Hypothermia induced alteration of repolarization - impact on acute and long-term outcome: a prospective cohort study

Abstract

BackgroundThe 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.MethodsIn 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.ResultsOne 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).ConclusionOur 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.

Electrocardiographic changes in patients undergoing targeted temperature management

“…Gachoka et al 15 reported none of 55 patients undergoing targeted temperature management developed Torsades de pointes or ventricular tachycardia. Ulmenstein et al 8 reported 13.7% of 95 patients had ventricular tachycardia and ventricular fibrillation, and Rosol et al, 9 the largest study to date, reported 11.3% of 193 patients developed ventricular tachycardia, ventricular fibrillation, or Torsades de pointes. Both latter studies showed no statistical difference in QT or QTc interval between those with and without ventricular arrhythmias.…”

“…In other studies, the QRS interval is noted to significantly decrease from hypothermia to after cessation of treatment. However, it is not noted to be associated with arrhythmias and likely to be a benign finding 8,12 …”

“…Accidental hypothermia studies have shown that hypothermia itself can cause adverse cardiac events, such as bradycardia, Osborn waves, atrial fibrillation, and QTc prolongation, predisposing patients to life‐threatening ventricular arrhythmias 7 . These arrhythmias are hypothesized to be due to serum electrolyte changes, including an increase in intracellular calcium, combined with myocardial repolarization variability that occurs with hypothermia 8 . Multiple case reports and studies demonstrate that hypothermia is associated with a significant prolongation in QT and QTc interval 9,10 …”

A Case of Severe QTc Prolongation During Targeted Temperature Management – What Can We Learn?

“…QTc prolongation is common during therapeutic hypothermia, which is conducted for neuroprotection after ventricular fibrillation and ventricular tachycardia cardiac arrests. Hypothermia affects the cardiac cell membrane via electrolyte disturbances in potassium, magnesium, calcium, and sodium, which in turn cause prolongation of ventricular repolarization and the possibility of ventricular arrhythmias [ 1 , 3 ]. The physiologic effects of TTM along with the use of class III antiarrhythmic drugs (i.e., amiodarone) for ventricular tachycardia/ventricular fibrillation cardiac arrests can lead to QTc prolongation, which can in turn potentiate fibrillation and malignant arrhythmias.…”

“…It has been shown to have neuroprotective effects through reduced brain metabolism, decreased neural apoptosis, decreased production of free radicals, and overall decreased inflammation. However, it also has several adverse cardiovascular effects due to its impact on electrolytes and the stability of the cardiac membrane, potentially leading to QTc prolongation and possible arrhythmias [ 1 – 3 ]. QTc prolongation is a known finding during hypothermia, and it is negatively correlated with temperature (i.e., lower temperatures are associated with prolonged QTc) [ 2 ].…”