Posts Tagged ‘stroke’
Background: Experimental evidence has indicated the benefit of simvastatin in the treatment of subarachnoid hemorrhage. However, no clinical data are available to answer whether a high-dose regimen is more effective than a normal-dose regimen, even though the biochemical actions and related neuroprotective mechanisms are thought to be dose related.
Objective: To determine whether 80 mg simvastatin daily (high dose) over 3 weeks initiated within 96 hours of the ictus will reduce the incidence of delayed ischemic deficits after subarachnoid hemorrhage compared with 40 mg simvastatin daily (normal dose), leading to improvements in clinical outcomes and thus cost-effectiveness.
Methods: The study design is a randomized, controlled, double-blind clinical trial (www.ClinicalTrials.gov; identifier: NCT01077206). Two hundred forty patients with aneurysmal subarachnoid hemorrhage (presenting within 96 hours of the ictus) from 6 neurosurgical centers are being recruited over 3 years. The primary outcome measure is the presence of delayed ischemic deficits. Secondary outcome measures include modified Rankin Disability Score at 3 months and cost-effectiveness analysis.
Background: Carotid endarterectomy is a low-risk treatment for carotid occlusive disease. Recent clinical trials have suggested that carotid angioplasty may be a viable alternative. One important issue that has not been evaluated is the long-term recurrent stenosis rate after either intervention.
Objective: To examine the risk of recurrent stenosis after carotid endarterectomy and to provide long-term data on the durability of carotid endarterectomy.
Methods: A total of 1335 sequential patients were followed up prospectively with annual carotid ultrasonography. All patients were maintained on antiplatelet therapy, and arteriotomies were closed with a patch graft. Operations were performed under general anesthesia with electroencephalographic monitoring and selective shunting. There were no changes in surgical technique during this study.
Background: Enrollment in the Stenting and Aggressive Medical Management for the Prevention of stroke in Intracranial Stenosis (SAMMPRIS) trial was halted owing to higher-than-expected 30-day stroke rates in the stenting arm. Improvement in periprocedural stroke rates from angioplasty and stenting for intracranial atherosclerotic disease (ICAD) requires an understanding of the mechanisms of these events.
Objective: To identify the types and mechanisms of periprocedural stroke after angioplasty and stenting for ICAD.
Methods: Patients who experienced a hemorrhagic or ischemic stroke or a cerebral infarct with temporary signs within 30 days of attempted angioplasty and stenting in SAMMPRIS were identified. Study records, including case report forms, procedure notes, and imaging were reviewed. Strokes were categorized as ischemic or hemorrhagic. Ischemic strokes were categorized as perforator territory, distal embolic, or delayed stent thrombosis. Hemorrhagic strokes were categorized as subarachnoid or intraparenchymal. Causes of hemorrhage (wire perforation, vessel rupture) were recorded.
Background: Delayed cerebral ischemia is common after aneurysmal subarachnoid hemorrhage (aSAH) and is a major contributor to poor outcome. Yet, although generally attributed to arterial vasospasm, neurological deterioration may also occur in the absence of vasospasm.
Objective: To determine the relationship between delayed infarction and angiographic vasospasm and compare the characteristics of infarcts related to vasospasm vs those unrelated.
Methods: A retrospective review of patients with aSAH admitted from July 2007 through June 2011. Patients were included if they were admitted within 48 hours of SAH, had a computed tomography scan both 24 to 48 hours following aneurysm treatment and ≥7 days after SAH, and had a catheter angiogram to evaluate for vasospasm. Delayed infarcts seen on late computed tomography but not postprocedurally were attributed to vasospasm if there was moderate or severe vasospasm in the corresponding vascular territory on angiography. Infarct volume was measured by perimeter tracing.
Objective: To demonstrate a rat brain perfusion model that provides a simplified reliable brain perfusion circuit, reduces variables during experiment and recovery, and therefore, permits more precise, reliable, and context-independent research data.
Methods: Rat forebrain perfusion was reduced surgically to that by one internal carotid artery without injury to the animal. The next day the fully awake rat was studied for brain ischemia painlessly, yet in the absence of anesthesia or other interventions that might bias or alter the biochemistry of the event. This model was rigorously validated with isotope cerebral blood studies during ischemia and with histology studies at 72 hrs post-ischemia. First application of this model was to compare ischemia injuries for global total versus global penumbra versus global shock ischemia in a single experimental context.