BACKGROUND AND PURPOSE:Aneurysm treatment by intrasaccular packing has been associated with a relatively high rate of recurrence. The use of mesh tubes has recently gained traction as an alternative therapy. This article summarizes the midterm results of using an endoluminal sleeve, the PED, in the treatment of aneurysms.

IntroductionThe purpose of this study was to evaluate the safety and efficacy of the recently available flow diverter “pipeline embolization device” (PED) for the treatment of intracranial aneurysms and dissections.MethodsEighty-eight consecutive patients underwent an endovascular treatment of 101 intracranial aneurysms or dissections using the PED between September 2009 and January 2011. The targeted vessels include 79 (78%) in the anterior circulation and 22 (22%) in the posterior circulation. We treated 96 aneurysms and 5 vessel dissections. Multiple devices were implanted in 67 lesions (66%).ResultsOne technical failure of the procedure was encountered. Immediate exclusion of the target lesion was not observed. Angiographic follow-up examinations were carried out in 80 patients (91%) with 90 lesions and revealed complete cure of the target lesion(s) in 47 (52%), morphological improvement in 32 lesions (36%), and no improvement in 11 lesions (12%). Six major complications were encountered: one fatal aneurysm rupture, one acute and one delayed PED thrombosis, and three hemorrhages in the dependent brain parenchyma.ConclusionOur experience reveals that the PED procedure is technically straightforward for the treatment of selected wide-necked saccular aneurysms, fusiform aneurysms, remnants of aneurysms, aneurysms with a high likelihood of failure with conventional endovascular techniques, and dissected vessels. While vessel reconstruction, performed after dissection, is achieved within days, remodeling of aneurysmal dilatations may take several months. Dual platelet inhibition is obligatory. Parenchymal bleeding into brain areas dependent on the target vessel is uncommon.

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Cerebral water accumulation was studied during induction of brain edema in dystrophin-null transgenic mice (mdx-␤geo) and control mice. Immunofluorescence and immunoelectron microscopic analyses of dystrophin-null brains revealed a dramatic reduction of AQP4 (aquaporin-4) in astroglial end-feet surrounding capillaries (blood-brain barrier) and at the glia limitans (cerebrospinal fluidbrain interface). The AQP4 protein is mislocalized, because immunoblotting showed that the total AQP4 protein abundance was unaltered. Brain edema was induced by i.p. injection of distilled water and 8-deamino-arginine vasopressin. Changes in cerebral water compartments were assessed by diffusion-weighted MRI with determination of the apparent diffusion coefficient (ADC). In dystrophin-null mice and control mice, ADC gradually decreased by 5-6% from baseline levels during the first 35 min, indicating the initial phase of intracellular water accumulation is similar in the two groups. At this point, the control mice sustained an abrupt, rapid decline in ADC to 58% ؎ 2.2% of the baseline at 52.5 min, and all of the animals were dead by 56 min. After a consistent delay, the dystrophin-null mice sustained a similar decline in ADC to 55% ؎ 3.4% at 66.5 min, when all of the mice were dead. These results demonstrate that dystrophin is necessary for polarized distribution of AQP4 protein in brain where facilitated movements of water occur across the blood-brain barrier and cerebrospinal fluid-brain interface. Moreover, these results predict that interference with the subcellular localization of AQP4 may have therapeutic potential for delaying the onset of impending brain edema. Brain edema is associated with many intracranial neuropathological states, such as head trauma, ischemic brain injury, neoplasms, and metabolic diseases including systemic hyponatremia. Although much investigation has addressed the underlying molecular mechanisms and pathophysiology of brain edema, little is known about the regulation of water transport across the blood-brain barrier, the cerebrospinal fluid (CSF)-brain interface, and between extracellular and intracellular compartments in brain parenchyma.It is well recognized that the aquaporin family of water channel proteins is the major pathway by which water rapidly crosses cell membranes (1). Manley et al. recently reported that AQP4 (aquaporin-4; ref. 18) negatively influences the outcome from brain edema (2), and other recent studies also have suggested that AQP4 contributes to the development of brain edema (3, 4). These observations are consistent with the distribution of AQP4 in brain, because the protein is expressed abundantly in a highly polarized distribution in ependymal cells and astroglial membranes facing capillaries and forming the glia limitans (5).Decreased expression of AQP4 protein without changes in the AQP4 mRNA levels was reported recently in brains of Dmd mdx mice (C57BL10 ScSn mdx), a strain carrying a spontaneous mutation that prevents expression of the longest isoform of dystrophin (6)....

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Undersized balloon angioplasty and deployment of an Enterprise stent is safe and effective for intracranial stenoses. Follow-up results were equal to or better than those reported for bare-metal balloon-expandable or self-expanding stents and yielded excellent protection from recurrent ischemia.

Preliminary data show that CLINA is a straightforward, effective, and safe option for patients with severe CV refractory to medical therapy. Dilation of spastic arteries starts within a few hours and is lasting. Indication for CLINA is peripheral and diffuse CV at any location.

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