Lynnette Murray.

D. James Cooper, M.D ., Jeffrey V. Rosenfeld, M.D., Lynnette Murray, B.App.Sci., Yaseen M. Arabi, M.D., Andrew R. Davies, M.B., B.S., Paul D’Urso, Ph.D., Thomas Kossmann, M.D., Jennie Ponsford, Ph.D., Ian Seppelt, M.B., B.S., Peter Reilly, M.D., and Rory Wolfe, Ph.D. For the DECRA Trial Investigators and the Australian and New Zealand Intensive Care Society Clinical Trials Group: Decompressive Craniectomy in Diffuse Traumatic Brain Injury Among patients who are hospitalized with severe traumatic brain injury, 60 percent either die or survive with serious disability.1-3 Of Australia’s population of 22 million,4 approximately 1000 patients annually sustain a severe traumatic brain injury, with associated lifetime costs estimated in $1 billion.5 In the United States, the annual burden of traumatic brain injury is a lot more than $60 billion.6 After severe traumatic brain injury, medical and surgical therapies are performed to reduce secondary brain injury.7-9 Increased intracranial pressure, which is due to cerebral edema typically, is an important secondary insult.7,9,10 Although few data regarding the monitoring of intracranial pressure can be found from randomized, controlled trials, such monitoring is preferred by international scientific practice suggestions, and first-tier therapies are accustomed to control intracranial pressure.11 However, many individuals with severe traumatic brain injury possess raised intracranial pressure that is refractory to first-tier therapies.11,12 In such instances, surgical decompressive craniectomy is conducted with increasing frequency to regulate intracranial pressure.10 We designed the multicenter, randomized, controlled Decompressive Craniectomy trial13,14 to check the efficacy of bifrontotemporoparietal decompressive craniectomy in adults under the age of 60 years with traumatic brain injury in whom first-tier intensive care and neurosurgical therapies had not preserved intracranial pressure below recognized targets.

Lately, several clinical trials have shown that the prices of target-lesion revascularization and myocardial infarction were higher with the paclitaxel-eluting stent that was found in the SYNTAX trial than with the second-era everolimus-eluting stent.25,26 Whether use of everolimus-eluting stents could have reduced or even eliminated the benefit of CABG over PCI with regards to the extent of relief from angina through the first year following the treatment is unknown. Finally, there were differences in the usage of both calcium-channel blockers and long-acting nitrates through the follow-up period, which may have mitigated the benefits of CABG regarding angina and other health status measures. In conclusion, among patients with still left or three-vessel primary coronary artery disease who were suitable candidates for either PCI or CABG, both strategies resulted in significant relief from angina and improvements in overall health status over the initial year of follow-up.