Cerebral monitoring in a pig model of cardiac arrest with 48 h of intensive care

Lauge Vammen; Cecilie Munch Johannsen; Andreas Magnussen; Amalie Ling Povlsen; Søren Riis Petersen; Arezo Azizi; Michael Pedersen; Anders Rosendal Korshoej; Steffen Ringgaard; Bo Løfgren; Lars W Andersen; Asger Granfeldt

doi:10.1186/s40635-022-00475-2

Cerebral monitoring in a pig model of cardiac arrest with 48 h of intensive care

Lauge Vammen, Cecilie Munch Johannsen, Andreas Magnussen, Amalie Ling Povlsen, Søren Riis Petersen, Arezo Azizi, Michael Pedersen, Anders Rosendal Korshoej, Steffen Ringgaard, Bo Løfgren, Lars W Andersen, Asger Granfeldt^*

^*Corresponding author af dette arbejde

Publikation: Bidrag til tidsskrift/Konferencebidrag i tidsskrift /Bidrag til avis › Tidsskriftartikel › Forskning › peer review

6 Citationer (Scopus)

Abstract

Background: Neurological injury is the primary cause of death after out-of-hospital cardiac arrest. There is a lack of studies investigating cerebral injury beyond the immediate post-resuscitation phase in a controlled cardiac arrest experimental setting. Methods: The aim of this study was to investigate temporal changes in measures of cerebral injury and metabolism in a cardiac arrest pig model with clinically relevant post-cardiac arrest intensive care. A cardiac arrest group (n = 11) underwent 7 min of no-flow and was compared with a sham group (n = 6). Pigs underwent intensive care with 24 h of hypothermia at 33 °C. Blood markers of cerebral injury, cerebral microdialysis, and intracranial pressure (ICP) were measured. After 48 h, pigs underwent a cerebral MRI scan. Data are presented as median [25th; 75th percentiles]. Results: Return of spontaneous circulation was achieved in 7/11 pigs. Time to ROSC was 4.4 min [4.2; 10.9]. Both NSE and NfL increased over time (p < 0.001), and were higher in the cardiac arrest group at 48 h (NSE 4.2 µg/L [2.4; 6.1] vs 0.9 [0.7; 0.9], p < 0.001; NfL 63 ng/L [35; 232] vs 29 [21; 34], p = 0.02). There was no difference in ICP at 48 h (17 mmHg [14; 24] vs 18 [13; 20], p = 0.44). The cerebral lactate/pyruvate ratio had secondary surges in 3/7 cardiac arrest pigs after successful resuscitation. Apparent diffusion coefficient was lower in the cardiac arrest group in white matter cortex (689 × 10^–6 mm²/s [524; 765] vs 800 [799; 815], p = 0.04) and hippocampus (854 [834; 910] vs 1049 [964; 1180], p = 0.03). N-Acetylaspartate was lower on MR spectroscopy in the cardiac arrest group (− 17.2 log [− 17.4; − 17.0] vs − 16.9 [− 16.9; − 16.9], p = 0.03). Conclusions: We have developed a clinically relevant cardiac arrest pig model that displays cerebral injury as marked by NSE and NfL elevations, signs of cerebral oedema, and reduced neuron viability. Overall, the burden of elevated ICP was low in the cardiac arrest group. A subset of pigs undergoing cardiac arrest had persisting metabolic disturbances after successful resuscitation.

Originalsprog	Engelsk
Artikelnummer	45
Tidsskrift	Intensive Care Medicine Experimental
Vol/bind	10
Nummer	1
ISSN	2197-425X
DOI	https://doi.org/10.1186/s40635-022-00475-2
Status	Udgivet - okt. 2022

Emneord

Heart Arrest
Acute myocardial infarction
Post-cardiac arrest care
Targeted temperature management

Adgang til dokumentet

10.1186/s40635-022-00475-2Licens: CC BY

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Citationsformater

Vammen, L., Munch Johannsen, C., Magnussen, A., Povlsen, A. L., Riis Petersen, S., Azizi, A., Pedersen, M., Korshoej, A. R., Ringgaard, S., Løfgren, B., Andersen, L. W., & Granfeldt, A. (2022). Cerebral monitoring in a pig model of cardiac arrest with 48 h of intensive care. Intensive Care Medicine Experimental, 10(1), Artikel 45. https://doi.org/10.1186/s40635-022-00475-2

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title = "Cerebral monitoring in a pig model of cardiac arrest with 48 h of intensive care",

abstract = "Background: Neurological injury is the primary cause of death after out-of-hospital cardiac arrest. There is a lack of studies investigating cerebral injury beyond the immediate post-resuscitation phase in a controlled cardiac arrest experimental setting. Methods: The aim of this study was to investigate temporal changes in measures of cerebral injury and metabolism in a cardiac arrest pig model with clinically relevant post-cardiac arrest intensive care. A cardiac arrest group (n = 11) underwent 7 min of no-flow and was compared with a sham group (n = 6). Pigs underwent intensive care with 24 h of hypothermia at 33 °C. Blood markers of cerebral injury, cerebral microdialysis, and intracranial pressure (ICP) were measured. After 48 h, pigs underwent a cerebral MRI scan. Data are presented as median [25th; 75th percentiles]. Results: Return of spontaneous circulation was achieved in 7/11 pigs. Time to ROSC was 4.4 min [4.2; 10.9]. Both NSE and NfL increased over time (p < 0.001), and were higher in the cardiac arrest group at 48 h (NSE 4.2 µg/L [2.4; 6.1] vs 0.9 [0.7; 0.9], p < 0.001; NfL 63 ng/L [35; 232] vs 29 [21; 34], p = 0.02). There was no difference in ICP at 48 h (17 mmHg [14; 24] vs 18 [13; 20], p = 0.44). The cerebral lactate/pyruvate ratio had secondary surges in 3/7 cardiac arrest pigs after successful resuscitation. Apparent diffusion coefficient was lower in the cardiac arrest group in white matter cortex (689 × 10–6 mm2/s [524; 765] vs 800 [799; 815], p = 0.04) and hippocampus (854 [834; 910] vs 1049 [964; 1180], p = 0.03). N-Acetylaspartate was lower on MR spectroscopy in the cardiac arrest group (− 17.2 log [− 17.4; − 17.0] vs − 16.9 [− 16.9; − 16.9], p = 0.03). Conclusions: We have developed a clinically relevant cardiac arrest pig model that displays cerebral injury as marked by NSE and NfL elevations, signs of cerebral oedema, and reduced neuron viability. Overall, the burden of elevated ICP was low in the cardiac arrest group. A subset of pigs undergoing cardiac arrest had persisting metabolic disturbances after successful resuscitation.",

keywords = "Heart Arrest, Acute myocardial infarction, Post-cardiac arrest care, Targeted temperature management",

author = "Lauge Vammen and {Munch Johannsen}, Cecilie and Andreas Magnussen and Povlsen, {Amalie Ling} and {Riis Petersen}, S{\o}ren and Arezo Azizi and Michael Pedersen and Korshoej, {Anders Rosendal} and Steffen Ringgaard and Bo L{\o}fgren and Andersen, {Lars W} and Asger Granfeldt",

year = "2022",

month = oct,

doi = "10.1186/s40635-022-00475-2",

language = "English",

volume = "10",

journal = "Intensive Care Medicine Experimental",

issn = "2197-425X",

publisher = "Springer Nature",

number = "1",

}

TY - JOUR

T1 - Cerebral monitoring in a pig model of cardiac arrest with 48 h of intensive care

AU - Vammen, Lauge

AU - Munch Johannsen, Cecilie

AU - Magnussen, Andreas

AU - Povlsen, Amalie Ling

AU - Riis Petersen, Søren

AU - Azizi, Arezo

AU - Pedersen, Michael

AU - Korshoej, Anders Rosendal

AU - Ringgaard, Steffen

AU - Løfgren, Bo

AU - Andersen, Lars W

AU - Granfeldt, Asger

PY - 2022/10

Y1 - 2022/10

N2 - Background: Neurological injury is the primary cause of death after out-of-hospital cardiac arrest. There is a lack of studies investigating cerebral injury beyond the immediate post-resuscitation phase in a controlled cardiac arrest experimental setting. Methods: The aim of this study was to investigate temporal changes in measures of cerebral injury and metabolism in a cardiac arrest pig model with clinically relevant post-cardiac arrest intensive care. A cardiac arrest group (n = 11) underwent 7 min of no-flow and was compared with a sham group (n = 6). Pigs underwent intensive care with 24 h of hypothermia at 33 °C. Blood markers of cerebral injury, cerebral microdialysis, and intracranial pressure (ICP) were measured. After 48 h, pigs underwent a cerebral MRI scan. Data are presented as median [25th; 75th percentiles]. Results: Return of spontaneous circulation was achieved in 7/11 pigs. Time to ROSC was 4.4 min [4.2; 10.9]. Both NSE and NfL increased over time (p < 0.001), and were higher in the cardiac arrest group at 48 h (NSE 4.2 µg/L [2.4; 6.1] vs 0.9 [0.7; 0.9], p < 0.001; NfL 63 ng/L [35; 232] vs 29 [21; 34], p = 0.02). There was no difference in ICP at 48 h (17 mmHg [14; 24] vs 18 [13; 20], p = 0.44). The cerebral lactate/pyruvate ratio had secondary surges in 3/7 cardiac arrest pigs after successful resuscitation. Apparent diffusion coefficient was lower in the cardiac arrest group in white matter cortex (689 × 10–6 mm2/s [524; 765] vs 800 [799; 815], p = 0.04) and hippocampus (854 [834; 910] vs 1049 [964; 1180], p = 0.03). N-Acetylaspartate was lower on MR spectroscopy in the cardiac arrest group (− 17.2 log [− 17.4; − 17.0] vs − 16.9 [− 16.9; − 16.9], p = 0.03). Conclusions: We have developed a clinically relevant cardiac arrest pig model that displays cerebral injury as marked by NSE and NfL elevations, signs of cerebral oedema, and reduced neuron viability. Overall, the burden of elevated ICP was low in the cardiac arrest group. A subset of pigs undergoing cardiac arrest had persisting metabolic disturbances after successful resuscitation.

AB - Background: Neurological injury is the primary cause of death after out-of-hospital cardiac arrest. There is a lack of studies investigating cerebral injury beyond the immediate post-resuscitation phase in a controlled cardiac arrest experimental setting. Methods: The aim of this study was to investigate temporal changes in measures of cerebral injury and metabolism in a cardiac arrest pig model with clinically relevant post-cardiac arrest intensive care. A cardiac arrest group (n = 11) underwent 7 min of no-flow and was compared with a sham group (n = 6). Pigs underwent intensive care with 24 h of hypothermia at 33 °C. Blood markers of cerebral injury, cerebral microdialysis, and intracranial pressure (ICP) were measured. After 48 h, pigs underwent a cerebral MRI scan. Data are presented as median [25th; 75th percentiles]. Results: Return of spontaneous circulation was achieved in 7/11 pigs. Time to ROSC was 4.4 min [4.2; 10.9]. Both NSE and NfL increased over time (p < 0.001), and were higher in the cardiac arrest group at 48 h (NSE 4.2 µg/L [2.4; 6.1] vs 0.9 [0.7; 0.9], p < 0.001; NfL 63 ng/L [35; 232] vs 29 [21; 34], p = 0.02). There was no difference in ICP at 48 h (17 mmHg [14; 24] vs 18 [13; 20], p = 0.44). The cerebral lactate/pyruvate ratio had secondary surges in 3/7 cardiac arrest pigs after successful resuscitation. Apparent diffusion coefficient was lower in the cardiac arrest group in white matter cortex (689 × 10–6 mm2/s [524; 765] vs 800 [799; 815], p = 0.04) and hippocampus (854 [834; 910] vs 1049 [964; 1180], p = 0.03). N-Acetylaspartate was lower on MR spectroscopy in the cardiac arrest group (− 17.2 log [− 17.4; − 17.0] vs − 16.9 [− 16.9; − 16.9], p = 0.03). Conclusions: We have developed a clinically relevant cardiac arrest pig model that displays cerebral injury as marked by NSE and NfL elevations, signs of cerebral oedema, and reduced neuron viability. Overall, the burden of elevated ICP was low in the cardiac arrest group. A subset of pigs undergoing cardiac arrest had persisting metabolic disturbances after successful resuscitation.

KW - Heart Arrest

KW - Acute myocardial infarction

KW - Post-cardiac arrest care

KW - Targeted temperature management

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U2 - 10.1186/s40635-022-00475-2

DO - 10.1186/s40635-022-00475-2

M3 - Journal article

C2 - 36284020

AN - SCOPUS:85140650478

SN - 2197-425X

VL - 10

JO - Intensive Care Medicine Experimental

JF - Intensive Care Medicine Experimental

IS - 1

M1 - 45

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