Having promised that #STRESS-L would be announced here first, the other place (Twitter / X) took of on its own!
So here are some thoughts not found elsewhere. Thread.
STRESS-L was published yesterday: https://jamanetwork.com/journals/jama/fullarticle/2811213
We recruited patients with established septic shock defined by being treated with noradrenaline for at least 24 hours. At the time of randomisation, patients had to be on 0.1 mcg/kg/min noradrenaline and tachycardic (HR>=95 bpm).
We treated 63 patients with standard care and 63 patients with standard care and landiolol to control the heart rate between 80 and 94.
Our primary outcome was Mean SOFA Score over 14 days whilst in ICU. There was no difference between groups in our primary outcome.
The study was halted early after 126 of an expected 340 participants as the intervention was unlikely to display benefit and could be harmful.
This last bit has been widely shared.
Similar trials in the field are Morelli (JAMA 2013) https://jamanetwork.com/journals/jama/fullarticle/1752246 and J-Land 3S (Kakihana, Lancet Resp Med, 2020) https://www.thelancet.com/journals/lanres/article/PIIS2213-2600(20)30037-0.
Morelli used esmolol but added levosimendan to patients who had a significant fall in cardiac output. J-Land 3S used landiolol but earlier than 24 hours (whereas STRESS-L treated AFTER 24 hours of noradrenaline).
To determine whether treating critically ill patients with severe septic shock with esmolol, a short-acting β-blocker, to reduce their heart rates, Morelli and coauthors conducted an open-label, randomized phase 2 study, involving 154 qualifying patients treated at a university hospital intensive...
I suppose I wonder what would make a difference (if any).
Positive inotropy? With Levosimendan? Does it matter??
Earlier application of the intervention?
Less Beta1 specificity?
It's sometimes frustrating when researchers say "we need more studies" but...
ENDS
Tony Whitehouse
Lars Mølgaard Saxhaug