Thiamine for the Treatment of Cardiac Arrest–Induced Neurological Injury: A Randomized, Blinded, Placebo‐Controlled Experimental Study
Background Thiamine supplementation has demonstrated protective effects in a mouse model of cardiac arrest. The aim of this study was to investigate the neuroprotective effects of thiamine in a clinically relevant large animal cardiac arrest model. The hypothesis was that thiamine reduces neurologic...
Main Authors: | , , , , , , , , , , , |
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Format: | Article |
Language: | English |
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Wiley
2023-04-01
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Series: | Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease |
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Online Access: | https://www.ahajournals.org/doi/10.1161/JAHA.122.028558 |
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author | Lauge Vammen Cecilie Munch Johannsen Cecilie Dahl Baltsen Casper Nørholt Mark Eggertsen Signe Mortensen Lasse Vormfenne Amalie Povlsen Michael W. Donnino Bo Løfgren Lars W. Andersen Asger Granfeldt |
author_facet | Lauge Vammen Cecilie Munch Johannsen Cecilie Dahl Baltsen Casper Nørholt Mark Eggertsen Signe Mortensen Lasse Vormfenne Amalie Povlsen Michael W. Donnino Bo Løfgren Lars W. Andersen Asger Granfeldt |
author_sort | Lauge Vammen |
collection | DOAJ |
description | Background Thiamine supplementation has demonstrated protective effects in a mouse model of cardiac arrest. The aim of this study was to investigate the neuroprotective effects of thiamine in a clinically relevant large animal cardiac arrest model. The hypothesis was that thiamine reduces neurological injury evaluated by neuron‐specific enolase levels. Methods and Results Pigs underwent myocardial infarction and subsequently 9 minutes of untreated cardiac arrest. Twenty minutes after successful resuscitation, the pigs were randomized to treatment with either thiamine or placebo. All pigs underwent 40 hours of intensive care and were awakened for assessment of functional neurological outcome up until 9 days after cardiac arrest. Nine pigs were included in both groups, with 8 in each group surviving the entire intensive care phase. Mean area under the curve for neuron‐specific enolase was similar between groups, with 81.5 μg/L per hour (SD, 20.4) in the thiamine group and 80.5 μg/L per hour (SD, 18.3) in the placebo group, with an absolute difference of 1.0 (95% CI, −57.8 to 59.8; P=0.97). Likewise, there were no absolute difference in neurological deficit score at the end of the protocol (2 [95% CI, −38 to 42]; P=0.93). There was no absolute mean group difference in lactate during the intensive care period (1.1 mmol/L [95% CI, −0.5 to 2.7]; P=0.16). Conclusions In this randomized, blinded, placebo‐controlled trial using a pig cardiac arrest model with myocardial infarction and long intensive care and observation for 9 days, thiamine showed no effect in changes to functional neurological outcome or serum levels of neuron‐specific enolase. Thiamine treatment had no effect on lactate levels after successful resuscitation. |
first_indexed | 2024-03-13T10:55:31Z |
format | Article |
id | doaj.art-a5f49d573b9545b38b81e55ce1713a92 |
institution | Directory Open Access Journal |
issn | 2047-9980 |
language | English |
last_indexed | 2024-03-13T10:55:31Z |
publishDate | 2023-04-01 |
publisher | Wiley |
record_format | Article |
series | Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease |
spelling | doaj.art-a5f49d573b9545b38b81e55ce1713a922023-05-17T04:33:58ZengWileyJournal of the American Heart Association: Cardiovascular and Cerebrovascular Disease2047-99802023-04-0112710.1161/JAHA.122.028558Thiamine for the Treatment of Cardiac Arrest–Induced Neurological Injury: A Randomized, Blinded, Placebo‐Controlled Experimental StudyLauge Vammen0Cecilie Munch Johannsen1Cecilie Dahl Baltsen2Casper Nørholt3Mark Eggertsen4Signe Mortensen5Lasse Vormfenne6Amalie Povlsen7Michael W. Donnino8Bo Løfgren9Lars W. Andersen10Asger Granfeldt11Department of Anesthesiology and Intensive Care Aarhus University Hospital Aarhus DenmarkDepartment of Anesthesiology and Intensive Care Aarhus University Hospital Aarhus DenmarkDepartment of Clinical Medicine Aarhus University Aarhus DenmarkDepartment of Anesthesiology and Intensive Care Aarhus University Hospital Aarhus DenmarkDepartment of Anesthesiology and Intensive Care Aarhus University Hospital Aarhus DenmarkDepartment of Clinical Medicine Aarhus University Aarhus DenmarkDepartment of Clinical Medicine Aarhus University Aarhus DenmarkDepartment of Clinical Medicine Aarhus University Aarhus DenmarkCenter for Resuscitation Science, Department of Emergency Medicine Beth Israel Deaconess Medical Center Boston MA USADepartment of Clinical Medicine Aarhus University Aarhus DenmarkDepartment of Anesthesiology and Intensive Care Aarhus University Hospital Aarhus DenmarkDepartment of Anesthesiology and Intensive Care Aarhus University Hospital Aarhus DenmarkBackground Thiamine supplementation has demonstrated protective effects in a mouse model of cardiac arrest. The aim of this study was to investigate the neuroprotective effects of thiamine in a clinically relevant large animal cardiac arrest model. The hypothesis was that thiamine reduces neurological injury evaluated by neuron‐specific enolase levels. Methods and Results Pigs underwent myocardial infarction and subsequently 9 minutes of untreated cardiac arrest. Twenty minutes after successful resuscitation, the pigs were randomized to treatment with either thiamine or placebo. All pigs underwent 40 hours of intensive care and were awakened for assessment of functional neurological outcome up until 9 days after cardiac arrest. Nine pigs were included in both groups, with 8 in each group surviving the entire intensive care phase. Mean area under the curve for neuron‐specific enolase was similar between groups, with 81.5 μg/L per hour (SD, 20.4) in the thiamine group and 80.5 μg/L per hour (SD, 18.3) in the placebo group, with an absolute difference of 1.0 (95% CI, −57.8 to 59.8; P=0.97). Likewise, there were no absolute difference in neurological deficit score at the end of the protocol (2 [95% CI, −38 to 42]; P=0.93). There was no absolute mean group difference in lactate during the intensive care period (1.1 mmol/L [95% CI, −0.5 to 2.7]; P=0.16). Conclusions In this randomized, blinded, placebo‐controlled trial using a pig cardiac arrest model with myocardial infarction and long intensive care and observation for 9 days, thiamine showed no effect in changes to functional neurological outcome or serum levels of neuron‐specific enolase. Thiamine treatment had no effect on lactate levels after successful resuscitation.https://www.ahajournals.org/doi/10.1161/JAHA.122.028558acute myocardial infarctionanimal experimentheart arrestneurological injurythiamine |
spellingShingle | Lauge Vammen Cecilie Munch Johannsen Cecilie Dahl Baltsen Casper Nørholt Mark Eggertsen Signe Mortensen Lasse Vormfenne Amalie Povlsen Michael W. Donnino Bo Løfgren Lars W. Andersen Asger Granfeldt Thiamine for the Treatment of Cardiac Arrest–Induced Neurological Injury: A Randomized, Blinded, Placebo‐Controlled Experimental Study Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease acute myocardial infarction animal experiment heart arrest neurological injury thiamine |
title | Thiamine for the Treatment of Cardiac Arrest–Induced Neurological Injury: A Randomized, Blinded, Placebo‐Controlled Experimental Study |
title_full | Thiamine for the Treatment of Cardiac Arrest–Induced Neurological Injury: A Randomized, Blinded, Placebo‐Controlled Experimental Study |
title_fullStr | Thiamine for the Treatment of Cardiac Arrest–Induced Neurological Injury: A Randomized, Blinded, Placebo‐Controlled Experimental Study |
title_full_unstemmed | Thiamine for the Treatment of Cardiac Arrest–Induced Neurological Injury: A Randomized, Blinded, Placebo‐Controlled Experimental Study |
title_short | Thiamine for the Treatment of Cardiac Arrest–Induced Neurological Injury: A Randomized, Blinded, Placebo‐Controlled Experimental Study |
title_sort | thiamine for the treatment of cardiac arrest induced neurological injury a randomized blinded placebo controlled experimental study |
topic | acute myocardial infarction animal experiment heart arrest neurological injury thiamine |
url | https://www.ahajournals.org/doi/10.1161/JAHA.122.028558 |
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