scholarly journals Targeted Temperature Management at 36°C after In-Hospital Cardiac Arrest Trial (TTM-36 IHCA Trial): Study Protocol for an Investigator-Initiated, Single-Center, Randomized, Controlled, Assessor-Blinded, Pilot Clinical Trial

2016 ◽  
Vol 9 (1) ◽  
pp. 7-15 ◽  
Author(s):  
Sang-Beom Jeon ◽  
Platelets ◽  
2017 ◽  
Vol 29 (5) ◽  
pp. 504-511 ◽  
Author(s):  
Anni Nørgaard Jeppesen ◽  
Anne-Mette Hvas ◽  
Anders Morten Grejs ◽  
Christophe Duez ◽  
Susanne Ilkjær ◽  
...  

2020 ◽  
pp. 204887262093430
Author(s):  
Johannes Grand ◽  
Christian Hassager ◽  
Markus B Skrifvars ◽  
Marjaana Tiainen ◽  
Anders M Grejs ◽  
...  

Background Comatose patients admitted after out-of-hospital cardiac arrest frequently experience haemodynamic instability and anoxic brain injury. Targeted temperature management is used for neuroprotection; however, targeted temperature management also affects patients’ haemodynamic status. This study assessed the haemodynamic status of out-of-hospital cardiac arrest survivors during prolonged (48 hours) targeted temperature management at 33°C. Methods Analysis of haemodynamic and vasopressor data from 311 patients included in a randomised, clinical trial conducted in 10 European hospitals (the TTH48 trial). Patients were randomly allocated to targeted temperature management at 33°C for 24 (TTM24) or 48 (TTM48) hours. Vasopressor and haemodynamic data were reported hourly for 72 hours after admission. Vasopressor load was calculated as norepinephrine (µg/kg/min) plus dopamine(µg/kg/min/100) plus epinephrine (µg/kg/min). Results After 24 hours, mean arterial pressure (mean±SD) was 74±9 versus 75±9 mmHg ( P=0.19), heart rate was 57±16 and 55±14 beats/min ( P=0.18), vasopressor load was 0.06 (0.03–0.15) versus 0.08 (0.03–0.15) µg/kg/min ( P=0.22) for the TTM24 and TTM48 groups, respectively. From 24 to 48 hours, there was no difference in mean arterial pressure ( Pgroup=0.32) or lactate ( Pgroup=0.20), while heart rate was significantly lower (average difference 5 (95% confidence interval 2–8) beats/min, Pgroup<0.0001) and vasopressor load was significantly higher in the TTM48 group ( Pgroup=0.005). In a univariate Cox regression model, high vasopressor load was associated with mortality in univariate analysis (hazard ratio 1.59 (1.05–2.42) P=0.03), but not in multivariate analysis (hazard ratio 0.77 (0.46–1.29) P=0.33). Conclusions In this study, prolonged targeted temperature management at 33°C for 48 hours was associated with higher vasopressor requirement but no sign of any detrimental haemodynamic effects.


Author(s):  
Thomas Hvid Jensen ◽  
Peter Juhl-Olsen ◽  
Bent Roni Ranghøj Nielsen ◽  
Johan Heiberg ◽  
Christophe Henri Valdemar Duez ◽  
...  

Abstract Background Transthoracic echocardiographic (TTE) indices of myocardial function among survivors of out-of-hospital cardiac arrest (OHCA) have been related to neurological outcome; however, results are inconsistent. We hypothesized that changes in average peak systolic mitral annular velocity (s’) from 24 h (h) to 72 h following start of targeted temperature management (TTM) predict six-month neurological outcome in comatose OHCA survivors. Methods We investigated the association between peak systolic velocity of the mitral plane (s’) and six-month neurological outcome in a population of 99 patients from a randomised controlled trial comparing TTM at 33 ± 1 °C for 24 h (h) (n = 47) vs. 48 h (n = 52) following OHCA (TTH48-trial). TTE was conducted at 24 h, 48 h, and 72 h after reaching target temperature. The primary outcome was 180 days neurological outcome assessed by Cerebral Performance Category score (CPC180) and the primary TTE outcome measure was s’. Secondary outcome measures were left ventricular ejection fraction (LVEF), global longitudinal strain (GLS), e’, E/e’ and tricuspid annular plane systolic excursion (TAPSE). Results Across all three scan time points s’ was not associated with neurological outcome (ORs: 24 h: 1.0 (95%CI: 0.7–1.4, p = 0.98), 48 h: 1.13 (95%CI: 0.9–1.4, p = 0.34), 72 h: 1.04 (95%CI: 0.8–1.4, p = 0.76)). LVEF, GLS, E/e’, and TAPSE recorded on serial TTEs following OHCA were neither associated with nor did they predict CPC180. Estimated median e’ at 48 h following TTM was 5.74 cm/s (95%CI: 5.27–6.22) in patients with good outcome (CPC180 1–2) vs. 4.95 cm/s (95%CI: 4.37–5.54) in patients with poor outcome (CPC180 3–5) (p = 0.04). Conclusions s’ assessed on serial TTEs in comatose survivors of OHCA treated with TTM was not associated with CPC180. Our findings suggest that serial TTEs in the early post-resuscitation phase during TTM do not aid the prognostication of neurological outcome following OHCA. Trial registration NCT02066753. Registered 14 February 2014 – Retrospectively registered,


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