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Background: Randomized-controlled trials have shown no beneficial short-term effects of blood pressure lowering treatment in the acute phase of stroke., Aim: We aimed to see whether blood pressure lowering treatment with candesartan in the acute phase can lead to benefits that become apparent over a longer period of follow-up., Methods: The Scandinavian Candesartan Acute Stoke Trial was a randomized- and placebo-controlled trial of candesartan in 2,029 patients with acute stroke and systolic blood pressure ≥140 mmHg. Trial treatment was given for seven-days, and the primary follow-up period was six-months. We have used the national patient registries and the cause of death registries in the Scandinavian countries to collect data on vascular events and deaths up to three-years from randomization. The primary end-point was the composite of stroke, myocardial infarction, or vascular death, and we used Cox proportional hazards regression model for analysis., Results: Long-term data were available for 1,256 of the 1,286 patients (98%) from Scandinavia. The risk of the primary composite end-point did not differ significantly between the groups (candesartan 178/632 events, placebo 203/624 events, hazard ratio = 0·87, 95% confidence interval 0·71-1·07). There were also no statistically significant differences for the secondary end-points stroke and all-cause death, or in any of the pre-specified subgroups., Conclusions: Treatment with candesartan in the acute phase of stroke was not associated with clear long-term clinical benefits. This result supports the conclusion from trials with short-term follow-up, that blood pressure lowering treatment with candesartan should not be given routinely to patients with acute stroke and raised blood pressure., (© 2015 World Stroke Organization.)

Background: The Scandinavian Candesartan Acute Stroke Trial (SCAST) showed no beneficial clinical effects of blood pressure lowering with the angiotensin receptor blocker candesartan in the acute phase of stroke. In the present analysis we wanted to see if the effects of blood pressure lowering are harmful in the subgroup of patients with carotid artery stenosis., Methods: SCAST was a randomized- and placebo-controlled, double-masked trial of 2029 patients with acute stroke and high systolic blood pressure (≥ 140 mmHg). Of 1733 patients with ischemic stroke 993 underwent carotid artery imaging, and the degree of stenosis was categorized as no/insignificant (0-49%, n = 806), moderate (50-69%, n = 97) or severe (≥ 70%, n = 90). The trial's two co-primary effect variables were the composite end-point of vascular death, stroke or myocardial infarction, and functional outcome at six-months, according to the modified Rankin Scale., Results: Among patients with moderate or severe carotid artery stenosis the vascular end-point occurred in 9 of 87 patients (10.3%) treated with candesartan and in 17 of 100 controls (17.0%), and there was no evidence of a different risk in patients with severe stenosis (adjusted hazard ratio 0.74, 95% confidence interval 0.28-1.96, P = 0.54). For functional outcome there was also no clear difference, although in patients with severe stenosis the risk of a poor outcome was somewhat higher than in any of the other groups (adjusted odds ratio 2.24, 95% confidence interval 0.71-7.09, P = 0.16). Progressive stroke also occurred more often in patients with carotid artery stenosis treated with candesartan (10 of 87 patients (11.5%) vs. 4 of 100 patients (4.0%)), with a trend towards an increased risk with increasing severity of stenosis (P-value for linear trend = 0.04)., Conclusions: There is no clear evidence that the effect of candesartan is qualitatively different in patients with carotid artery stenosis, but there are signals that patients with severe stenosis are at particularly high risk of stroke progression and poor functional outcome., (© 2014 World Stroke Organization.)

Introduction: The National Institutes of Health Stroke Scale (NIHSS) and Scandinavian Stroke Scale (SSS) are both validated measures of neurologic impairment and have been used in many acute stroke trials. Methods for interconverting SSS and NIHSS are needed., Methods: Conversion equations were developed using linear regression (both unadjusted, and adjusted for age and sex) using a random 50% of the data at both baseline and 90 days. The remaining 50% of data were used to test the accuracy of the models produced., Results: Data from 5 acute stroke trials (2004 patients) were included. Fitted models at baseline were NIHSS = 25.68 - 0.43 * SSS (R(2) = 0.57, prediction error [PE] -0.2, P = .20), and SSS = 50.37 - 1.63 * NIHSS (R(2) = 0.59, PE 0.2, P = .35). The 90-day models were NIHSS = 22.99 - 0.39 * SSS (R(2) = 0.82, PE -0.3, P = .001), and SSS = 56.68 - 2.20 * NIHSS (R(2) = 0.80, PE -0.4, P = .08). Adjustment did not materially improve the R(2) values., Conclusion: Total scores for NIHSS and SSS may be interconverted with good precision; the mathematic conversion equations may prove useful in clinical practice and in comparison of data from observational studies and randomized trials.