Study finds no difference in survival when lowering cardiac arrest patients’ temperature to 33°C vs. 36°C
American Heart Association Late-Breaking Clinical Trial Report LBCT 1/Abstract: 17279 (Hall E)
- Lowering cardiac arrest patients’ body temperature to 33°C compared to 36°C made no difference in survival in an international study of more than 900 patients.
- The lower temperature was potentially associated with more side effects.
- Lowering cardiac arrest patients’ body temperature is standard treatment to protect the brain.
DALLAS, Nov. 17, 2013 — Lowering cardiac arrest patients’ body temperatures to 33°C (91.4°F) instead of 36°C (96.8°F) did not improve survival or neurological/cognitive function in a late-breaking clinical trial presented at the American Heart Association’s Scientific Sessions 2013.
Cardiac arrest causes the heart to stop suddenly. With no blood flow or oxygen getting to the brain, nerve cells begin to die. The brain injury can continue to evolve even after the blood flow is restored; this is called reperfusion injury.
To help protect the brain, guidelines recommend cooling resuscitated cardiac arrest patients who remain comatose soon after hospital arrival in a process called therapeutic hypothermia. Body temperature is then slowly raised to normal levels.
In the Target Temperature Management After Cardiac Arrest (TTM) Trial, the largest trial to-date to study hypothermia in cardiac arrest patients, researchers looked at outcomes of 939 patients treated in 36 intensive care units in Sweden, Denmark, the United Kingdom, Netherlands, Italy, Norway, Switzerland, Australia, Luxembourg and the Czech Republic. They randomly chose half the patients to be cooled to 33°C and the other half to 36°C.
At end of the trial, about half of the patients in each group had died: 50 percent in the 33°C group and 48 percent in the 36°C group. After six months, 54 percent of the lower temperature group had died or had poor neurological outcomes, compared to 52 percent in the warmer temperature group.
Although the colder temperature was associated a numerical increase in side effects, the difference was not significant. More patients cooled to 33°C (93 percent) had side effects including pneumonia, electrolyte disturbances and bleeding, compared to those cooled to 36°C (90 percent).
“Given these findings, we may need to re-examine current guidelines” said Niklas Nielsen, M.D., Ph.D., the study’s lead author and a consultant in intensive care medicine in the Department of Anesthesia and Intensive Care at Helsingborg Hospital and Lund University in Sweden.
The American Heart Association and International Liaison Committee on Resuscitation (ILCOR) currently recommend lowering body temperature to 32ºC-34ºC (89.6ºF-93.2ºF). A Late-Breaking Clinical Trial presented at the American Heart Association’s Scientific Sessions 2012 found in a very small study population that cooling patients to 32°C was associated with a better chance of survival and greater functional ability after recovery than cooling them to 34°C.
“We won’t let the results swing the pendulum the other way and have no temperature control,” Nielsen said. “Our findings suggest that milder temperature control is equally beneficial and may avoid some of the side effects we saw, but the optimal temperature remains unclear.”
Researchers next will examine subgroups of patients within the study to see if any may benefit from the lower cooling temperature, Nielsen said.
Co-authors are Jørn Wetterslev, M.D., Ph.D.; Tobias Cronberg, M.D., Ph.D.; David Erlinge, M.D., Ph.D.; Yvan Gasche, M.D.; Christian Hassager, M.D., D.M.Sci.; Janneke Horn, M.D., Ph.D.; Jan Hovdenes, M.D., Ph.D.; Jesper Kjaergaard, M.D., D.M.Sci.; Michael Kuiper, M.D., Ph.D.; Tommaso Pellis, M.D.; Pascal Stammet, M.D.; Michael Wanscher, M.D., Ph.D.; Matt P. Wise, M.D., D.Phil.; Anders Åneman, M.D., Ph.D.; Nawaf Al-Subaie, M.D.; Søren Boesgaard, M.D., D.M.Sci.; John Bro-Jeppesen, M.D.; Iole Brunetti, M.D.; Jan Frederik Bugge, M.D., Ph.D.; Christopher D. Hingston, M.D.; Nicole P. Juffermans, M.D., Ph.D.; Matty Koopmans, R.N., M.Sc.; Lars Køber, M.D., D.M.Sci.; Jørund Langørgen, M.D.; Gisela Lilja, O.T.; Jacob Eifer Møller, M.D., D.M.Sci.; Malin Rundgren, M.D., Ph.D.; Christian Rylander, M.D., Ph.D.; Ondrej Smid, M.D.; Christophe Werer, M.D.; Per Winkel, M.D., D.M.Sci.; Hans Friberg, M.D., Ph.D. and the TTM-trial investigators. Disclosures
The study was funded by independent grants from the Swedish Heart Lung Foundation; AFA Insurance Foundation; Swedish Research Council, regional research support, Region Skåne; governmental funding of clinical research within the Swedish National Health Services; Thelma Zoega Foundation; Krapperup Foundation; Thure Carlsson Foundation; Hans-Gabriel and Alice Trolle-Wachtmeister Foundation; Skåne University Hospital; Sweden, TrygFonden, Denmark; and the European Clinical Research Infrastructures Network.
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Note: Actual presentation is 4:57 p.m. CT/5:57 p.m. ET, Sunday, Nov. 17, 2013, in Hall E.