Stroke; a journal of cerebral circulation
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Familial aggregation of intracranial aneurysms (IA) strongly suggests a genetic contribution to pathogenesis. However, genetic risk factors have yet to be defined. For families affected by aortic aneurysms, specific gene variants have been identified, many affecting the receptors to transforming growth factor-beta (TGF-beta). In recent work, we found that aortic and intracranial aneurysms may share a common genetic basis in some families. We hypothesized, therefore, that mutations in TGF-beta receptors might also play a role in IA pathogenesis. ⋯ Mutations in TGF-beta receptor genes are not a major cause of IA. However, we identified rare variants in ENG and TGFBR3 that may be important for IA pathogenesis in a subset of families.
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The purpose of this study was to estimate the safety and efficacy of abciximab treatment in combination with prophylactic heparin, acetylsalicylic acid (ASA), and clopidogrel application in cases of thrombus formation complicating endovascular coil embolization in cerebral aneurysms. ⋯ Abciximab was safe as rescue treatment in cases of thrombus formation during endovascular aneurysm coiling. In our study the use of Abciximab, in combination with prophylactic anticoagulation and antiaggregation, does not lead to additional intracranial hemorrhages or any extracranial bleeding complications.
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Randomized Controlled Trial Multicenter Study
Quality of life after intracerebral hemorrhage: results of the Factor Seven for Acute Hemorrhagic Stroke (FAST) trial.
Neurological impairment and physical disability are frequent and important complications of stroke with serious consequences for health-related quality of life (HRQOL). Little data exist, however, on the risk factors for poor HRQOL after intracerebral hemorrhage, the deadliest and most disabling form of stroke. ⋯ The vast majority of survivors after intracerebral hemorrhage have very poor HRQOL. Critical care interventions designed to control blood pressure or prevent neuroworsening may improve HRQOL in intracerebral hemorrhage survivors.
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Review
Reporting standards for angioplasty and stent-assisted angioplasty for intracranial atherosclerosis.
Intracranial cerebral atherosclerosis causes ischemic stroke in a significant number of patients. Technological advances over the past 10 years have enabled endovascular treatment of intracranial atherosclerotic stenosis. The number of patients treated with angioplasty or stent-assisted angioplasty for this condition is increasing. Given the lack of universally accepted definitions, the goal of this document is to provide consensus recommendations for reporting standards, terminology, and written definitions when reporting clinical and radiological evaluation, technique, and outcome of endovascular treatment using angioplasty or stent-assisted angioplasty for stenotic and occlusive intracranial atherosclerosis. ⋯ In summary, the definitions proposed represent recommendations for constructing useful research data sets. The intent is to facilitate production of scientifically rigorous results capable of reliable comparisons between and among similar studies. In some cases, the definitions contained here are recommended by consensus of a panel of experts in this writing group for consistency in reporting and publication. These definitions should allow different groups to publish results that are directly comparable.
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Cognitive dysfunction occurs in 9% to 23% of patients during the first month after carotid endarterectomy (CEA). A 4-basepair (AAAT) tandem repeat polymorphism (either 3 or 4 repeats) has been described in the promoter region of inducible nitric oxide synthase (iNOS), a gene with complex roles in ischemic injury and preconditioning against ischemic injury. We investigated whether the 4-repeat variant (iNOS(+)) affects the incidence of cognitive dysfunction after CEA. ⋯ We demonstrate an iNOS promoter polymorphism variant provides protection against moderate/severe cognitive dysfunction 1 month after CEA. Further, this protection appears to involve cognitive domains localized ipsilateral to the operative carotid artery.