https://nova.newcastle.edu.au/vital/access/ /manager/Index ${session.getAttribute("locale")} 5 https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:22216 Wed 11 Apr 2018 14:00:50 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:35216 .05). Conclusion: White matter changes after stroke may be localized rather than a global phenomenon.]]> Wed 06 Apr 2022 13:57:07 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:31270 Thu 09 Dec 2021 11:04:26 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:24016 Thu 04 Nov 2021 10:39:04 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:9613 Sat 24 Mar 2018 08:39:38 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:9555 1.2, was independently scored by 1 expert and 2 inexperienced raters blinded to calculated volumes and clinical information. Visual mismatch was compared with region-of-interest-based volumetric calculation, which was used as the gold standard. Results: Volumetric calculation demonstrated perfusion-diffusion mismatch in 85/99 patients. Visual TTP-DWI mismatch was correctly classified by the experienced rater in 82% of the cases (sensitivity: 0.86; specificity: 0.54) compared to 73% for the inexperienced raters (sensitivity: 0.75; specificity: 0.57). The interrater reliability for TTP-DWI mismatch was moderate (к= 0.50). Visual T max -DWI mismatch performed better (agreement – 93 and 87%, sensitivity – 95 and 88%, specificity – 77 and 82% for the experienced and inexperienced raters, respectively). Conclusions: The assessment of visual TTP-DWI mismatch at the MRI console is insufficiently reliable for use in clinical trials. Differences in perfusion analysis technique and visual inaccuracies combine to make visual TTP-DWI mismatch substantially different to volumetric T max -DWI mismatch. Automated software that applies perfusion thresholds may improve the reproducibility of real-time mismatch assessment.]]> Sat 24 Mar 2018 08:34:38 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:16030 Sat 24 Mar 2018 08:21:18 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:10749 Sat 24 Mar 2018 08:08:20 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:21715 Sat 24 Mar 2018 08:06:26 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:21405 P=0·03) and a trend to lower absolute growth (-0·17ml versus 9·6ml, P=0·07). Reperfusion was increased in the tissue plasminogen activator group (58% versus 25%, P=0·03) and was associated with increased rates of good neurological (86% versus 28% P<0·001) and functional (modified Rankin scale 0-2 73% versus 34%, P=0·01) outcomes. Reperfusion was strongly associated with lower relative (80% versus 189%, P<0·001) and absolute (-2·5ml versus 40ml, P<0·001) infarct growth. Conclusions: Thrombolysis 4·5-6h after stroke onset reduced infarct growth and increased the rate of reperfusion, which was associated with good neurological and functional outcome.]]> Sat 24 Mar 2018 08:05:00 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:19908 max) with PH was examined using receiver operating characteristic analysis and multivariate logistic regression. Result: Of 132 patients, 70 were treated with thrombolysis, and 14 (10.6%) developed PH on follow-up imaging. Baseline National Institutes of Health Stroke Scale score (P=0.033) and thrombolysis (P=0.003) were both predictive of PH. Receiver operating characteristic analysis revealed that T_max>14 s (area under the curve=0.748; P=0.002) and relative cerebral blood flow <30% of contralateral mean (area under the curve=0.689, P=0.021) were the optimal thresholds, and the Bayesian information criterion (+2.6) indicated that T_max was more strongly associated with PH than relative cerebral blood flow. T_{max14 s volumes of >5 mL allowed prediction of PH with sensitivity of 79%, specificity of 68%, and negative likelihood ratio of 3.16. Tmax>14 s volume and thrombolysis were both independently predictive of PH in a multivariate logistic regression model (P<0.05). Conclusions: Tmax >14 s was the CTP parameter most strongly associated with PH. This outperformed relative cerebral blood flow <30%, which closely equates to CTP estimates of ischemic core volume. Although ischemic core volume on CTP is useful in the pretreatment prediction of PH, severe hypoperfusion on Tmax is more strongly associated and may allow better prediction of the likely anatomic location of hemorrhage.]]>} Sat 24 Mar 2018 08:03:47 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:20340 6 seconds, ratio>1.2) in 3/119 (2.5%) patients. Diffusion lesion reversal between baseline and 3 to 6 hours DWI was also uncommon (7/65, 11%) and often transient. Clinically relevant DLR is uncommon and rarely alters perfusion-diffusion mismatch. The acute diffusion lesion is generally a reliable signature of the infarct core.]]> Sat 24 Mar 2018 08:02:57 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:21179 4 seconds for lesion region of interest. The MR-Tmax >6 seconds perfusion lesion was automatically segmented and registered to CTP. Receiver-operating characteristic analysis determined the optimal CT-Tmax threshold to match MR-Tmax >6 seconds. Agreement of these CT parameters with MR perfusion-diffusion mismatch in coregistered slabs was assessed (mismatch ratio >1.2, absolute mismatch >10 mL, infarct core <70 mL). Results: In analysis of 49 patients (mean onset to CT, 213 minutes; mean CT to MR, 31 minutes), constraining relCBF <31% within the automated relTTP perfusion lesion region of interest reduced the median magnitude of volumetric error (vs diffusion-weighted imaging) from 47.5 mL to 15.8 mL (P<0.001). The optimal CT-Tmax threshold to match MR-Tmax >6 seconds was 6.2 seconds (95% confidence interval, 5.6–7.3 seconds; sensitivity, 91%; specificity, 70%; area under the curve, 0.87). Using CT-Tmax >6 seconds “penumbra” and relTTP-constrained relCBF “core,” CT-based and MRI-based mismatch status was concordant in 90% (kappa=0.80). Conclusions: Quantitative CTP mismatch classification using relCBF and Tmax is similar to perfusion-diffusion MRI. The greater accessibility of CTP may facilitate generalizability of mismatch-based selection in clinical practice and trials.]]> Sat 24 Mar 2018 07:58:05 AEDT ]]> https://nova.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://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:16967 Sat 24 Mar 2018 07:55:24 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:19728 P<0.001) and smaller baseline diffusion lesion volume (Rho −0.70, P<0.001). In 30 patients without reperfusion at day 3 to 5, deterioration in collateral quality between baseline and subacute imaging was strongly associated with absolute (P=0.02) and relative (P<0.001) infarct growth. The deterioration in collateral grade correlated with increased mean Tmax hypoperfusion severity (Rho −0.68, P<0.001). Deterioration in Tmax hypoperfusion severity was also significantly associated with absolute (P=0.003) and relative (P=0.002) infarct growth. Collateral flow is dynamic and failure is associated with infarct growth.]]> Sat 24 Mar 2018 07:53:45 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:19726 2 ml VLCBV threshold defined in EPITHET predicted PH with 100% sensitivity, 72% specificity, 35% positive predictive value, and 100% negative predictive value. Pooling EPITHET and DEFUSE (163 patients, including 23 with PH), regression models using VLCBV (p<0.001) and tPA (p=0.02) predicted PH independent of clinical factors better than models using diffusion or time to maximum>8 seconds lesion volumes. Excluding VLCBV in regions without reperfusion improved specificity from 61 to 78% in the pooled analysis. Interpretation: VLCBV predicts PH after stroke thrombolysis and appears to be a more powerful predictor than baseline diffusion or hypoperfusion lesion volumes. Reperfusion of regions of VLCBV is strongly associated with post-thrombolysis PH. VLCBV may be clinically useful to identify patients at significant risk of hemorrhage following reperfusion.]]> Sat 24 Mar 2018 07:53:44 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:19328 Sat 24 Mar 2018 07:52:14 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:21366 4 to >8 s. Hemorrhagic transformation was classified according to the European Cooperative Acute Stroke Studies criteria. Results: Of the 175 patients, 28 had definite atrial fibrillation, 30 probable atrial fibrillation, 111 no atrial fibrillation, and six were excluded due to insufficient imaging data. At baseline, patients with definite atrial fibrillation had more severe hypoperfusion (median time to maximum >8 s, volume 48 vs. 29 ml, P = 0·02) compared with patients with no atrial fibrillation. At outcome, patients with definite atrial fibrillation had greater infarct growth (median volume 47 vs. 8 ml, P = 0·001), larger infarcts (median volume 75 vs. 23 ml, P = 0·001), more frequent parenchymal hematoma grade hemorrhagic transformation (30% vs. 10%, P = 0·03), worse functional outcomes (median modified Rankin scale score 4 vs. 3, P = 0·03), and higher mortality (36% vs. 16%, P = 0·03) compared with patients with no atrial fibrillation. Definite atrial fibrillation was independently associated with increased parenchymal hematoma (odds ratio = 6·05, 95% confidence interval 1·60–22·83) but not poor functional outcome (modified Rankin scale 3–6, odds ratio = 0·99, 95% confidence interval 0·35–2·80) or mortality (odds ratio = 2·54, 95% confidence interval 0·86–7·49) three-months following stroke, after adjusting for other baseline imbalances. Conclusion: Atrial fibrillation is associated with greater volumes of more severe baseline hypoperfusion, leading to higher infarct growth, more frequent severe hemorrhagic transformation and worse stroke outcomes.]]> Sat 24 Mar 2018 07:51:25 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:27117 Sat 24 Mar 2018 07:41:36 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:27975 Sat 24 Mar 2018 07:38:43 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:26463 1). Results: Overall, 152 patients (82 left hemisphere) were included. Median diffusion lesion volume was 37.0 ml, and median baseline National Institutes of Health Stroke Score was 13. In the left hemisphere, the strongest determinants of nonfavorable outcome were infarction of the uncinate fasciculus, followed by precuneus, angular gyrus and total diffusion lesion volume. In the right hemisphere, the strongest determinants of nonfavorable outcome were infarction of the parietal lobe followed by the putamen. Conclusions: Assessment of infarct location using CART demonstrates regional characteristics associated with poor outcome. Prognostically important locations include limbic, default-mode and language areas in the left hemisphere, and visuospatial and motor regions in the right hemisphere.]]> Sat 24 Mar 2018 07:27:16 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:28115 Sat 24 Mar 2018 07:24:58 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:41084 Fri 22 Jul 2022 17:11:20 AEST ]]>