          = {http://dx.doi.org/10.1089/ther.2014.0027},
  volume       = {5},
  year         = {2015},
}