ObjectiveTo compare transradial artery access (TRA) to the gold standard of transfemoral artery access (TFA) in mechanical thrombectomy (MT) for stroke caused by anterior circulation large vessel occlusion.MethodsThe clinical outcomes, procedural speed, angiographic efficacy and safety of both techniques were analysed in 375 consecutive cases over an 18-month period in a high volume statewide neurointerventional service.ResultsThere was no significant difference in patient characteristics, stroke parameters, imaging techniques or intracranial techniques. The median time elapsed between CT scanning and reperfusion was 96.5 min (IQR 68–123) in the TFA group and 95 min (IQR 68–123) in the TRA group (p=0.456). Of 336 patients who were independent at presentation 58% (124/214) of the TFA group and 67% (82/122) of the TRA group had a modified Rankin score of 0–2 at 90-day follow-up (p=0.093). Cross-over from radial to femoral was 4.6% (4/130) compared with 1.6% cross-over from femoral to radial (4/245), but did not meet the predetermined level of statistical significance (OR 2.92, 95% CI 0.81 to 10.52), p=0.088) and did not impact median procedural speed. Adequate angiographic reperfusion, first pass reperfusion, embolisation to new territory and symptomatic intracranial haemorrhage were similar in both groups. There was a significant difference in major access site complications requiring an additional procedure. None of the TRA cases had a major access site complication but 6.5% (16/245) of the TFA cases did (p=0.003).ConclusionThis study suggests that using TRA for anterior circulation MT is fast, efficacious, safe and not inferior to the gold standard of TFA.

1 The mechanism of flecainide-induced unexpected death remains uncertain. Phase-2 ventricular arrhythmias occur during infarct evolution. We examined whether flecainide (0.74 and 1.48 mM, representing the peak unbound plasma and total blood concentrations, respectively, at 'therapeutic' dosage) has proarrhythmic activity on phase-2 arrhythmia susceptibility during infarct evolution. 2 To achieve this, we used the Langendorff-perfused rat heart preparation (n ¼ 8 per group) in which baseline phase-2 arrhythmia susceptibility is low. Left main coronary occlusion evoked phase-1 (acute ischaemia-induced) ventricular arrhythmias including fibrillation (VF) in all hearts. By 90 min, hearts were relatively arrhythmia-free. 3 Randomized and blinded switch of perfusion to flecainide at 90 min caused no increase over baseline in the incidence of VF, tachycardia (VT) or premature beats (VPB) during the following 150 min of ischaemia, or during reperfusion (begun 240 min after the onset of ischaemia). 4 In separate hearts, catecholamines (313 nM norepinephrine and 75 nM epinephrine) were coperfused with flecainide from 90 min of ischaemia. Catecholamine perfusion increased heart rate, coronary flow and QT interval, and shortened PR interval (all Po0.05), actions that were not altered by flecainide. Catecholamine perfusion caused a weak nonsignificant increase in phase-2 VPB, VT and VF incidence, but there was no proarrhythmic interaction with flecainide. 5 In conclusion, the present findings suggest that the increased risk of death associated with clinical use of flecainide is not due to facilitation of phase-2 ventricular arrhythmias.