Is Stent Retraction to ReLieve Arterial Cerebral VaSospasm Caused by SAH (Stent-ReLACSS) Using PRELAX the Long-awaited Solution for Treatment of Posthemorrhagic Cerebral Vasospasm? : Treatment of Posthemorrhagic Cerebral Vasospasm with PRESET and PRELAX: Technical Aspects, Efficacy, and Safety Margins in a Case Series.

PURPOSE: Recent observational studies have indicated the efficacy of stent retriever devices for the treatment of posthemorrhagic cerebral vasospasm (CVS), both by deployment and on-site withdrawal into the microcatheter (stent angioplasty, SA) and deployment followed by retraction through the target vessel similar to thrombectomy (Stent Retraction to reLieve Arterial Cerebral vaSospasm caused by SAH, Stent-ReLACSS). This article reports the findings with each application of pRESET and pRELAX in the treatment of CVS. METHODS: We retrospectively enrolled 25 patients with severe CVS following aneurysmal subarachnoid hemorrhage. For the SA group, a stent retriever or a pRELAX was temporarily deployed into a narrow vessel segment and retrieved into the microcatheter after 3 min. For the Stent-ReLACSS group, a pRELAX was temporarily deployed into a narrow vessel and pulled back unfolded into the internal carotid artery. If intra-arterial vasodilators were administered, they were given exclusively after mechanical vasospasmolysis to maximize the effectiveness of the stent treatment. RESULTS: In this study fifteen patients and 49 vessels were treated with SA. All were technically successful without periprocedural complications; however, 8/15 patients (53.3%) required additional treatment of the CVS. A total of 10 patients and 23 vessel segments were treated with Stent-ReLACSS. All maneuvers were technically successful without periprocedural complications and all vessels showed significant angiographic improvement. No recurrent CVS requiring further endovascular treatment occurred in-hospital, and neither territorial ischemia in the treated vessels nor vascular injury were observed in follow-up angiography. CONCLUSION: Based on the presented data it appears that Stent-ReLACSS with pRELAX does not pose any additional risks when used to treat CVS and might be superior to SA, especially concerning mid-term and long-term efficacy. The mechanism of action may be an effect on the endothelium rather than mechanical vasodilation. As many patients with CVS are diagnosed too late, prophylactic treatment of high-risk patients (e.g., poor grade, young, female) is potentially viable.

Intracranial stenting as a bail-out option for posthemorrhagic cerebral vasospasm: a single-center experience with long-term follow-up.

BACKGROUND: Cerebral vasospasm (CVS) is a leading cause of morbidity and mortality in patients after aneurysmal subarachnoid hemorrhage (aSAH). Endovascular treatment, including intraarterial infusion of drugs with vasodilation effects, and balloon- and stentriever angioplasty, are helpful but may achieve only short-term effects. There is a clinical need for long-lasting treatment of refractory recurrent vasospasm. We report our experience in stent implantation as a treatment for recurrent severe post-SAH vasospasm. METHODS: A retrospective analysis of our institutional database of 883 patients with SAH, managed between January 2010 and December 2021, was performed. Six patients were identified as having received intracranial stenting in the context of post-SAH cerebral vasospasm. All patients were initially treated with intra-arterial infusion of nimodipine and/or milrinone. Self-expanding intracranial stents were implanted during endovascular aneurysm treatment to enable access despite impaired perfusion (Group 1) or as a bail-out strategy after failed intraarterial drug infusion or mechanical treatment (Group 2). All stented patients received dual antiplatelet therapy (DAPT) for 6 months. RESULTS: Nine vessels in six patients with severe post-SAH vasospasm were stented. The stents were deployed in 16 vessel segments. All attempted implantations were technically successful. All patients demonstrated radiographic and clinical improvement of the vessel narrowing. No recurrent vasospasm or permanent vessel occlusion of the stented vessels was encountered. A thrombus formation in a Group 1 patient resolved under 4 mg eptifibatide IA infusion. During long-term angiographic follow-up, neither in-stent stenosis nor stent occlusion was found. CONCLUSIONS: Endovascular implantation of self-expanding stents is a potential ultima ratio strategy for patients with severe refractory post-SAH cerebral vasospasm. Stents with reduced thrombogenicity (avoiding DAPT) and bioabsorbable self-expanding stents might further advance this concept.

Volumetric analysis of intracranial vessels: a novel tool for evaluation of cerebral vasospasm.

PURPOSE: Together with other diagnostic modalities, computed tomography angiography (CTA) is commonly used to indicate endovascular vasospasm treatment after subarachnoid hemorrhage (SAH), despite the fact that objective, user-independent parameters for evaluation of CTA are lacking. This exploratory study was designed to investigate whether quantification of vasospasm by automated volumetric analysis of the middle cerebral artery M1 segment from CTA data could be used as an objective parameter to indicate endovascular vasospasm treatment. METHODS: We retrospectively identified SAH patients who underwent transcranial Doppler sonography (TCD), CTA, and CT perfusion (CTP), with or without subsequent endovascular treatment. We determined vessel volume/vessel length of the M1 segments from CTA data and used receiver operating characteristic curve analysis to determine the optimal threshold of vessel volume to predict vasospasm requiring endovascular treatment. In addition, blinded investigators independently analyzed TCD, CTA, and CTP data. RESULTS: Of 45 CTA examinations with corresponding CTP and TCD examinations (24 SAH patients), nine indicated the need for endovascular vasospasm treatment during examination. In our patients, vessel volume < 5.8 µL/mm was moderately sensitive but fairly specific to detect vasospasm requiring endovascular treatment (sensitivity, 67%; specificity, 78%; negative predictive value (NPV), 89%; positive predictive value (PPV), 46%). For CTA, CTP, and TCD, we found NPVs of 96%, 92%, and 89%, PPVs of 40%, 35%, and 35%, sensitivities of 89%, 78%, and 67%, and specificities of 67%, 64%, and 69%, respectively. CONCLUSION: Vessel volumes could provide a new objective parameter for the interpretation of CTA data and could thereby improve multimodal assessment of vasospasm in SAH patients.