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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.

Purpose To compare the diagnostic performance of T1 mapping and MR elastography (MRE) for staging of hepatic fibrosis and grading inflammation with histopathology as standard of reference. Methods 68 patients with various liver diseases undergoing liver biopsy for suspected fibrosis or with an established diagnosis of cirrhosis prospectively underwent look-locker inversion recovery T1 mapping and MRE. T1 relaxation time and liver stiffness (LS) were measured by two readers. Hepatic fibrosis and inflammation were histopathologically staged according to a standardized fibrosis (F0–F4) and inflammation (A0–A2) score. For statistical analysis, independent t test, and Mann–Whitney U test and ROC analysis were performed, the latter to determine the performance of T1 mapping and MRE for fibrosis staging and inflammation grading, as compared to histopathology. Results Histopathological analysis diagnosed 9 patients with F0 (13.2%), 21 with F1 (30.9%), 11 with F2 (16.2%), 10 with F3 (14.7%), and 17 with F4 (25.0%). Both T1 mapping and MRE showed significantly higher values for patients with significant fibrosis (F0-1 vs. F2-4; T1 mapping p < 0.0001, MRE p < 0.0001) as well as for patients with severe fibrosis or cirrhosis (F0-2 vs. F3-4; T1 mapping p < 0.0001, MRE p < 0.0001). T1 values and MRE LS were significantly higher in patients with inflammation (A0 vs. A1-2, both p = 0.01). T1 mapping showed a tendency toward lower diagnostic performance without statistical significance for significant fibrosis (F2-4) (AUC 0.79 vs. 0.91, p = 0.06) and with a significant difference compared to MRE for severe fibrosis (F3-4) (AUC 0.79 vs. 0.94, p = 0.03). For both T1 mapping and MRE, diagnostic performance for diagnosing hepatic inflammation (A1-2) was low (AUC 0.72 vs. 0.71, respectively). Conclusion T1 mapping is able to diagnose hepatic fibrosis, however, with a tendency toward lower diagnostic performance compared to MRE and thus may be used as an alternative to MRE for diagnosing hepatic fibrosis, whenever MRE is not available or likely to fail due to intrinsic factors of the patient. Both T1 mapping and MRE are probably not sufficient as standalone methods to diagnose hepatic inflammation with relatively low diagnostic accuracy.