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.
Subject(s)
Hypothermia, Induced , Myocardial Infarction , Out-of-Hospital Cardiac Arrest , Percutaneous Coronary Intervention , Biomarkers , Coma/diagnosis , Coma/etiology , Coma/therapy , Humans , Hypothermia, Induced/adverse effects , Myocardial Infarction/diagnosis , Myocardial Infarction/etiology , Myocardial Infarction/therapy , Out-of-Hospital Cardiac Arrest/diagnosis , Out-of-Hospital Cardiac Arrest/therapy , Percutaneous Coronary Intervention/adverse effects , Troponin I , Troponin TABSTRACT
BACKGROUND: We studied the associations between ischemia and hypothermia duration, that is, the hypothermic to ischemic ratio (H/I ratio), with mortality in patients included in a trial on two durations of targeted temperature management (TTM) at 33°C. METHODS: The TTH48 (NCT01689077) trial compared 24 and 48 hours of TTM in patients after cardiac arrest. We calculated the hypothermia time from return of spontaneous circulation (ROSC) until the patient reached 37°C after TTM and the ischemic time from CA to ROSC. We compared continuous variables with the Mann-Whitney U test. Using COX regression, we studied the independent association of the logarithmically transformed H/I ratio and time to death as well as interaction between time to ROSC, hypothermia duration, and intervention group. We visualized the predictive ability of variables with receiver operating characteristic curve analysis. RESULTS: Of the 338 patients, 237 (70%) survived for 6 months. The H/I ratio was 155 (IQR 111-238) in survivors and 114 (IQR 80-169) in non-survivors (P < .001). In a Cox regression model including factors associated with outcome in univariate analysis, the logarithmically transformed H/I ratio was a significant predictor of outcome (hazard ratio 0.52 (0.37-0.72, P = .001)). After removing an outlier, we found no interaction between time to ROSC and intervention group (P = .55) or hypothermia duration in quartiles (P = .07) with mortality. There was no significant difference in the area under the curve (AUC) between time to ROSC and H/I ratio (ΔAUC 0.03 95% CI -0.006-0.07, P = .10). CONCLUSIONS: We did not find any consistent evidence of a modification of the effect of TTM based on ischemia duration.
Subject(s)
Hypothermia, Induced/mortality , Hypothermia, Induced/methods , Hypothermia/mortality , Ischemia/mortality , Out-of-Hospital Cardiac Arrest/mortality , Out-of-Hospital Cardiac Arrest/therapy , Aged , Europe/epidemiology , Female , Humans , Male , Middle Aged , Survival Analysis , Time FactorsABSTRACT
EEG reactivity (EEG-R) is regarded as an important parameter in coma prognosis but knowledge is sparse on the nature of EEG changes due to different kinds of stimulation and their prognostic significance. EEG-R was quantified in a study of 39 comatose neurosurgical patients. Six 30-second standardized visual, auditory, and painful stimulations were applied. EEG-R in the delta, theta, alpha, and beta band was normalized in z-scores as the power of a stimulation epoch relative to average power of 6 resting epochs. Outcome measure was 3 months Glasgow Outcome Scale. Increase in EEG activity was related to poor outcome, was more common (13.4% of tests), and grew continuously during the 30-second stimulation epoch. Decrease in EEG activity was related to good outcome, was rarer (2.5%), and peaked around 15 seconds. Pain was the most provocative stimulation (20.4%) followed by sound (8.7%) and eye-opening (6.7%). Discrimination between good (n = 6) and poor (n = 33) outcome was best in the theta and alpha bands for pain stimulation in the first 10-20 seconds and for sound stimulation in the first 5 to 10 seconds, eye-opening did not discriminate. Increase in activity predicted poor outcome with a high specificity 100% (CI = 52%-100%) and a modest sensitivity of 39% (CI = 23%-58%). Decrease in activity predicted good outcome with a high specificity of 100% (CI = 87%-100%) and a modest sensitivity of 33% (CI = 6%-76%). This quantitative study reveals new knowledge about the nature of EEG-R, which contribute to the development of more reliable and objective clinical procedures for outcome prediction.