Kinetics of 2 different high-sensitive troponins during targeted temperature management in out-of-hospital cardiac arrest patients with acute myocardial infarction: a post hoc sub-study of a randomised clinical trial

Alf Inge Larsen, Anders Morten Grejs, Simon Tilma Vistisen, Kristian Strand, Øyvind Skadberg, Anni Nørgaard Jeppesen, Christophe H V Duez, Hans Kirkegaard, Eldar Søreide, Alf Inge Larsen, Anders Morten Grejs, Simon Tilma Vistisen, Kristian Strand, Øyvind Skadberg, Anni Nørgaard Jeppesen, Christophe H V Duez, Hans Kirkegaard, Eldar Søreide

Abstract

Introduction: Short term hypothermia has been suggested to have cardio protective properties in acute myocardial infarction (AMI) by reducing infarct size as assessed by troponins. There are limited data on the kinetics of these biomarkers in comatose out-of-hospital cardiac arrest (OHCA) patients, with and without AMI, undergoing targeted temperature management (TTM) in the ICU.

Purpose: The aim of this post hoc analyses was to evaluate and compare the kinetics of two high-sensitivity cardiac troponins in OHCA survivors, with and without acute myocardial infarction (AMI), during TTM of different durations [24 h (standard) vs. 48 h (prolonged)].

Methods: In a sub-cohort (n = 114) of the international, multicentre, randomized controlled study "TTH48" we measured high-sensitive troponin T (hs-cTnT), high-sensitive troponin I (hs-cTnI) and CK-MB at the following time points: Arrival, 24 h, 48 h and 72 h from reaching the target temperature range of 33 ± 1 °C. All patients diagnosed with an AMI at the immediate coronary angiogram (CAG)-18 in the 24-h group and 25 in the 48-h group-underwent PCI with stent implantation. There were no stent thromboses.

Results: Both the hs-cTnT and hs-cTnI changes over time were highly influenced by the cause of OHCA (AMI vs. non-AMI). In contrast to non-AMI patients, both troponins remained elevated at 72 h in AMI patients. There was no difference between the two time-differentiated TTM groups in the kinetics for the two troponins.

Conclusion: In comatose OHCA survivors with an aetiology of AMI levels of both hs-cTnI and hs-cTnT remained elevated for 72 h, which is in contrast to the well-described kinetic profile of troponins in normotherm AMI patients. There was no difference in kinetic profile between the two high sensitive assays. Different duration of TTM did not influence the kinetics of the troponins.

Trial registration: Clinicaltrials.gov Identifier: NCT01689077, 20/09/2012.

Keywords: Myocardial Infarction; Out of hospital cardiac arrest; Targeted temperature management; Troponins.

Conflict of interest statement

Anders Grejs reports to have received speaker fees from Novartis and MSD. All other authors declare no conflict of interest. Authorship: All authors had access to the data and participated in writing the manuscript according to the Vancouver protocol.

© 2022. The Author(s).

Figures

Fig. 1
Fig. 1
Kinetics of TnI, TnT and CK-mb in comatose survivors after OHCA. AMI compared to non-AMI. Pooled analyses of both treatment arms 24 and 48 h of TTM. Patients stratified by acute myocardial infarction (AMI) or non-AMI. hs-cTnT, hs-cTnI, CK-MB is log transformed, (mean ± SE). The units are ng/l. TNT; high sensitive troponin T, TNI; high sensitive troponin I, CK-MB; Creatine kinase MB, OHCA; out of hospital cardiac arrest, TTM; target temperature management
Fig. 2
Fig. 2
Kinetics of TnI, TnT and CK-mb in comatose survivors after OHCA treated with TTM in the TTH48 trial stratified by cause of event (AMI vs. non-AMI) and treatment group (TTM 24 h vs. TTM 48 h). Patients stratified by AMI and length of TTM, (mean ± SE). hs-cTnT, hs-cTnI, CK-MB. The units are ng/l. TNI; high sensitive troponin I, TNT; high sensitive troponin T, CK-MB; Creatin kinase MB, OHCA; out of hospital cardiac arrest, TTM; target temperature management
Fig. 3
Fig. 3
Changes in serum creatinine during 72 h as a function of aetiology (AMI or not AMI), treatment group (TTM 24 h vs. TTM 48 h) and the combination of these. Patients stratified by AMI or no-AMI, (mean ± SE). sCr; serum creatinine, AMI; acute myocardial infarction, TTM; target temperature management
Fig. 4
Fig. 4
Kinetics of TnI, TnT and CK-mb in comatose survivors after OHCA treated with TTM in the TTH48 trial. Duration of TTM. Patients stratified by treatment group, (mean ± SE). The units are ng/l. TNI; high sensitive troponin I, TNT; high sensitive troponin T, MB; Creatine kinase MB, TTM; target temperature management
Fig. 5
Fig. 5
Effect of age > 63 and female gender on the levels troponins. Patients stratified by age and gender, (mean ± SE). The units are ng/l. TNI; high sensitive troponin I, TNT; high sensitive troponin T
Fig. 6
Fig. 6
Summary of results for TNI, TNT and CK-MB, treatment length, AMI versus non ami, age and gender. The units are ng/l. TNI; high sensitive troponin I, TNT; high sensitive troponin T, AMI; acute myocardial infarction. (mean ± SE)

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