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1.
  • Staaf, Gert, et al. (författare)
  • Pure motor stroke from presumed lacunar infarct - Long-term prognosis for survival and risk of recurrent stroke
  • 2001
  • Ingår i: Stroke: a journal of cerebral circulation. - American Heart Association. - 1524-4628. ; 32:11, s. 2592-2596
  • Tidskriftsartikel (refereegranskat)abstract
    • Background and Purpose-A low risk of recurrent stroke and death after lacunar infarction has previously been reported, but follow-up has been limited to less than or equal to5 years. Methods-One hundred eighty patients with pure motor stroke, collected between 1983 and 1986 from a hospital-based stroke registry, were followed up until at least 10 years after the index stroke. Two patients were lost to follow-up. Survival status was determined from the official population registry and compared with survival rates of the Swedish population, matched for age and sex. Cox proportional hazards regression analyses were used to identify independent prognostic predictors. Results-During follow-up 106 (60%) of the 178 patients died, most commonly as a result of coronary heart disease. During the first 5 years after the stroke, survival rates were similar to those of the general population. Beyond this time the risk of death was increased among patients with pure motor stroke, with an excess of 10 to 15 percent units compared with the general population. Independent determinants for death were age (P <0.01), male sex (P <0.01), and nonuse of acetylsalicylic acid (P=0.02). Recurrent stroke occurred in 42 (23.5%) of the patients, corresponding to an annual risk of 2.4%. Hypertension (P=0.025) and diabetes (P=0.024) were independent risk factors for recurrent stroke. Conclusions-For the first few years after lacunar infarct, the risk of death was similar to that of the general population, but later a clear excess of death was observed. The long-term prognosis in lacunar infarction appears less favorable than previously reported.
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  • Ahmed, Niaz, et al. (författare)
  • Effect of intravenous nimodipine on blood pressure and outcome after acute stroke
  • 2000
  • Ingår i: Stroke. - 0039-2499 .- 1524-4628. ; 31:6, s. 1250-1255
  • Tidskriftsartikel (refereegranskat)abstract
    • <p>Background and Purpose-The Intravenous Nimodipine West European Stroke Trial (INWEST) found a correlation between nimodipine-induced reduction in blood pressure (BP) and an unfavorable outcome in acute stroke. We sought to confirm this correlation with and without adjustment for prognostic variables and to investigate outcome in subgroups with increasing levels of BP reduction. Methods-Patients with a clinical diagnosis of ischemic stroke (within 24 hours) were consecutively allocated to receive placebo (n=100), 1 mg/h (low-dose) nimodipine (n=101), or 2 mg/h (high-dose) nimodipine (n=94). The correlation between average BP change during the first 2 days and the outcome at day 21 was analysed. Results-Two hundred sixty-five patients were included in this analysis (n=92, 93, and 80 for placebo, low dose, and high dose. respectively). Nimodipine treatment resulted in a statistically significant reduction in systolic BP (SBP) and diastolic BP (DBP) from baseline compared with placebo during the first few days. In multivariate analysis, a significant correlation between DBP reduction and worsening of the neurological score was round for the high-close group (beta=0.49, P=0.048). Patients with a DBP reduction of greater than or equal to 20% in the high-dose group had a significantly increased adjusted OR for the compound outcome variable death or dependency (Barthel Index &lt;60) (n/N=25/26, OR 10.16, 95% CI 1.02 to 101.74) and death alone (n/N=9/26, OR 4.3361 95% CI 1.131 16.619) compared with all placebo patients (n/N=62/92 and 14/92. respectively). There was no correlation between SEP change and outcome. Conclusions-DBP, but not SEP, reduction was associated with neurological worsening after the intravenous administration of high-dose nimodipine after acute stroke. For low-dose nimodipine, the results were not conclusive. These results do not confirm or exclude a neuroprotective property of nimodipine.</p>
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  • Aho, Leena, et al. (författare)
  • Beta-amyloid aggregation in human brains with cerebrovascular lesions.
  • 2006
  • Ingår i: Stroke. - 0039-2499 .- 1524-4628. ; 37:12, s. 2940-5
  • Tidskriftsartikel (refereegranskat)abstract
    • <p><strong>BACKGROUND AND PURPOSE:</strong> The present study assessed beta-amyloid (Abeta) protein aggregates in postmortem human brains in subjects who had experienced stroke to examine the proposed association between ischemic stress and the accumulation of Abeta reported in rodents.</p> <p><strong>METHODS:</strong> A sample of 484 postmortem brains from nondemented subjects, lacking isocortical neurodegenerative pathology with verified cerebrovascular lesions, and 57 age-matched controls were assessed with respect to Abeta, Abeta40, and Abeta42 aggregates in the cortex and thalamus by immunohistochemical techniques.</p> <p><strong>RESULTS:</strong> The load of Abeta aggregates did not display a significant association with cerebrovascular lesions. The load of Abeta, Abeta40, and Abeta42 aggregates increased with age, and there was a tendency toward higher odds ratios for Abeta aggregates, though not statistically significant, in subjects with acute cerebrovascular lesions. In the oldest subjects with cerebrovascular lesions and with both thalamic and cortical Abeta aggregates, the load of thalamic Abeta42 was significantly higher than the load of Abeta40.</p> <p><strong>CONCLUSIONS:</strong> Our findings indicate that cerebrovascular disease does not influence the load of Abeta, whereas a shift of aggregation from the Abeta40 to the Abeta42 residue is noted in the thalamus but only in aged subjects. It is impossible, however, to state whether this result is attributable to increased Abeta production, its insufficient elimination, or other susceptibility factors.</p>
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