https://ogma.newcastle.edu.au/vital/access/ /manager/Index en-au 5 https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:46485 70 ml (n = 9), and no perfusion lesion/lack of penumbral tissue (n = 20). The revised perfusion lesion volumes were significantly smaller compared to the original RAPID volumes (median 68 ml IQR 34–102 ml vs. 42 ml 16–92 ml, p = 0.036). Of the patients who met the revised mismatch criteria, 40% receiving alteplase had modified Rankin Scale (mRS) 0–1 at 3-month compared to 28% with placebo (Adjusted Odds Ratio (OR) = 2.23, CI 1.08–4.58, p = 0.028). In contrast, in the original mismatch cohort, 35% receiving alteplase had mRS 0–1 at 3-month compared to 30% with placebo (adjusted OR = 1.88, p = 0.056). Conclusions: These data reinforce the benefit of alteplase in the later time window, and suggest that differences in automated perfusion imaging software outputs may be clinically relevant.]]> Wed 13 Mar 2024 07:51:52 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:49270 Wed 10 May 2023 12:03:17 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:41666 Wed 10 Aug 2022 12:13:25 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:56246 Tue 20 Aug 2024 16:04:27 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:31435 P < 0.001). For every millilitre of penumbra salvaged, 7.2 days of disability-adjusted life-year days were saved (ß = -7.2, 95% confidence interval, -10.4 to -4.1 days, P < 0.001). Each minute of earlier onset-to-treatment time resulted in a saving of 4.4 disability-free days after stroke (1.3-7.5 days, P = 0.006). However, after adjustment for imaging variables, onset-to-treatment time was not significantly associated with savings in disability-adjusted life-year days. Pretreatment perfusion computed tomography can (independently of clinical variables) predict significant gains, or loss, of disability-free life in patients undergoing reperfusion therapy for stroke. The effect of earlier treatment on disability-free life appears explained by salvage of penumbra, particularly when the ischaemic core is not too large.]]> Thu 17 Feb 2022 09:30:10 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:31270 Thu 09 Dec 2021 11:04:26 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:21715 Sat 24 Mar 2018 08:06:26 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:17780 1.2 and total coregistered mismatch volume was ≥10 mL. The primary outcome was a comparison of infarct growth in alteplase vs placebo patients with coregistered mismatch. Of 99 patients with baseline diffusion-weighted imaging and perfusion-weighted imaging, coregistration of both images was possible in 95 patients. Coregistered mismatch was present in 93% (88/95) compared to 85% (81/95) with standard volumetric mismatch. In the coregistered mismatch patients, of whom 45 received alteplase and 43 received placebo, the primary outcome measure of geometric mean infarct growth was significantly attenuated by a ratio of 0.58 with alteplase compared to placebo (1.02 vs 1.77; 95% CI, 0.33–0.99; P=0.0459). When using coregistration techniques to determine the presence of mismatch at study entry, alteplase significantly attenuated infarct growth. This highlights the necessity for a randomized, placebo-controlled, phase III clinical trial of alteplase using penumbral selection beyond 3 hours.]]> Sat 24 Mar 2018 07:57:41 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:17758 Sat 24 Mar 2018 07:57:21 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:19971 Sat 24 Mar 2018 07:54:29 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:26876 Sat 24 Mar 2018 07:41:43 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:27117 Sat 24 Mar 2018 07:41:36 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:23444 Sat 24 Mar 2018 07:13:32 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:23824 1·2, and absolute mismatch >10 ml) will be randomized to either tissue plasminogen activator or placebo. Study outcome: The primary outcome measure will be modified Rankin Scale 0–1 at day 90. Clinical secondary outcomes include categorical shift in modified Rankin Scale at 90 days, reduction in the National Institutes of Health Stroke Score by 8 or more points or reaching 0–1 at day 90, recurrent stroke, or death. Imaging secondary outcomes will include symptomatic intracranial haemorrhage, reperfusion and or recanalization at 24 h and infarct growth at day 90.]]> Sat 24 Mar 2018 07:12:50 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:23766 Sat 24 Mar 2018 07:11:08 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:55776 Sat 22 Jun 2024 12:11:18 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:44500 7, intracerebral haemorrhage volume <70 mL, no identified or suspected secondary cause of intracerebral haemorrhage, no thrombotic events within the previous 12 months, no planned surgery in the next 24 h, and no use of anticoagulation), had contrast extravasation on CT angiography (the so-called spot sign), and were treatable within 4·5 h of symptom onset and within 1 h of CT angiography. Patients were randomly assigned (1:1) to receive either 1 g of intravenous tranexamic acid over 10 min followed by 1 g over 8 h or matching placebo, started within 4·5 h of symptom onset. Randomisation was done using a centralised web-based procedure with randomly permuted blocks of varying size. All patients, investigators, and staff involved in patient management were masked to treatment. The primary outcome was intracerebral haemorrhage growth (>33% relative or >6 mL absolute) at 24 h. The primary and safety analyses were done in the intention-to-treat population. The trial is registered at ClinicalTrials.gov (NCT01702636). Findings: Between March 1, 2013, and Aug 13, 2019, we enrolled and randomly assigned 100 participants to the tranexamic acid group (n=50) or the placebo group (n=50). Median age was 71 years (IQR 57-79) and median intracerebral haemorrhage volume was 14·6 mL (7·9-32·7) at baseline. The primary outcome was not different between the two groups: 26 (52%) patients in the placebo group and 22 (44%) in the tranexamic acid group had intracerebral haemorrhage growth (odds ratio [OR] 0·72 [95% CI 0·32-1·59], p=0·41). There was no evidence of a difference in the proportions of patients who died or had thromboembolic complications between the groups: eight (16%) in the placebo group vs 13 (26%) in the tranexamic acid group died and two (4%) vs one (2%) had thromboembolic complications. None of the deaths was considered related to study medication. Interpretation: Our study does not provide evidence that tranexamic acid prevents intracerebral haemorrhage growth, although the treatment was safe with no increase in thromboembolic complications. Larger trials of tranexamic acid, with simpler recruitment methods and an earlier treatment window, are justified. Funding: National Health and Medical Research Council, Royal Melbourne Hospital Foundation.]]> Mon 13 Nov 2023 13:34:03 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:41084 Fri 22 Jul 2022 17:11:20 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:41586 Fri 05 Aug 2022 14:51:46 AEST ]]>