AnStroke 2017.

Study characteristics
Methods	Setting: single‐centre, Sweden Design: RCT, 2 arms, parallel assignment, single‐blind Start date: 14 November 2013 (reported in protocol) Completion date: 30 September 2016 (reported in protocol)
Participants	106 men and women randomised: experimental (GA) = 54 and comparator (CSA) = 52; procedure interrupted in GA = 8 and CSA = 7; 1 consent withdrawn in GA arm and 0 lost to follow‐up, 90 analysed Mean age: 72 years (range: 65–80 years) Gender (men/women): 49/51 Mean NIHSS score: 18 (score range: 15–22) Mean ASPECTS: 10 (score range: 8–10) 7 (15.6%) participants were converted from CSA to GA 66 (73.3%) participants received IV r‐tPA before EVT  Diagnostic criteria: AIS with LVO in anterior cerebral circulation  Inclusion criteria Aged ≥ 18 years Confirmed occlusion in anterior cerebral circulation by CTA and NIHSS score ≥ 10 (if right‐sided occlusion) or ≥ 14 (if left‐sided occlusion) Treatment initiated within 8 hours after onset of symptoms  Exclusion criteria Not eligible for randomisation because of anaesthesiological concerns (airway, agitation, etc.) at the discretion of the attending anaesthetist Occlusion of posterior cerebral circulation intracerebral haemorrhage Neurological recovery or recanalisation before or during angiography Premorbidity mRS score ≥ 4 or other comorbidities contraindicating embolectomy
Interventions	Experimental: GA Induced by propofol and remifentanil, maintained with sevoflurane and remifentanil, and aiming for normoventilation  Comparator: CSA performed by remifentanil infusion Blood pressure monitoring SBP, DBP, MAP recorded every 5 minutes from before start of induction of anaesthesia until extubation in neurointerventional suite. Last recorded MAP before induction of anaesthesia was defined as baseline MAP. Intraprocedural MAP expressed as fractions of baseline MAP. Occurrence of > 20% and > 40% fall in MAP from baseline was noted, and total time spent under these limits was calculated. Dopamine, ephedrine, phenylephrine, or noradrenaline was used for inotropic and vasoactive treatment at the discretion of the attending anaesthesiologist. Treatment goal was SBP 140–180 mmHg in all participants before recanalisation. Excluded medications: not reported
Outcomes	Primary outcome (specified) Neurological outcome in the 2 different arms (time frame: 90 days) Neurological outcome measured as mRS, 90 days poststroke Primary outcome (collected) Neurological outcome in the 2 different arms. Neurological outcome measured as mRS, 90 days poststroke Secondary outcomes (specified) NIHSS. Change in NIHSS score on day 3, day 7, and 3 months compared to admission to hospital Degree of recanalisation and reperfusion (time frame: 1 day (after completed embolectomy)). Measured as modified TICI score Periprocedural complications (time frame: perioperatively) Infarction magnitude (time frame: day 1 to day 90). CT scan day 1 including CT perfusion MRI on day 3 (2–4) and 3 months brain damage markers (GFAP, Tau, S‐100B) before, 2, 24, 48, 72 hours, and 3 months after the procedure Quantitative EEG changes days 1, 2, and 3 months after onset Time consumption from: stroke onset to CTA, CTA to start of anaesthesia/sedation, stroke onset to start of embolectomy, and duration of embolectomy Hospital length of stay (time frame: approximately 7–14 days) Secondary outcomes (collected) NIHSS. Change in score 24 hours after procedure, day 3, days 4–7, or at hospital discharge Degree of recanalisation and reperfusion 1 day after completed embolectomy. Measured as mTICI score Hospital mortality MRI day 3 cerebral infarction volume (infarction magnitude at 3 months was not collected)  Mortality at 3 months New stroke detected clinically and with MRI/CT at 3 months  There was no collected hospital length of stay
Notes	Conflicts of interest: (quote) "none". Funding: (quote) "The study was supported by Swedish State Support for Clinical Research (ALFGBG‐75130 and ALFGBG‐590861), The Gothenburg Medical Society, John and Britt Wennstroms/Per‐Olof Ahls Fund, Sahlgrenska University Hospital Foundations, and Swedish Stroke Association". Protocol: NCT01872884
Risk of bias
Bias	Authors' judgement	Support for judgement
Random sequence generation (selection bias)	Low risk	Quote: "patients were randomly allocated in blocks to either GA or CS".
Allocation concealment (selection bias)	Low risk	Quote: "1:1 ratio using sealed non‐transparent envelopes".
Blinding of participants and personnel (performance bias)	High risk	Not described, but due to the nature of the interventions, we assumed that blinding of personnel was not possible.
Blinding of outcome assessment (detection bias)	Low risk	Quote: "The review of the neuroradiologic and angiographic data was done by experienced neuroradiologists, blinded to neurological outcome". Quote: "A vascular neurologist, blinded to treatment allocation and mTICI score, assessed mRS score by direct examination (n = 81, 90%) or by telephone interview (n = 9, 10%) 3 months after stroke".
Incomplete outcome data (attrition bias)	High risk	There were no losses. Crossover occurred in 7 (15.6%) participants who were converted from CSA to GA.
Selective reporting (reporting bias)	Low risk	All prespecified outcomes were reported.
Other bias	Low risk	No evidence of other bias related to this study.