Restenosis After Balloon Angioplasty for Cerebral Vasospasm

Sédat, Jacques; Chau, Yves; Popolo, Margherita; Gindre, S.; Rami, Laurent; Orban, J.-C.

doi:10.1007/s00270-008-9419-0

Cited by 10 publications

(10 citation statements)

References 15 publications

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“…Although the specific mechanism of action responsible for the effects of TBA are not well understood, several are likely to be at play, including but probably not limited to disruption or dysfunction of smooth muscle cells, extracellular matrix, or connections between the basement membranes of the cells. 30,39,48 Although it has been shown that TBA causes smooth muscle and endothelial cell flattening, some extracellular matrix disruption, and denudation of the endothelial lining, TBA is not thought to cause major irreversible structural damage. 29,30 These mechanisms usually result in a robust patency after angioplasty, with resilience to further spasm, but it should be noted that these vessels may also become less responsive to pharmacological vasodilators.…”

Section: Intraarterial Vasodilatorsmentioning

confidence: 99%

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Endovascular options in the treatment of delayed ischemic neurological deficits due to cerebral vasospasm

Eddleman

Hurley

Naidech

et al. 2009

FOC

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The second leading cause of death and disability in patients with aneurysmal subarachnoid hemorrhage (SAH) is delayed cerebral ischemia due to vasospasm. Although up to 70% of patients have been shown to have angiographic evidence of vasospasm, only 20–30% will present with clinical changes, including mental status changes and neurological deficits that necessitate acute management. Endovascular capabilities have progressed to become viable options in the treatment of cerebral vasospasm. The rationale for intraarterial therapy includes the fact that morbidity and mortality rates have not changed in recent years despite optimized noninvasive medical care. In this report, the authors discuss the most common endovascular options—namely intraarterial vasodilators and transluminal balloon angioplasty—from the standpoint of mechanism, efficacy, limitations, and complications as well as the treatment algorithms for cerebral vasospasm used at our institution.

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Section: Intraarterial Vasodilatorsmentioning

confidence: 99%

“…10,18,23,36,39,43,48 The most feared complication is vessel rupture, which can occur when there is discordant balloon diameter to vessel size. Occasionally, in the absence of a prespasm baseline angiographic study, the "normal" size of a spastic vessel must be estimated based on anatomical assumptions.…”

Section: Intraarterial Vasodilatorsmentioning

confidence: 99%

Endovascular options in the treatment of delayed ischemic neurological deficits due to cerebral vasospasm

Eddleman

Hurley

Naidech

et al. 2009

FOC

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“…In a review by Hoh and Ogilvy [74], balloon angioplasty had an approximately 5% risk of major complication, including an approximate 1% risk of vessel perforation/rupture, which is usually fatal [17,18,63,71,72,73,74,75,76]. Recently, some authors described the occurrence of delayed stenosis after angioplasty [77,78]. Although uncommon, recurrence of vasospasm after angioplasty may also occur [79].…”

Section: Endovascular Therapy In Sah-induced Cerebral Vasospasmmentioning

confidence: 99%

Current Options for the Management of Aneurysmal Subarachnoid Hemorrhage-Induced Cerebral Vasospasm: A Comprehensive Review of the Literature

2013

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Objectives: Cerebral vasospasm is one of the leading causes of morbi-mortality following aneurysmal subarachnoid hemorrhage. The aim of this article is to discuss the current status of vasospasm therapy with emphasis on endovascular treatment. Methods: A comprehensive review of the literature obtained by a PubMed search. The most relevant articles related to medical, endovascular and alternative therapies were selected for discussion. Results: Current accepted medical options include the oral nimodipine and ‘triple-H' therapy (hypertension, hypervolemia and hemodilution). Nimodipine remains the only modality proven to reduce the incidence of infarction. Although widely used, ‘triple-H' therapy has not been demonstrated to significantly change overall outcome after cerebral vasospasm. Indeed, both induced hypervolemia and hemodilution may have deleterious effects, and more recent physiologic data favor normovolemia with induced hypertension or optimization of cardiac output. Endovascular options include percutaneous transluminal balloon angioplasty (PTA) and intra-arterial (IA) infusion of vasodilators. Multiple case reports and case series have been encountered in the literature using different drug regimens with diverse mechanisms of action. Compared with PTA, IA drug infusion has the advantages of distal penetration and a better safety profile. Its main disadvantages are the more frequent need for repeat treatments and its systemic hemodynamic repercussions. Alternative options using intraventricular/cisternal drug therapy and flow augmentation strategies have also shown possible benefits; however, their use is not yet as well established. Conclusion: Blood pressure or cardiac output optimization should be the mainstay of hyperdynamic therapy. Endovascular treatment appears to have a positive impact on neurological outcome compared with the natural history of the disease. The role of intraventricular therapy and flow augmentation strategies in association with medical and endovascular treatment may, in the future, play a growing role in the management of patients with severe refractory vasospasm.

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“…Restenosis after balloon angioplasty for atherosclerosis is a well-known phenomenon [9][10][11], however, its occurrence in a delayed fashion following its use for cerebral vasospasm is rare [12][13][14]. We report a patient who underwent successful angioplasty for internal carotid artery (ICA) post-SAH vasospasm, who went on to develop delayed progressive severe focal restenosis.…”

Section: Introductionmentioning

confidence: 98%

Delayed progressive bilateral supraclinoid internal carotid artery stenosis in a patient with a ruptured basilar artery aneurysm

Safain

Malek

2015

Journal of Clinical Neuroscience

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Restenosis After Balloon Angioplasty for Cerebral Vasospasm

Cited by 10 publications

References 15 publications

Endovascular options in the treatment of delayed ischemic neurological deficits due to cerebral vasospasm

Endovascular options in the treatment of delayed ischemic neurological deficits due to cerebral vasospasm

Current Options for the Management of Aneurysmal Subarachnoid Hemorrhage-Induced Cerebral Vasospasm: A Comprehensive Review of the Literature

Delayed progressive bilateral supraclinoid internal carotid artery stenosis in a patient with a ruptured basilar artery aneurysm

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