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Background Since its approval, the use of alteplase had been limited to patients aged ≤80 years. Aims TESPI trial had been designed to evaluate whether alteplase treatment within 3 h in patients with acute ischemic stroke aged >80 years resulted in favorable benefit/risk ratio compared with standard care. The meta-analysis of randomized controlled trials was updated to put findings in the context of all available evidence. Methods TESPI was a multicenter, open-label with blinded outcome evaluation, randomized, controlled trial. Main clinical endpoints were 90-day favorable functional outcome (mRS score 0–2) and mortality and symptomatic intracerebral hemorrhage. The trial was prematurely terminated for ethical reasons after publication of IST-3 trial which provided evidence of treatment benefit in elderly. Results Of the planned 600 patients, 191 (88 assigned to alteplase) were enrolled. Overall, 24/83 (28.9%) alteplase patients had a favorable outcome compared to 22/95 (23.2%) controls (non-significant absolute difference of 5.7% for alteplase; OR 1.35, 95% CI 0.69–2.64, P = 0.381). Rates of death were non-significantly lower in the alteplase patients (18.1% vs. 26.5%); rates of symptomatic intracerebral hemorrhage were similar between the two groups (5.9% vs. 5.1%). The updated meta-analysis showed consistent results with prior estimates and add weights. Conclusions The effects of alteplase observed in this interrupted trial did not reach statistical significance, probably for the small numbers, but are consistent with and add weight to the sum total of the randomized evidence demonstrating that alteplase is beneficial in patients with acute ischemic stroke aged over 80 years, particularly if given within 3 h.

Objective: To assess the impact on stroke outcome of statin use in the acute phase after IV thrombolysis. Methods: Multicenter study on prospectively collected data of 2,072 stroke patients treated with IV thrombolysis. Outcome measures of efficacy were neurologic improvement (NIH Stroke Scale [NIHSS] ≤ 4 points from baseline or NIHSS = 0) and major neurologic improvement (NIHSS ≤ 8 points from baseline or NIHSS = 0) at 7 days and favorable (modified Rankin Scale [mRS] ≤ 2) and excellent functional outcome (mRS ≤ 1) at 3 months. Outcome measures of safety were 7-day neurologic deterioration (NIHSS ≥ 4 points from baseline or death), symptomatic intracerebral hemorrhage type 2 with NIHSS ≥ 4 points from baseline or death within 36 hours, and 3-month death. Results: Adjusted multivariate analysis showed that statin use in the acute phase was associated with neurologic improvement (odds ratio [OR] 1.68, 95% confidence interval [CI] 1.26-2.25; p < 0.001), major neurologic improvement (OR 1.43, 95% CI 1.11-1.85; p = 0.006), favorable functional outcome (OR 1.63, 95% CI 1.18-2.26; p = 0.003), and a reduced risk of neurologic deterioration (OR: 0.31, 95% CI 0.19-0.53; p < 0.001) and death (OR 0.48, 95% CI 0.28-0.82; p = 0.007). Conclusion: Statin use in the acute phase of stroke after IV thrombolysis may positively influence short- and long-term outcome. © 2013 American Academy of Neurology.

We performed angio-CT following i.v. administration of an iodinated contrast medium and analyzed the pixel contrast time-density curves from 4 to 10 min postinjection to derive vascular and volume BBB permeability images. This was performed by applying multiple regression analysis of pixel contrast curves versus blood contrast and integrated blood contrast curves. The two regression coefficients, mapped pixel by pixel, correspond respectively to vascular volume and BBB unidirectional transport rate. Initial application in a small number of normal subjects and patients allowed us to characterize areas of steady-state contrast enhancement according to changes of vascular volume and BBB permeability.

We performed a Cr dynamic study during the first pass of an intravenously injected bolus of a iodinated contrast medium, followed by generation of the regional arm-brain circulation time (rABCF) image, in 11 patients with vascular malformations. All lesions could be detected as changes of rABCT, and the comparison with values of normal arteries and veins allowed the deduction of the hemodynamic conditions of the lesions. Seven cases showed evidence of altered distribution of rABCT in the corresponding brain hemisphere, suggesting a perfusion reserve impairment.

To clarify the relationships between early hyperperfusion (i.e. the hallmark of early, efficient recanalization in animal stroke models) and ultimate infarction, we have compared acute-stage perfusion PET images and chronic-stage CT scans in patients with middle cerebral artery (MCA) stroke. We used PET and the oxygen-15 (15O) equilibrium method to obtain cerebral blood flow (CBF), cerebral blood volume (CBV), oxygen extraction fraction (OEF) and cerebral metabolic rate of oxygen consumption (CMRO2) parametric images in 30 consecutive, still symptomatic, first-ever MCA territory stroke patients without sign of haemorrhage at admission CT scan. Each subject was studied twice, first within 5-18 h of stroke onset, and, in survivors, approximately 1 month later; a plain CT scan (co-registered with PET) was performed approximately 1 month after onset. Following initial screening based on acute-stage perfusion images, 10 survivors with focal hyperperfusion in the appropriate MCA territory confirmed by computer were declared eligible. In each patient, the topography and volume of both hyperperfusion and infarction (delineated on late CT scan) were recorded, and all PET parameters were obtained for both areas and both times. The hyperperfused areas affected the cortical MCA territory, often widely so and in a patchy fashion; they were topographically distinct from, and consistently larger than (P < 0.01, Wilcoxon sign test) the final infarcts, which were small and generally deep-seated. In none of the nine patients in whom it was successfully performed did transcranial Doppler reveal MCA stem occlusion. In the hyperperfused regions, the acute-stage perfusion, blood volume and oxygen consumption were significantly increased, and the OEF significantly reduced, while all these variables had significantly returned toward normality in the chronic-stage PET study. The ultimately infarcted area did not exhibit significant hyperperfusion in the acute stage. The areas with acute-stage hyperperfusion exhibited haemodynamic and metabolic abnormalities consistent with post-recanalization hyperperfusion, i.e. vasodilatation and "luxury perfusion'. Increased oxidative metabolism, previously reported only in animals, presumably reflects an overshoot of protein synthesis. The fact that the areas with hyperperfusion, though extensive, were topographically distinct from the infarcted region, suggests that spontaneous non-haemorrhagic hyperperfusion, when documented 5-18 h after onset, is a harmless and even perhaps beneficial phenomenon. These results have implications for clinical trials.