Key result
Target temperature management significantly prolonged ventricular repolarization parameters, but these changes were not associated with the 13.7% incidence of ventricular arrhythmias during hypothermia.
Why the study?
Does target temperature management alter repolarization and impact acute and long-term outcomes in patients with successful resuscitation after cardiac arrest?
Cohort (n=95)
Yes
Does target temperature management alter repolarization and impact acute and long-term outcomes in patients with successful resuscitation after cardiac arrest?
While target temperature management significantly prolongs ventricular repolarization, this temporary prolongation does not predict the occurrence of ventricular arrhythmias and is not a useful prognostic marker.
TTM-induced repolarization prolongation was unassociated with arrhythmias or acute outcomes; leaves open post-TTM TpTe as a long-term prognostic marker.
BACKGROUND: The effects of target temperature management (TTM) on the heart aren't thoroughly studied yet. Several studies showed the prolongation of various ECG parameters including Tpeak-Tend-time under TTM. Our study's goal is to evaluate the acute and long-term outcome of these prolongations. METHODS: In this study we included patients with successful resuscitation after cardiac arrest who were admitted to the Charité Virchow Klinikum Berlin or the Heart and Vascular Centre of the Ruhr University Bochum between February 2006 and July 2013 (Berlin) or May 2014 to November 2015 (Bochum). For analysis, one ECG during TTM was recorded after reaching the target temperature (33-34 °C) or in the first 6 h of TTM. If possible, another ECG was taken after TTM. The patients were being followed until February 2016. Primary endpoint was ventricular arrhythmia during TTM, secondary endpoints were death and hospitalization due to cardiovascular diseases during follow-up. RESULTS: One hundred fifty-eight patients were successfully resuscitated in the study period of which 95 patients had usable data (e.g. ECGs without artifacts). During TTM significant changes for different parameters of ventricular de- and repolarization were noted: QRS (103.2 ± 23.7 vs. 95.3 ± 18.1; p = 0.003),QT (405.8 ± 76.4 vs. 373.8 ± 75.0; p = 0.01), QTc (474.9 ± 59.7 vs. 431.0 ± 56.8; p < 0.001), JT (302.8 ± 69.4 vs. 278.5 ± 75.2; p = 0.043), JTc (354.3 ± 60.2 vs. 318.7 ± 59.1; p = 0.001). 13.7% of the patients had ventricular arrhythmias during TTM, however these patients showed no difference regarding their ECG parameters in comparison to those were no ventricular arrhythmias occurred. We were able to follow 69 Patients over an average period of 35 ± 31 months. The 14 (21.5%) patients who died during the follow-up had significant prolongations of the TpTe-time in the ECGs without TTM (103.9 ± 47.2 vs. 75.8 ± 28.6; p = 0.023). CONCLUSION: Our results show a significant prolongation of ventricular repolarization during TH. However, there was no significant difference between the ECG parameters of those who developed a ventricular arrhythmia and those who did not. The temporary prolongation of the repolarization during TTM seems to be less important for the prognosis of the patient. Whereas the prolongation of the repolarization in the basal ECG is associated with a higher mortality in our study.
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Ulmenstein et al. (2017) conducted a cohort in Cardiac arrest (n=95). Target temperature management (TTM) vs. Normothermia (after TTM) was evaluated on Ventricular arrhythmia during TTM. Target temperature management significantly prolonged ventricular repolarization parameters, but these changes were not associated with the 13.7% incidence of ventricular arrhythmias during hypothermia.
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