Intracranial Stenting as a Bail-out Option for Posthemorrhagic Cerebral Vasospasm: A Single-Center Experience with Long-Term Follow-Up

Intracranial Stenting as a Bail-out Option for Posthemorrhagic Cerebral Vasospasm: A Single-Center Experience with Long-Term Follow-Up | Research Square window.SnipcartSettings = { analytics: { enabled: false } }; (function() { var accessVector = localStorage.getItem('access_vector') || ''; window.dataLayer = window.dataLayer || []; if (accessVector) { window.dataLayer.push({ user: { profile: { profileInfo: { snid: accessVector } } } }); } })(); (function(w,d,s,l,i){w[l]=w[l]||[];w[l].push({'gtm.start':new Date().getTime(),event:'gtm.js'});var f=d.getElementsByTagName(s)[0],j=d.createElement(s),dl=l!='dataLayer'?'&l='+l:'';j.async=true;j.src='https://www.googletagmanager.com/gtm.js?id='+i+dl;f.parentNode.insertBefore(j,f);})(window,document,'script','dataLayer','GTM-K279D39R'); Browse Preprints In Review Journals COVID-19 Preprints AJE Video Bytes Research Tools Research Promotion AJE Professional Editing AJE Rubriq About Preprint Platform In Review Editorial Policies Our Team Advisory Board Help Center Sign In Submit a Preprint Cite Share Download PDF Research Article Intracranial Stenting as a Bail-out Option for Posthemorrhagic Cerebral Vasospasm: A Single-Center Experience with Long-Term Follow-Up Ali Khanafer, Alexandru Cimpoca, Pervinder Bhogal, Hansjörg Bäzner, and 2 more This is a preprint; it has not been peer reviewed by a journal. https://doi.org/ 10.21203/rs.3.rs-1801216/v1 This work is licensed under a CC BY 4.0 License Status: Under Review Version 1 posted 10 You are reading this latest preprint version Abstract Background: Cerebral vasospasm is a leading cause of morbidity and mortality in patients after subarachnoid hemorrhage (SAH). Endovascular treatment, including intraarterial infusion of drugs with vasodilation effects, and balloon- and stentriever angioplasty, are helpful but can achieve only short-term effects in some patients. A need remains 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 or as a bail-out strategy after failed intraarterial drug infusion or mechanical treatment. All stented patients received dual antiplatelet therapy (DAPT). 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 thromboembolic occlusion of the stented vessels was encountered. In 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 would further advance this concept. Subarachnoid hemorrhage posthemorrhagic cerebral vasospasm endovascular treatment self-expanding stent Figures Figure 1 Figure 2 Figure 3 Introduction Cerebral vasospasm (CVS) is one of the leading causes of neurological deterioration after subarachnoid hemorrhage (SAH). CVS is responsible for a morbidity and mortality incidence of approximately 20% [ 1 , 2 ]. Among patients with SAH, 50–70% develop CVS, and approximately 30% present neurologic deficits [ 3 , 4 ]. Despite limited accuracy, transcranial Doppler sonography (TCD) and transcranial color-coded Doppler (TCCD) remain preferred diagnostic methods in intensive care units for the detection of vasospasm, because of their logistic simplicity [ 5 ]. Magnetic resonance angiography (MRA), particularly computed tomography angiography (CTA) with computed tomography perfusion (CTP), is more reliable in CVS detection. Digital subtraction angiography (DSA) remains the gold standard for detecting and quantifying CVS [ 6 ]. Conservative management by intravenous or oral administration of calcium channel blockers has yielded poor results [ 7 ]. Endovascular management strategies allow for effective treatment of CVS. These strategies include Short-term intra-arterial administration of nimodipine [ 8 ], milrinone [ 9 , 10 ], or verapamil [ 11 ]; long-term intra-arterial selective infusion of nimodipine [ 12 ]; and mechanical dilatation of large arteries with non-compliant balloons, compliant balloons [ 13 – 17 ], or stentrievers [ 18 – 22 ]. The substantial logistic efforts required for diagnosis and endovascular treatment outside the intensive care unit, and the complex cardiovascular and respiratory monitoring required before and during treatment, may lead to treatment delays and consequently poor outcomes. In addition, despite the development of pharmacological and endovascular treatment options, the treatment of post-SAH CVS remains a challenge because of its frequent occurrence. Here, we report our experience in the use of intracranial stenting in the treatment of patients with post-SAH CVS. Methods Study Population Between January 2010 and December 2021, we treated a total of 883 patients with SAH. The management strategy followed in our neurovascular center is as follows: - Early diagnosis of SAH according to computed tomography (CT)/CTA or magnetic resonance imaging (MRI)/MRA, followed by DSA. - Early endovascular or microsurgical aneurysm treatment based on individualized multidisciplinary decision-making - Early external cerebrospinal fluid drainage when deemed necessary - Administration of intravenous or per os nimodipine starting on the first clinical day of stay, if tolerated. During this period, 275 patients were diagnosed with post-SAH CVS. We retrospectively evaluated our database and identified 76 patients with recurrent CVS after initial short-term intra-arterial (IA) administration of milrinone (Corotrop, Sanofi-Avantis). These patients were treated with repeated IA administration of vasodilators and/or interventional mechanical vasodilatation of the vessel segments affected by CVS. The mechanical treatments applied were stent retriever-assisted angioplasty, pRELAX device-assisted angioplasty, and intracranial implantation of self-expandable stents. In six of these patients with CVS, intracranial self-expanding stent implantation was performed. The clinical data files and the imaging results were available for retrospective evaluation. The patients’ demographics and clinical characteristics are listed in Table 1. Table 1: Demographics and clinical characteristics of patients. Patients Group Age (years) Gender HH Fisher Days between SAH and vasospasm Days between SAH and stent-implantation 1 1 61 F 1 3 0 0 2 1 48 F 3 2 0 0 3 2 52 F 3 4 4 15 4 2 49 F 5 4 7 8 5 2 41 M 5 4 6 7 6 2 67 F 3 4 5 6 Data Analysis All six case histories were analyzed individually. Vasospasm was either prospectively diagnosed during the hospital stay or retrospectively identified by analysis of the imaging material by a neuroradiologist (with 3 years of experience in neuroradiological imaging), as supervised by the senior author. The six patients who underwent intracranial stenting were initially treated with IA vasodilators as soon as the vasospasms were angiographically diagnosed. After review of clinical data files and all imaging results (CT, MRI/MRA, and DSA) of the patients treated with intracranial stenting, the patients were divided into the following two groups: - Group 1: Intracranial stenting during endovascular therapy of a ruptured aneurysm, to allow for catheter access despite narrowing of the parent artery and in the context of stent-assisted coiling - Group 2: Intracranial stenting for recurrent vasospasm after failed IA infusion of vasodilators and/or mechanical treatment, particularly in patients with severe CVS who were at risk of brain infarction Follow-up Early follow-up catheter angiography was performed before discharge according to routine clinical protocols. The first mid-term angiographic follow-up was performed 3–6 months after discharge. Clinical assessment was performed with the modified Rankin Scale (mRS) during the acute post-SAH period, discharge, and follow-up visits. Statistical Analysis For categorical variables, results are described as percentages. Continuous variables are reported as mean and standard deviation. Results Group 1: Intracranial stenting of refractory CVS during endovascular treatment of the ruptured aneurysm This group consisted of two patients and represented our first experience in intracranial stenting as a treatment for recurrent CVS. Both patients showed CVS on day 1 during the first DSA examination to locate the source of hemorrhage. At that time, we suspected that the current SAH was not the first. This suspicion was confirmed in one patient, according to information provided by the family regarding a severe headache 7 days earlier. Both patients showed neurological deficits due to CVS; therefore, endovascular treatment could not be delayed. Endovascular coil occlusion of the ruptured aneurysm was planned for both patients. Initial treatment with IA vasodilators was performed in both patients for approximately 30 minutes immediately before the start of endovascular coiling of the ruptured aneurysm. After an infusion of 8 mg milirinone into the internal carotid artery (ICA), the affected vessel segments showed sufficient vasodilation to enable coil occlusion of the aneurysms. During the endovascular coiling of the ruptured aneurysms, recurrent vasospasm was detected in both patients. Concurrently the implanted coils shifted into the parent vessels. Vasospasm and coil displacement resulted in a substantial perfusion delay of the dependent vasculature. To be able to continue the treatment, prevent the increase in CVS, and prevent ischemic changes, we implanted a self-expanding stent in the parent artery. Consequently, the covered vessel segments dilated, the perfusion of the distal vessels improved, and we completed the treatment Fig. 1. The post-procedural CT imaging showed no ischemic lesions due to CVS. On day 1 after aneurysm coiling, one patient showed generalized moderate vasospasm in the proximal segments of the middle and anterior cerebral artery, excluding the stented M1-M2 vessel segments. In both patients, the injection of IA vasodilators for 30 min induced significant dilatation of the affected vessels and vessel segments. After that, the patients showed no further recurrent vasospasm, ischemic lesions, or new neurological deficits during the remainder of their clinical stay. Group 2: Intracranial stenting of refractory CVS after failure of IA vasodilators or mechanical treatment This group included four patients with a mean age of 52.2 years (range 41–67 years). Three of these patients were in poor clinical condition, and the clinical management was complicated by periprocedural and postprocedural issues. One patient was diagnosed with periprocedural dissection of the left ICA after endovascular treatment of a giant left ICA aneurysm with pCONUS-assisted coiling. This dissection caused an ischemic lesion 6 days later by increasing vasoconstriction due to vasospasm. Another patient was found to have an intracerebral hemorrhage in the brain's left frontal lobe after a new external ventricular drain was inserted 5 days after endovascular treatment of a giant aneurysm of the right ICA with flow diversion-assisted coiling. The third patient showed a new postoperative hemorrhage on non-contrast CT performed immediately after microsurgical clipping of an aneurysm of the right middle cerebral artery (MCA) bifurcation. Beyond the recurrent generalized CVS, all these conditions increased the intracranial pressure in the patients and complicated their clinical management. One patient underwent hemicraniectomy as a result of the rebleeding. The fourth patient experienced only headaches at the beginning of the clinical stay. One day later, the patient showed rapid high-grade neurological deficits due to CVS. All patients in this group showed recurrent CVS and therefore underwent at least one independent therapy session before stent implantation and multiple endovascular procedures (median 3; 2–3). Except for patients in group 1, intracranial stenting as a treatment for CVS was not performed in the first vasospasm treatment session. Three patients also underwent interventional mechanical treatment with a stent retriever or pRELAX device. In two patients, we performed IA continuous selective infusion of nimodipine for 3–6 days because of generalized CVS in other vascular segments. At the beginning of our experience, we used intracranial stenting in CVS to dilate the most affected or relevant vessel segments by using only one stent. Later, with increasing experience, we have decided to insert as many as four stents in a patient with generalized recurrent CVS. The concerning vessel segments in these patients were ICA bifurcation, A1, A2, AcomA, M1, and M2. We performed stenting of two to five vessel segments on each patient. A total of 18 artery segments were covered with stents. Ten stents were used, and we successfully implanted the stents into the spastic segments after IA vasodilator infusion in all cases. The medications and interventional characteristics are listed in Table 2. After the stenting procedures, all vessel segments showed satisfactory vasodilation and improved perfusion of the distal vasculature Figs. 2, 3. Three patients required further endovascular CVS treatment, but not for the stent-covered segments. No evidence of any luminal narrowing of the stented vessels was observed. No thromboembolic or spasm-related ischemic lesions were detectable in the supply area of the treated segments in control CT or MRI after stent implantation. Most patients (five of six, 83.3%) showed neurological improvement at discharge, and all patients showed neurological improvement at the 6-month follow-up. A good clinical outcome (mRS ≤ 2) was achieved in five of six patients Table 3. Table 2: Radiological and interventional findings of the patients in both groups. Patients no. Group Loading Medication Stents Vessels Segments Ischemia after Stent postprocedural bleeding 1 1 1 x 500 mg ASA 1 x 75 mg Prasugrel 1 x Solitaire 4/15 ACA ri A1-A2 no no 2 1 1 x 4 mg Eptifibatide 2 x 500 mg ASA 1 x 600 mg Clopidogrel 1 x LVIS Jr. 2,5/24 MCA ri Caro-bi-M1-M2 no no 3 2 1 x 500 mg ASA 1 x 30 mg Prasugrel 1 x Enterprise 4/39 MCA ri M1-M2 no no 4 2 1 x 12.4 mg Eptifibatide 1 x 500 mg ASA 1 x 180 mg Ticagrelor 1 x Enterprise 2 4/30 MCA ri M1-M2 no no 5 2 1 x 500 mg ASA 1 x 10 mg Prasugrel 1x Enterprise 4/16 1x Enterprise 4/23 MCA ri ACA ri M1 A1-A2 no no 6 2 1 x 12.4 mg Eptifibatide 1 x 500 mg ASA 1 x 180 mg Ticagrelor 1 x Neuroform Atlas 3/15 1 x Baby Leo 2/12 1 x Neuroform Atlas 4/24 1 x Neuroform Atlas 4,5/30 ACA ri ACA ri MCA le ACA le A2 A1 M1+Caro-bi A1-A2 no no Table 3: Clinical and radiological findings of the patients in both groups. Patients no. Group TCDD before the stenting mRS before stenting TCDD 1 day after the stenting mRS on discharge mRS 90 days mRS 180 days last mRS 1 1 _ 2 50 1 0 0 0 2 1 160 5 90 3 2 0 0 3 2 250 intubated 100 4 3 3 3 4 2 240 5 95 4 3 2 2 5 2 180 5 80 3 2 2 2 6 2 160 4 n.a. 0 0 0 0 Complications One technical complication occurred. In the first group, one patient had an occlusion of the stent-covered MCA, but the thrombus formation resolved with the administration of eptifibatide IA (Integrilin, GlaxoSmithKline) Fig. 1. This complication did not lead to clinical consequences. The patient showed no associated ischemic lesions after the procedure. No complications occurred in the patients in group 2. No peri- or post-procedural hemorrhage or vascular injuries were encountered. Discussion Although the endovascular or microsurgical treatment of ruptured aneurysms has substantially improved during the past three decades, similar progress in the treatment of CVS is lacking. The past 20 years have seen a mindset shift from a fatalistic acceptance of poor outcomes due to CVS toward active attempts to address these outcomes. The search for a safe and efficacious treatment for CVS has been ongoing since the 1970s [ 23 ]. Balloon dilatation of proximal arteries (mainly the distal ICA and the proximal MCA) is an acceptable option, but the risk of vessel dissection and even rupture remains a concern. Intraarterial infusion of vasodilator drugs may work, but this treatment modality requires major logistic efforts and may fail. In recent years, endovascular mechanical vessel dilatation using stent retrievers (e.g., Solitaire, Medtronic; pRESET, or phenox) has been established [ 18 – 22 ]. The indications for this treatment are not yet well defined, particularly because the incidence of delayed cerebral ischemia (DCI) is approximately 30%. However, CVS is diagnosed in 70% of patients, and the areas of ischemia often do not correspond to vascular territories that demonstrate large proximal vessel vasospasm. This shift in interest away from targeting large vessel vasospasms has been supported by the failure of clazosentan, a potent vasodilator, to improve patient outcomes [ 24 – 27 ]. Nevertheless, evidence suggests that the treatment of CVS can improve clinical outcomes. Jabbar et al. [ 28 ] have compared two patient cohorts from two institutions treated between 2005 and 2012, including 1057 patients. All patients underwent daily TCD ultrasonography to detect CVS. Patients in group A were treated immediately after any suspicion of CVS, regardless of the TCD results. Patients in group B were treated by endovascular means only after persistent CVS despite induced hypertension for 2–4 hours or when a mean flow velocity above 160 cm/sec was gradually exceeded for two consecutive days. In comparison, more patients were treated in group A. In group A, 24.4% of patients (n = 121/495) underwent the first endovascular treatment on day 6 ± 3.64, and in group B, 14.4% (n = 81/562) underwent the first endovascular treatment on day 8.9 ± 4.78; differences in the odds (p < 0.0001, OR 1.92 95% CI 1.41–2.63) were observed in the rate of treatment and the timing (p < 0.0001). The rate of DCI was lower in cohort A (20.8% vs. 29%, p = 0.0023, OR 0.64, 95% CI 0.48–0.85), as confirmed by multivariate analysis (p = 0.001, adjusted OR 0.59, 95% CI 0.44–0.8). The rates of DCI were higher in patients undergoing endovascular treatment for delayed ischemic neurologic deficit than in those undergoing endovascular treatment solely because of TCD measurements (64% vs. 44.7%, p = 0.0277). The rate of unfavorable outcomes after SAH was also lower in cohort A (44% vs. 56%, p = 0.0404) and remained significant in multivariate analysis (p < 0.0001, adjusted OR 0.55, 95% CI 0.4–0.77). This study demonstrated that early identification and aggressive treatment might result in better functional outcomes. Non-selective IA injection of vasodilators was one of the first endovascular treatments for CVS. Despite improving cerebral flow after the injection of vasodilators, this treatment can lead to an iatrogenic steal phenomenon due to more significantly improved inflow in the non-spastic arteries [ 29 ]. To avoid the iatrogenic steal phenomenon and improve outcomes in the distal vessels, distal vasospasm was suggested to be best treated with medication after initial mechanical treatment of the proximal vasospasm. Balloon angioplasty [ 13 – 17 ] and stentoplasty [ 18 – 22 ] have shown therapeutic efficacy and sustained improvement. Although balloon angioplasty was initially believed to damage the extracellular matrix, thus explaining angioplasty’s mechanism of action, evidence has indicated that balloon angioplasty of an arterial segment instead induces paralysis of the vessel without necessarily damaging the underlying extracellular matrix [ 20 , 30 ]. The induced vessel paralysis after angioplasty is affected by the contractile state of the vessel. Contracted vessels, such as vasospastic vessels, require less dilatation to become paralyzed; therefore, vessels with CVS are predisposed to paralysis after mechanical dilation and thus can be treated with devices with lower radial force [ 20 ]. The reason for this paralysis and the requirement for decreased dilatation to induce the same degree of paralysis in contracted vessels than in vessels in a relaxed state is not fully understood. Damage to the underlying contractile apparatus within the smooth muscle cells, which stiffen when contracted and may potentially be more prone to mechanical disruption, has been suggested to explain this phenomenon [ 31 ]. This finding suggests that mechanical angioplasty should be performed before chemical angioplasty, because it would be likely to have more significant effects. Simultaneously, lower forces might be required, thus potentially explaining why stentrievers have shown some success in treating CVS despite having much lower radial force than balloons. Kwon et al. [ 20 ], in a series of patients treated with both chemical angioplasty and stentoplasty, have compared patients in whom the stent was deployed initially followed by injection of a vasodilator (nicardipine) and those in whom a vasodilator was injected first, and stentoplasty was performed second. In the vasodilator-first group, 71.4% of treated vessel segments (10/14) showed vasodilation after stentoplasty, but 60% of patients (3/5) developed recurrent vasospasm requiring repeated angioplasty. In the stentriever-first group, 82.1% of segments (32/39) showed vasodilatation after stentoplasty, but none of the patients developed radiological or clinical evidence of recurrent vasospasm. This small clinical study corroborated the initial hypothesis suggested by Bhogal et al., building on the work of Fischell et al. [ 30 , 31 ] The use of permanently implanted stents has also been reported. Andic et al. [ 32 ] have analyzed data from 15 consecutive patients with 18 aneurysms, eight of whom underwent stent-assisted coiling. In most cases (n = 6), an LVIS Jr (MicoVention) stent was implanted, with a Solitaire (Medtronic) or Acclino (Acandis) used in the remainder. In a single case, Y-stenting with the use of two LVIS Jr stents was used to treat an MCA bifurcation aneurysm. The authors observed moderate to complete dilatation in the spastic parent arteries after deployment of the stents in patients treated with stent-assisted coiling. In one case, refractory vasospasm occurred after the treatment of two aneurysms (a basilar bifurcation aneurysm and an MCA bifurcation aneurysm), and the authors found no evidence of recurrent vasospasm in the stented segments but observed widespread recurrent vasospasm in the segments previously treated with chemical angioplasty. Although these findings were based on only a small series, this article highlights the potential for braided and laser-cut stents to effectively treat and prevent recurrent CVS. Subsequently, Bhambri et al. [ 33 ] described a novel method of using drug-eluting stents to treat CVS. The authors developed polymer-coated laser-cut stents and used various methods to coat the stent: dip coating, spin coating, and electrospinning. The laser-cut and polymer-coated stents were also loaded with different doses of verapamil with varying drug release pharmacokinetics. In all cases, the combined stent demonstrated an initial burst phase of drug release followed by sustained drug release. Varying the concentration of the verapamil changed these different phases by altering the construction of the polymer coating. This preliminary in vitro study suggests the potential promise of further developing stents that release vasodilating drugs. However, to date, no further studies on this technology have been published. Despite the development of endovascular techniques and their demonstrated effectiveness in treating recurrent vasospasm, some of these therapies remain unsuccessful. The possible reasons for the failure of endovascular treatment are as follows: Steal phenomenon, particularly with intra-arterial vasodilator treatment Distal location: difficult navigation and dilatation of CVS in distal vessel segments for endovascular mechanical treatments Tortuosity and curved vessels: complex dilatation of spastic vessels in a curved course, such as the transition from the A1 to the A2 segment, particularly for balloon angioplasty Some endovascular treatments have a short-term maximal dilatation effect, but CVS is a dynamic and potentially long-term pathology during the first 3 weeks after SAH. Therefore, recurrent CVS may not be successfully treated in some cases despite multiple repeated endovascular treatments sessions. Consequently, the search for a therapeutic solution for refractory CVS continues. Intracranial stenting of vessels with vasospasm is an ultima ratio treatment in patients with severe recurrent vasospasm. We have attempted to induce permanent dilatation of vessels with resistant spasms by stent implantation. The implanted stents' relatively low and continuous radial force provides a good solution for distal and curved vessel segments. The implanted device is intended to avoid the steal phenomenon and enhance vasodilator drugs' effects, particularly on the peripheral vessels. By improving perfusion in the proximal vessels, we have also observed a reduction of CVS in the distal vessels. This level of improvement occurred only after stent implantation and therefore cannot be explained by the earlier IA administration of the vasodilator. The idea of treating CVS with intracranial stenting arose from incidental experience during the management of complications during aneurysm coil occlusion. During coiling, impaired perfusion of the parent vessel and the dependent vasculature was observed, owing to inadvertent displacement of the implanted coils. Stents were implanted to maintain the coils inside the aneurysm and restore normal blood flow. The vessels where the stents were implanted had shown CVS before and during the coiling despite the IA vasodilator administration. After stenting, we observed decreased vasospasms with similar perfusion improvement in the distal supply territory ( Fig. 1 ) . One of the two patients with incidental treatment was diagnosed with high-grade CVS after day 1, but not within or distal to the stented vessel. The stents used were not dedicated to treating CVS, but we believe that they may be valuable in extreme situations in which few choices are available. After our initial two incidental experiences and the excellent long-term outcome, we decided to perform this treatment in the four described cases after several unsuccessful chemical and mechanical treatments. In the first two patients, we implanted only one stent in the MCA in the M1-M2 junction. With experience, in the third patient, we implanted two stents in the middle and anterior cerebral artery ipsilaterally. In the last patient, four stents were implanted, two on each side. The stent implantations were always performed under dual antiplatelet therapy (DAPT). Overall, only one temporary thromboembolic occlusion occurred as a periprocedural complication. None of the patients showed postprocedural hemorrhage, in-stent stenosis, or DCI in the vascular territories of the stented vessels. Detection and repetition of endovascular treatment of resistant spasms increase the risk of periprocedural complications and radiation exposure [ 34 ] Endovascular treatment may not always be feasible, owing to the complicated clinical management of patients with SAH, particularly respiratory and cardiovascular management. Intracranial stenting can be an unduly aggressive treatment for CVS, particularly because DAPT is required in the acute phase after SAH. Nonetheless, we believe that it is a viable treatment option as a last resort in refractory vasospasm to avoid life-threatening DCI after the failure of chemical and mechanical treatments. Of note, we observed that three of the used devices were Neuroform Atlas stents (Stryker). All sizes of this stent system can be implanted via a low profile 0.017 inch inner diameter microcatheter, thus making the navigation of distal vessel segments less traumatic and more manageable in patients with difficult probing conditions, particularly with associated CVS. This treatment method has several limitations. The need for DAPT during the acute phase after SAH is a reason for concern. Therefore, the ruptured aneurysm should be secured. All patients showed neurological improvement through intracranial stenting of recurrent CVS after the failure of various treatment methods. None of our patients showed postprocedural hemorrhage or any other persistent complication. This ultima ratio treatment has not been described in the English literature to our knowledge. Stenting, although not commonly used in this manner, is very effective over the long term and is safe if the medication is adjusted precisely. Limitations Our study has several limitations inherent to single-center retrospective data analyses. We present anecdotal experience in highly selected patients. The operator’s experience and skills influence the outcomes. The complexity of vasospasm and DCI poses a major logistic challenge for interventionists, intensivists, and neurosurgeons, far beyond the straightforward procedure of deploying a stent in a proximal brain artery. Stenting proximal arteries is only one piece in the armamentarium for the treatment of post-SAH vasospasm. Conclusion Endovascular treatment of post-SAH recurrent CVS with intracranial stenting is both practical and safe. This therapy is considered an ultima ratio after the failure of standard pharmacological and interventional measures. Peri- and post-procedural antiplatelet medication is essential to prevent thromboembolic complications. Abbreviations CT: computed tomography CTA: computed tomography angiography CTP: computed tomography perfusion CVS: cerebral vasospasm DAPT: dual antiplatelet therapy DCI: delayed cerebral ischemia DSA: digital subtraction angiography IA: intra-arterial ICA: internal carotid artery ICA: internal carotid artery MCA: middle cerebral artery MRA: magnetic resonance angiography MRI: magnetic resonance imaging mRS: modified Rankin Scale SAH: subarachnoid hemorrhage TCCD: transcranial color-coded doppler TCD: transcranial Doppler sonography Declarations Ethics approval and consent to participate This study was ethically approved by the Ethics Committee of the Landesärztekammer Baden-Wüttemberg (F-2016-128) Liebknechtstr. 33 . 70565 Stuttgart and adhered to the Declaration of Helsinki 2013. For Germany there are currently no valid guidelines for the treatment of vasospasm available. The outdated guidelines (AWMF 030/073) were stating: “An endovascular therapy of ischemic deficit due to vasospasm may be considered and carried. Randomized trials are missing and therefore there is no general recommendation possible”. The data presented in this manuscript have not be derived from a study protocol. There were generated through clinical routine and represent anecdotal observations. All patients (or their legal representatives) provided written consent to the anonymized analysis and publication of the data. Consent for publication Not applicable. Availability of data and materials The datasets used and/or analysed during the current study available from the corresponding author on reasonable request. Competing interests The authors have no conflict of interest in this regard. Funding This study was not funded. Authors' contributions A.K., P.B. and H.H. contributed to the conceptualization and design of the study, A.K. and A.C. organized the data curation, A.K., P.B. and H.B. analyzed and interpreted the patient data, A.K., P.B. and H.H. organized the methodology, H.H. and H.B. were the project administrators, H.H.,P.B. and O.G. performed the supervision, A.K. wrote the original draft, H.H., A.K., P.B. and A.C. reviewed and edited the manuscript. All authors have read and agreed to the published version of the manuscript. Acknowledgements Not applicable. References Keyrouz SG, Diringer MN. Clinical review: Prevention and therapy of vasospasm in subarachnoid hemorrhage. Crit Care. 2007;11:220. Esmaeeli S, Hrdlicka CM, Bastos AB, Wang J, Gomez-Paz S, Hanafy KA, et al. Robotically assisted transcranial Doppler with artificial intelligence for assessment of cerebral vasospasm after subarachnoid hemorrhage. J Neurocritical Care. 2020;13:32–40. 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Choi BJ, Lee TH, Lee JI, Ko JK, Park HS, Choi CH. Safety and Efficacy of Transluminal Balloon Angioplasty Using a Compliant Balloon for Severe Cerebral Vasospasm after an Aneurysmal Subarachnoid Hemorrhage. J Korean Neurosurg Soc. 2011;49:157–62. Chen C-T, Chen C-C, Wang AY-C, Wu Y-M, Chin S-C, Hsieh P-C, et al. Early strategy of scepter XC balloon angioplasty and simultaneous Nimodipine infusion for vasospasm following ruptured aneurysm. BMC Neurol. 2020;20:271. Bhogal P, Paraskevopoulos D, Makalanda HL. The use of a stent-retriever to cause mechanical dilatation of a vasospasm secondary to iatrogenic subarachnoid haemorrhage. Interv Neuroradiol. 2017;23:330–5. Badger CA, Jankowitz BT, Shaikh HA. Treatment of cerebral vasospasm secondary to subarachnoid hemorrhage utilizing the Comaneci device. Interv Neuroradiol J Peritherapeutic Neuroradiol Surg Proced Relat Neurosci. 2020;:1591019920945554. Kwon H-J, Lim J-W, Koh H-S, Park B, Choi S-W, Kim S-H, et al. Stent-Retriever Angioplasty for Recurrent Post-Subarachnoid Hemorrhagic Vasospasm - A Single Center Experience with Long-Term Follow-Up. Clin Neuroradiol. 2019;29:751–61. Bhogal P, Loh Y, Brouwer P, Andersson T, Söderman M. Treatment of cerebral vasospasm with self-expandable retrievable stents: proof of concept. J Neurointerventional Surg. 2017;9:52–9. Su YS, Ali MS, Pukenas BA, Favilla CG, Zanaty M, Hasan DM, et al. Novel Treatment of Cerebral Vasospasm Using Solitaire Stent Retriever−Assisted Angioplasty: Case Series. World Neurosurg. 2020;135:e657–63. Sen J, Belli A, Albon H, Morgan L, Petzold A, Kitchen N. Triple-H therapy in the management of aneurysmal subarachnoid haemorrhage. Lancet Neurol. 2003;2:614–21. Macdonald RL, Kassell NF, Mayer S, Ruefenacht D, Schmiedek P, Weidauer S, et al. Clazosentan to Overcome Neurological Ischemia and Infarction Occurring After Subarachnoid Hemorrhage (CONSCIOUS-1). Stroke. 2008;39:3015–21. Macdonald RL, Higashida RT, Keller E, Mayer SA, Molyneux A, Raabe A, et al. Clazosentan, an endothelin receptor antagonist, in patients with aneurysmal subarachnoid haemorrhage undergoing surgical clipping: a randomised, double-blind, placebo-controlled phase 3 trial (CONSCIOUS-2). Lancet Neurol. 2011;10:618–25. Macdonald RL, Higashida RT, Keller E, Mayer SA, Molyneux A, Raabe A, et al. Randomized Trial of Clazosentan in Patients With Aneurysmal Subarachnoid Hemorrhage Undergoing Endovascular Coiling. Stroke. 2012;43:1463–9. Macdonald RL, Higashida RT, Keller E, Mayer SA, Molyneux A, Raabe A, et al. Randomised trial of clazosentan, an endothelin receptor antagonist, in patients with aneurysmal subarachnoid hemorrhage undergoing surgical clipping (CONSCIOUS-2). Acta Neurochir Suppl. 2013;115:27–31. Jabbarli R, Pierscianek D, Rölz R, Darkwah Oppong M, Kaier K, Shah M, et al. Endovascular treatment of cerebral vasospasm after subarachnoid hemorrhage: More is more. Neurology. 2019;93:e458–66. Levitt MR, Morton RP, Haynor DR, Cohen W, Ghodke BV, Hallam DK, et al. Angiographic perfusion imaging: real-time assessment of endovascular treatment for cerebral vasospasm. J Neuroimaging Off J Am Soc Neuroimaging. 2014;24:387–92. Fischell TA, Grant G, Johnson DE. Determinants of smooth muscle injury during balloon angioplasty. Circulation. 1990;82:2170–84. Bhogal P, Pederzani G, Grytsan A, Loh Y, Brouwer PA, Andersson T, et al. The unexplained success of stentplasty vasospasm treatment - Insights using mechanistic mathematical modeling. Clin Neuroradiol. 2019;29:763–74. Andic C, Kardes O, Durdag E, Gedikoglu M, Akin S. Efficacy of endovascular treatment and feasibility of stent-assisted coiling in the presence of severe and symptomatic vasospasm. J NeuroInterventional Surg. 2017;9:1075–80. Bhambri P, Sarvi A, Wong JH, Sundararaj U, Mitha AP. Verapamil eluting stents as a possible treatment for vasospasm after subarachnoid hemorrhage. J NeuroInterventional Surg. 2017;9:875–9. Loftus ML, Minkowitz S, Tsiouris AJ, Min RJ, Sanelli PC. Utilization Guidelines for Reducing Radiation Exposure in the Evaluation of Aneurysmal Subarachnoid Hemorrhage: A Practice Quality Improvement Project. AJR Am J Roentgenol. 2010;195:176–80. Additional Declarations No competing interests reported. Cite Share Download PDF Status: Under Review Version 1 posted Editorial decision: Major revision 22 Jul, 2022 Reviews received at journal 19 Jul, 2022 Reviewers agreed at journal 16 Jul, 2022 Reviews received at journal 14 Jul, 2022 Reviewers agreed at journal 06 Jul, 2022 Reviewers invited by journal 05 Jul, 2022 Editor assigned by journal 05 Jul, 2022 Editor invited by journal 05 Jul, 2022 Submission checks completed at journal 05 Jul, 2022 First submitted to journal 27 Jun, 2022 You are reading this latest preprint version Research Square lets you share your work early, gain feedback from the community, and start making changes to your manuscript prior to peer review in a journal. As a division of Research Square Company, we’re committed to making research communication faster, fairer, and more useful. We do this by developing innovative software and high quality services for the global research community. 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Also discoverable on Platform About Our Team In Review Editorial Policies Advisory Board Help Center Resources Author Services Accessibility API Access RSS feed Manage Cookie Preferences © Research Square 2026 | ISSN 2693-5015 (online) Privacy Policy Terms of Service Do Not Sell My Personal Information {"props":{"pageProps":{"initialData":{"identity":"rs-1801216","acceptedTermsAndConditions":true,"allowDirectSubmit":false,"archivedVersions":[],"articleType":"Research Article","associatedPublications":[],"authors":[{"id":118806461,"identity":"a3163277-2b87-476c-83a8-70f2e530d367","order_by":0,"name":"Ali Khanafer","email":"data:image/png;base64,iVBORw0KGgoAAAANSUhEUgAAAZAAAAAyAQMAAABI0h/eAAAABlBMVEX///8AAABVwtN+AAAACXBIWXMAAA7EAAAOxAGVKw4bAAAA5UlEQVRIiWNgGAWjYHACZmYQyd7AwPgYym8gTgvPAQZmYwYGAyCfkXgtbNJgLQwEtOjOPsBsXFBzR56HvfdZdUHFn2j+dqCWHxXbcGoxO5fAnDzj2DPDHp7jZrdnnDHInXGYsYGx58xt3FrO8H8+zMN2mHG/RBrbbd42g9wGoBZmxjZ8WhiYD/P8O2zfI/+MrRikZT4xWpJ52w4n9kiwsTGDtGwgRosxb9/h5B6eNGZpnjPGuRuBWg7i9wsDUOW3w7Y97McYP/NUyOXOO3/44IMfFbi1YAcHSFQ/CkbBKBgFowANAACLKlHPWrY4CwAAAABJRU5ErkJggg==","orcid":"","institution":"Neuroradiologische Klinik, Klinikum Stuttgart","correspondingAuthor":true,"submittingAuthor":false,"prefix":"","firstName":"Ali","middleName":"","lastName":"Khanafer","suffix":""},{"id":118806462,"identity":"2ed5c7a2-ef34-4e73-9b97-6b0f8da9c0d9","order_by":1,"name":"Alexandru Cimpoca","email":"","orcid":"","institution":"Neuroradiologische Klinik, Klinikum Stuttgart","correspondingAuthor":false,"submittingAuthor":false,"prefix":"","firstName":"Alexandru","middleName":"","lastName":"Cimpoca","suffix":""},{"id":118806463,"identity":"64a4b8f4-3e61-426f-b5f1-a61d459bc989","order_by":2,"name":"Pervinder Bhogal","email":"","orcid":"","institution":"The Royal London Hospital","correspondingAuthor":false,"submittingAuthor":false,"prefix":"","firstName":"Pervinder","middleName":"","lastName":"Bhogal","suffix":""},{"id":118806464,"identity":"4e1dc6b4-f3d8-495e-85d1-8a917df7fb3a","order_by":3,"name":"Hansjörg Bäzner","email":"","orcid":"","institution":"Neurologische Klinik, Klinikum Stuttgart","correspondingAuthor":false,"submittingAuthor":false,"prefix":"","firstName":"Hansjörg","middleName":"","lastName":"Bäzner","suffix":""},{"id":118806465,"identity":"f0bef555-a163-433c-ab51-c776ec102556","order_by":4,"name":"Oliver Ganslandt","email":"","orcid":"","institution":"Neurochirurgische Klinik, Klinikum Stuttgart","correspondingAuthor":false,"submittingAuthor":false,"prefix":"","firstName":"Oliver","middleName":"","lastName":"Ganslandt","suffix":""},{"id":118806466,"identity":"47691708-4b4a-4159-b7bb-ab6afdcfa312","order_by":5,"name":"Hans Henkes","email":"","orcid":"","institution":"Neuroradiologische Klinik, Klinikum Stuttgart","correspondingAuthor":false,"submittingAuthor":false,"prefix":"","firstName":"Hans","middleName":"","lastName":"Henkes","suffix":""}],"badges":[],"createdAt":"2022-06-27 20:44:11","currentVersionCode":1,"declarations":"","doi":"10.21203/rs.3.rs-1801216/v1","doiUrl":"https://doi.org/10.21203/rs.3.rs-1801216/v1","draftVersion":[],"editorialEvents":[],"editorialNote":"","failedWorkflow":false,"files":[{"id":23829476,"identity":"b570242b-fa97-44ac-a476-be057ed9e896","added_by":"auto","created_at":"2022-07-13 19:01:38","extension":"png","order_by":1,"title":"Figure 1","display":"","copyAsset":false,"role":"figure","size":11374351,"visible":true,"origin":"","legend":"\u003cp\u003eDiagnostic imaging in a 48-year-old woman. (\u003cstrong\u003ea\u003c/strong\u003e) DSA of the right ICA in posterior-anterior projection showed an MCA bifurcation aneurysm with recurrent CVS despite endovascular treatment with IA milrinone 1 day earlier. (\u003cstrong\u003eb\u003c/strong\u003e)\u003cstrong\u003e \u003c/strong\u003eAngiogram after IA infusion of 8 mg milrinone over 30 min, showing improvement in CVS. (\u003cstrong\u003ec\u003c/strong\u003e)\u003cstrong\u003e \u003c/strong\u003eThe implanted coils shifted dorsally into the parent vessel and caused a perfusion delay in the dependent vasculature. (\u003cstrong\u003ed\u003c/strong\u003e)\u003cstrong\u003e \u003c/strong\u003eA microcatheter (Echelon 10 90°, Medtronic) and microguidewire (X-celerator 10, Medtronic) were navigated into the M2 segment of the MCA after exchange by using a low-profile microcatheter (Marathon, Medtronic) and microguidewire (Mirage, Medtronic). (\u003cstrong\u003ee\u003c/strong\u003e)\u003cstrong\u003e \u003c/strong\u003eAngiogram of the right\u003cstrong\u003e \u003c/strong\u003eICA after stent deployment, showing occlusion of the stent-covered MCA (M2-segment). (\u003cstrong\u003ef\u003c/strong\u003e)\u003cstrong\u003e \u003c/strong\u003eAn\u003cstrong\u003e \u003c/strong\u003eLVIS (2.5/24 mm) stent (MicroVention) is deployed in the distal ICA and M1-M2 branches. (\u003cstrong\u003eg\u003c/strong\u003e)\u003cstrong\u003e \u003c/strong\u003eRecanalization of the stent-covered MCA after intravenous eptifibatide administration. (\u003cstrong\u003eh\u003c/strong\u003e) Advancement of the coil embolization through the implanted stent. (\u003cstrong\u003ei\u003c/strong\u003e)\u003cstrong\u003e \u003c/strong\u003eAngiogram of the right\u003cstrong\u003e \u003c/strong\u003eICA after completion of coil occlusion of the aneurysm. Follow-up angiography at 3\u003cstrong\u003e \u003c/strong\u003emonths (\u003cstrong\u003ej\u003c/strong\u003e) and 5 years (\u003cstrong\u003ek\u003c/strong\u003e, \u003cstrong\u003el\u003c/strong\u003e), showing no evidence of in-stent stenosis.\u003c/p\u003e\u003cp\u003e\u003cbr\u003e\u003c/p\u003e","description":"","filename":"11.png","url":"https://assets-eu.researchsquare.com/files/rs-1801216/v1/82fabe5d7d5773e6c0705e16.png"},{"id":23830202,"identity":"4460bcce-253c-4bd7-9d70-1a31b5838b6a","added_by":"auto","created_at":"2022-07-13 19:06:38","extension":"png","order_by":2,"title":"Figure 2","display":"","copyAsset":false,"role":"figure","size":7386905,"visible":true,"origin":"","legend":"\u003cp\u003eDiagnostic imaging in a 41-year-old man with post-SAH recurrent CVS. (\u003cstrong\u003ea\u003c/strong\u003e) DSA of the right ICA in posterior-anterior projection, showing persistent severe CVS of the MCA and ACA despite treatment with IA administration of milrinone. (\u003cstrong\u003eb-c\u003c/strong\u003e) An Enterprise (4/16 mm) stent (Cerenovus) was deployed into the M1 branch showing sufficient vasodilatation. (\u003cstrong\u003ed\u003c/strong\u003e) Another Enterprise (4/23 mm) stent was deployed into the A1-A2 branches of the ACA. (\u003cstrong\u003ee-f\u003c/strong\u003e) Angiogram after stent deployment, showing sufficient vasodilatation. (\u003cstrong\u003eg-h\u003c/strong\u003e)\u003cstrong\u003e \u003c/strong\u003eFollow-up angiography after 3 and 6 months, demonstrating regular blood flow without evidence of in-stent stenoses or any other issue.\u003c/p\u003e\u003cp\u003e\u003cbr\u003e\u003c/p\u003e","description":"","filename":"22.png","url":"https://assets-eu.researchsquare.com/files/rs-1801216/v1/1fc52bea4561ca07ec70fec4.png"},{"id":23829474,"identity":"6f048089-dcde-4518-9594-9d985aaca41a","added_by":"auto","created_at":"2022-07-13 19:01:38","extension":"png","order_by":3,"title":"Figure 3","display":"","copyAsset":false,"role":"figure","size":11951111,"visible":true,"origin":"","legend":"\u003cp\u003eDiagnostic imaging in a 67-year-old woman with post-SAH recurrent CVS. (\u003cstrong\u003ea\u003c/strong\u003e)\u003cstrong\u003e \u003c/strong\u003eDSA of the right\u003cstrong\u003e \u003c/strong\u003eICA in posterior-anterior projection, showing persistent severe CVS of the ACA despite treatment with IA milrinone. (\u003cstrong\u003eb\u003c/strong\u003e)\u003cstrong\u003e \u003c/strong\u003eDSA of the left ICA in posterior-anterior projection, showing persistent severe CVS of the MCA and ACA despite treatment with IA administration of milrinone. (\u003cstrong\u003ec\u003c/strong\u003e)\u003cstrong\u003e \u003c/strong\u003eMechanical angioplasty with a pRESET LITE\u003cstrong\u003e \u003c/strong\u003e(4/20 mm) stentriever deployed in the spastic right ACA A1-A2 segments. (\u003cstrong\u003ed\u003c/strong\u003e)\u003cstrong\u003e \u003c/strong\u003eAngiogram after IA infusion of 8 mg milrinone and finishing mechanical angioplasty with a stentriever, showing persistent CVS. (\u003cstrong\u003ee\u003c/strong\u003e)\u003cstrong\u003e \u003c/strong\u003eA Neuroforom Atlas (3/15 mm) stent was deployed in the spastic A2 branch. (\u003cstrong\u003ef\u003c/strong\u003e)\u003cstrong\u003e \u003c/strong\u003eA Baby Leo (2/12 mm) stent (Balt Extrusion) was deployed in a spastic A1 branch. \u003cstrong\u003eg \u003c/strong\u003eAngiogram of the right\u003cstrong\u003e \u003c/strong\u003eICA in posterior-anterior projection after stent deployment, showing sufficient vasodilatation of the ACA.\u003cstrong\u003e (h\u003c/strong\u003e)\u003cstrong\u003e \u003c/strong\u003eAngiogram of the left\u003cstrong\u003e \u003c/strong\u003eICA in posterior-anterior projection after stent deployment in the ACA (A1-A2; Neuroforom Atlas 4.5/30) and MCA (M1-M2 Neuroforom Atlas 4/24), showing sufficient vasodilatation. (\u003cstrong\u003ei-j\u003c/strong\u003e)\u003cstrong\u003e \u003c/strong\u003eAngiogram at 11 days and\u003cstrong\u003e (k-l\u003c/strong\u003e)\u003cstrong\u003e \u003c/strong\u003eat 3\u003cstrong\u003e \u003c/strong\u003emonth follow-up, showing no evidence of vessel injuries or in-stent stenosis.\u003c/p\u003e\u003cp\u003e\u003cbr\u003e\u003c/p\u003e","description":"","filename":"33.png","url":"https://assets-eu.researchsquare.com/files/rs-1801216/v1/52eb1bac31e9bbe8406cad3b.png"},{"id":23830204,"identity":"9e6efc19-ef94-4ca3-b23a-c1a10c22bbe7","added_by":"auto","created_at":"2022-07-13 19:06:41","extension":"pdf","order_by":0,"title":"","display":"","copyAsset":false,"role":"manuscript-pdf","size":398667,"visible":true,"origin":"","legend":"","description":"","filename":"manuscript.pdf","url":"https://assets-eu.researchsquare.com/files/rs-1801216/v1/45e28c05-2517-432a-bf96-5a5fa1f11d2e.pdf"}],"financialInterests":"No competing interests reported.","formattedTitle":"Intracranial Stenting as a Bail-out Option for Posthemorrhagic Cerebral Vasospasm: A Single-Center Experience with Long-Term Follow-Up","fulltext":[{"header":"Introduction","content":"\u003cp\u003eCerebral vasospasm (CVS) is one of the leading causes of neurological deterioration after subarachnoid hemorrhage (SAH). CVS is responsible for a morbidity and mortality incidence of approximately 20% [\u003cspan citationid=\"CR1\" class=\"CitationRef\"\u003e1\u003c/span\u003e, \u003cspan citationid=\"CR2\" class=\"CitationRef\"\u003e2\u003c/span\u003e]. Among patients with SAH, 50\u0026ndash;70% develop CVS, and approximately 30% present neurologic deficits [\u003cspan citationid=\"CR3\" class=\"CitationRef\"\u003e3\u003c/span\u003e, \u003cspan citationid=\"CR4\" class=\"CitationRef\"\u003e4\u003c/span\u003e]. Despite limited accuracy, transcranial Doppler sonography (TCD) and transcranial color-coded Doppler (TCCD) remain preferred diagnostic methods in intensive care units for the detection of vasospasm, because of their logistic simplicity [\u003cspan citationid=\"CR5\" class=\"CitationRef\"\u003e5\u003c/span\u003e]. Magnetic resonance angiography (MRA), particularly computed tomography angiography (CTA) with computed tomography perfusion (CTP), is more reliable in CVS detection. Digital subtraction angiography (DSA) remains the gold standard for detecting and quantifying CVS [\u003cspan citationid=\"CR6\" class=\"CitationRef\"\u003e6\u003c/span\u003e]. Conservative management by intravenous or oral administration of calcium channel blockers has yielded poor results [\u003cspan citationid=\"CR7\" class=\"CitationRef\"\u003e7\u003c/span\u003e]. Endovascular management strategies allow for effective treatment of CVS. These strategies include\u003c/p\u003e \u003cp\u003e \u003cul\u003e \u003cli\u003e \u003cp\u003eShort-term intra-arterial administration of nimodipine [\u003cspan citationid=\"CR8\" class=\"CitationRef\"\u003e8\u003c/span\u003e], milrinone [\u003cspan citationid=\"CR9\" class=\"CitationRef\"\u003e9\u003c/span\u003e, \u003cspan citationid=\"CR10\" class=\"CitationRef\"\u003e10\u003c/span\u003e], or verapamil [\u003cspan citationid=\"CR11\" class=\"CitationRef\"\u003e11\u003c/span\u003e];\u003c/p\u003e \u003c/li\u003e \u003cli\u003e \u003cp\u003elong-term intra-arterial selective infusion of nimodipine [\u003cspan citationid=\"CR12\" class=\"CitationRef\"\u003e12\u003c/span\u003e]; and\u003c/p\u003e \u003c/li\u003e \u003cli\u003e \u003cp\u003emechanical dilatation of large arteries with non-compliant balloons, compliant balloons [\u003cspan additionalcitationids=\"CR14 CR15 CR16\" citationid=\"CR13\" class=\"CitationRef\"\u003e13\u003c/span\u003e\u0026ndash;\u003cspan citationid=\"CR17\" class=\"CitationRef\"\u003e17\u003c/span\u003e], or stentrievers [\u003cspan additionalcitationids=\"CR19 CR20 CR21\" citationid=\"CR18\" class=\"CitationRef\"\u003e18\u003c/span\u003e\u0026ndash;\u003cspan citationid=\"CR22\" class=\"CitationRef\"\u003e22\u003c/span\u003e].\u003c/p\u003e \u003c/li\u003e \u003c/ul\u003e \u003c/p\u003e \u003cp\u003eThe substantial logistic efforts required for diagnosis and endovascular treatment outside the intensive care unit, and the complex cardiovascular and respiratory monitoring required before and during treatment, may lead to treatment delays and consequently poor outcomes. In addition, despite the development of pharmacological and endovascular treatment options, the treatment of post-SAH CVS remains a challenge because of its frequent occurrence.\u003c/p\u003e \u003cp\u003eHere, we report our experience in the use of intracranial stenting in the treatment of patients with post-SAH CVS.\u003c/p\u003e"},{"header":"Methods","content":"\u003cp\u003e\u003cstrong\u003eStudy Population\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eBetween January 2010 and December 2021, we treated a total of 883 patients with SAH.\u003c/p\u003e\n\u003cp\u003eThe management strategy followed in our neurovascular center is as follows:\u003c/p\u003e\n\u003cp\u003e- Early diagnosis of SAH according to computed tomography (CT)/CTA or magnetic resonance imaging (MRI)/MRA, followed by DSA.\u003c/p\u003e\n\u003cp\u003e- Early endovascular or microsurgical aneurysm treatment based on individualized multidisciplinary decision-making\u003c/p\u003e\n\u003cp\u003e- Early external cerebrospinal fluid drainage when deemed necessary\u0026nbsp;\u003c/p\u003e\n\u003cp\u003e- Administration of intravenous or\u0026nbsp;\u003cem\u003eper os\u003c/em\u003e nimodipine starting on the first clinical day of stay, if tolerated.\u003c/p\u003e\n\u003cp\u003eDuring this period, 275 patients were diagnosed with post-SAH CVS. We retrospectively evaluated our database and identified 76 patients with recurrent CVS after initial short-term intra-arterial (IA) administration of milrinone (Corotrop, Sanofi-Avantis). These patients were treated with repeated IA administration of vasodilators and/or interventional mechanical vasodilatation of the vessel segments affected by CVS. The mechanical treatments applied were stent retriever-assisted angioplasty, pRELAX device-assisted angioplasty, and intracranial implantation of self-expandable stents. In six of these patients with CVS, intracranial self-expanding stent implantation was performed. The clinical data files and the imaging results were available for retrospective evaluation. The patients\u0026rsquo; demographics and clinical characteristics are listed in Table 1.\u003c/p\u003e\n\u003cp\u003e\u003cstrong style='font-weight: 700; color: rgb(0, 0, 0); font-family: \"Times New Roman\"; font-size: medium; font-style: normal; font-variant-ligatures: normal; font-variant-caps: normal; letter-spacing: normal; orphans: 2; text-align: start; text-indent: 0px; text-transform: none; white-space: normal; widows: 2; word-spacing: 0px; -webkit-text-stroke-width: 0px; text-decoration-style: initial; text-decoration-color: initial;'\u003eTable 1: Demographics and clinical characteristics of patients.\u003c/strong\u003e\u0026nbsp;\u003c/p\u003e\n\u003ctable border=\"0\" cellpadding=\"0\" cellspacing=\"0\" width=\"0\"\u003e\n \u003ctbody\u003e\n \u003ctr\u003e\n \u003ctd width=\"15.919629057187016%\"\u003e\n \u003cp\u003e\u003cstrong\u003ePatients\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"8.65533230293663%\"\u003e\n \u003cp\u003eGroup\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"9.273570324574962%\"\u003e\n \u003cp\u003eAge \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp;(years)\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"9.737248840803709%\"\u003e\n \u003cp\u003eGender\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"7.2642967542503865%\"\u003e\n \u003cp\u003eHH\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"8.809891808346213%\"\u003e\n \u003cp\u003eFisher\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"13.446676970633694%\"\u003e\n \u003cp\u003eDays between SAH and vasospasm\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"13.446676970633694%\"\u003e\n \u003cp\u003eDays between SAH and stent-implantation\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"bottom\" width=\"13.446676970633694%\"\u003e\u003cbr\u003e\u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd width=\"15.919629057187016%\"\u003e\n \u003cp\u003e1\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"8.65533230293663%\"\u003e\n \u003cp\u003e1\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"9.273570324574962%\"\u003e\n \u003cp\u003e61\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"9.737248840803709%\"\u003e\n \u003cp\u003eF\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"7.2642967542503865%\"\u003e\n \u003cp\u003e1\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"8.809891808346213%\"\u003e\n \u003cp\u003e3\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"13.446676970633694%\"\u003e\n \u003cp\u003e0\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"13.446676970633694%\"\u003e\n \u003cp\u003e0\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"bottom\" width=\"13.446676970633694%\"\u003e\u003cbr\u003e\u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd width=\"15.919629057187016%\"\u003e\n \u003cp\u003e2\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"8.65533230293663%\"\u003e\n \u003cp\u003e1\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"9.273570324574962%\"\u003e\n \u003cp\u003e48\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"9.737248840803709%\"\u003e\n \u003cp\u003eF\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"7.2642967542503865%\"\u003e\n \u003cp\u003e3\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"8.809891808346213%\"\u003e\n \u003cp\u003e2\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"13.446676970633694%\"\u003e\n \u003cp\u003e0\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"13.446676970633694%\"\u003e\n \u003cp\u003e0\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"bottom\" width=\"13.446676970633694%\"\u003e\u003cbr\u003e\u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd width=\"15.919629057187016%\"\u003e\n \u003cp\u003e3\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"8.65533230293663%\"\u003e\n \u003cp\u003e2\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"9.273570324574962%\"\u003e\n \u003cp\u003e52\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"9.737248840803709%\"\u003e\n \u003cp\u003eF\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"7.2642967542503865%\"\u003e\n \u003cp\u003e3\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"8.809891808346213%\"\u003e\n \u003cp\u003e4\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"13.446676970633694%\"\u003e\n \u003cp\u003e4\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"13.446676970633694%\"\u003e\n \u003cp\u003e15\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"bottom\" width=\"13.446676970633694%\"\u003e\u003cbr\u003e\u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd width=\"15.919629057187016%\"\u003e\n \u003cp\u003e4\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"8.65533230293663%\"\u003e\n \u003cp\u003e2\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"9.273570324574962%\"\u003e\n \u003cp\u003e49\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"9.737248840803709%\"\u003e\n \u003cp\u003eF\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"7.2642967542503865%\"\u003e\n \u003cp\u003e5\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"8.809891808346213%\"\u003e\n \u003cp\u003e4\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"13.446676970633694%\"\u003e\n \u003cp\u003e7\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"13.446676970633694%\"\u003e\n \u003cp\u003e8\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"bottom\" width=\"13.446676970633694%\"\u003e\u003cbr\u003e\u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd width=\"15.919629057187016%\"\u003e\n \u003cp\u003e5\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"8.65533230293663%\"\u003e\n \u003cp\u003e2\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"9.273570324574962%\"\u003e\n \u003cp\u003e41\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"9.737248840803709%\"\u003e\n \u003cp\u003eM\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"7.2642967542503865%\"\u003e\n \u003cp\u003e5\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"8.809891808346213%\"\u003e\n \u003cp\u003e4\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"13.446676970633694%\"\u003e\n \u003cp\u003e6\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"13.446676970633694%\"\u003e\n \u003cp\u003e7\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"bottom\" width=\"13.446676970633694%\"\u003e\u003cbr\u003e\u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd width=\"15.919629057187016%\"\u003e\n \u003cp\u003e6\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"8.65533230293663%\"\u003e\n \u003cp\u003e2\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"9.273570324574962%\"\u003e\n \u003cp\u003e67\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"9.737248840803709%\"\u003e\n \u003cp\u003eF\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"7.2642967542503865%\"\u003e\n \u003cp\u003e3\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"8.809891808346213%\"\u003e\n \u003cp\u003e4\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"13.446676970633694%\"\u003e\n \u003cp\u003e5\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"13.446676970633694%\"\u003e\n \u003cp\u003e6\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"bottom\" width=\"13.446676970633694%\"\u003e\u003cbr\u003e\u003c/td\u003e\n \u003c/tr\u003e\n \u003c/tbody\u003e\n\u003c/table\u003e\n\u003cp\u003e\u003cbr\u003e\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eData Analysis\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eAll six case histories were analyzed individually. Vasospasm was either prospectively diagnosed during the hospital stay or retrospectively identified by analysis of the imaging material by a neuroradiologist (with 3 years of experience in neuroradiological imaging), as supervised by the senior author. The six patients who underwent intracranial stenting were initially treated with IA vasodilators as soon as the vasospasms were angiographically diagnosed. After review of clinical data files and all imaging results (CT, MRI/MRA, and DSA) of the patients treated with intracranial stenting, the patients were divided into the following two groups:\u003c/p\u003e\n\u003cp\u003e- Group 1: Intracranial stenting during endovascular therapy of a ruptured aneurysm, to allow for catheter access despite narrowing of the parent artery and in the context of stent-assisted coiling\u003c/p\u003e\n\u003cp\u003e- Group 2: Intracranial stenting for recurrent vasospasm after failed IA infusion of vasodilators and/or mechanical treatment, particularly in patients with severe\u0026nbsp;CVS who were at risk of brain infarction\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eFollow-up\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eEarly follow-up catheter angiography was performed before discharge according to routine clinical protocols. The first mid-term angiographic follow-up was performed 3\u0026ndash;6 months after discharge. Clinical assessment was performed with the modified Rankin Scale (mRS) during the acute post-SAH period, discharge, and follow-up visits.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eStatistical Analysis\u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp;\u0026nbsp;\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eFor categorical variables, results are described as percentages. Continuous variables are reported as mean and standard deviation.\u0026nbsp;\u003c/p\u003e"},{"header":"Results","content":"\u003cp\u003e\u003cstrong\u003eGroup 1: Intracranial stenting of refractory CVS during endovascular treatment of the ruptured aneurysm\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eThis group consisted of two patients and represented our first experience in intracranial stenting as a treatment for recurrent CVS. Both patients showed CVS on day 1 during the first DSA examination to locate the source of hemorrhage. At that time, we suspected that the current SAH was not the first. This suspicion was confirmed in one patient, according to information provided by the family regarding a severe headache 7 days earlier. Both patients showed neurological deficits due to CVS; therefore, endovascular treatment could not be delayed. Endovascular coil occlusion of the ruptured aneurysm was planned for both patients. Initial treatment with IA vasodilators was performed in both patients for approximately 30 minutes immediately before the start of endovascular coiling of the ruptured aneurysm. After an infusion of 8 mg milirinone into the internal carotid artery (ICA), the affected vessel segments showed sufficient vasodilation to enable coil occlusion of the aneurysms. During the endovascular coiling of the ruptured aneurysms, recurrent vasospasm was detected in both patients. Concurrently the implanted coils shifted into the parent vessels. Vasospasm and coil displacement resulted in a substantial perfusion delay of the dependent vasculature.\u003c/p\u003e\n\u003cp\u003eTo be able to continue the treatment, prevent the increase in CVS, and prevent ischemic changes, we implanted a self-expanding stent in the parent artery. Consequently, the covered vessel segments dilated, the perfusion of the distal vessels improved, and we completed the treatment Fig. 1. The post-procedural CT imaging showed no ischemic lesions due to CVS. On day 1 after aneurysm coiling, one patient showed generalized moderate vasospasm in the proximal segments of the middle and anterior cerebral artery, excluding the stented M1-M2 vessel segments. In both patients, the injection of IA vasodilators for 30 min induced significant dilatation of the affected vessels and vessel segments. After that, the patients showed no further recurrent vasospasm, ischemic lesions, or new neurological deficits during the remainder of their clinical stay.\u003c/p\u003e\n\u003ch3\u003e\u003cstrong\u003eGroup 2: Intracranial stenting of refractory CVS after failure of IA vasodilators or mechanical treatment\u003c/strong\u003e\u003c/h3\u003e\n\u003cp\u003eThis group included four patients with a mean age of 52.2 years (range 41\u0026ndash;67 years). Three of these patients were in poor clinical condition, and the clinical management was complicated by periprocedural and postprocedural issues.\u0026nbsp;\u003c/p\u003e\n\u003cp\u003eOne patient was diagnosed with periprocedural dissection of the left ICA after endovascular treatment of a giant left ICA aneurysm with pCONUS-assisted coiling. This dissection caused an ischemic lesion 6 days later by increasing vasoconstriction due to vasospasm. Another patient was found to have an intracerebral hemorrhage in the brain\u0026apos;s left frontal lobe after a new external ventricular drain was inserted 5 days after endovascular treatment of a giant aneurysm of the right ICA with flow diversion-assisted coiling. The third patient showed a new postoperative hemorrhage on non-contrast CT performed immediately after microsurgical clipping of an aneurysm of the right\u0026nbsp;middle cerebral artery\u0026nbsp;(MCA) bifurcation.\u003c/p\u003e\n\u003cp\u003eBeyond the recurrent generalized CVS, all these conditions increased the intracranial pressure in the patients and complicated their clinical management. One patient underwent hemicraniectomy as a result of the rebleeding. The fourth patient experienced only headaches at the beginning of the clinical stay. One day later, the patient showed rapid high-grade neurological deficits due to CVS. All patients in this group showed recurrent CVS and therefore underwent at least one independent therapy session before stent implantation and multiple endovascular procedures (median 3; 2\u0026ndash;3).\u003c/p\u003e\n\u003cp\u003eExcept for patients in group 1, intracranial stenting as a treatment for CVS was not performed in the first vasospasm treatment session. Three patients also underwent interventional mechanical treatment with a stent retriever or pRELAX device. In two patients, we performed IA continuous selective infusion of nimodipine for 3\u0026ndash;6 days because of generalized CVS in other vascular segments. At the beginning of our experience, we used intracranial stenting in CVS to dilate the most affected or relevant vessel segments by using only one stent. Later, with increasing experience, we have decided to insert as many as four stents in a patient with generalized recurrent CVS. The concerning vessel segments in these patients were ICA bifurcation, A1, A2, AcomA, M1, and M2. We performed stenting of two to five vessel segments on each patient. A total of 18 artery segments were covered with stents. Ten stents were used, and we successfully implanted the stents into the spastic segments after IA vasodilator infusion in all cases. The medications and interventional characteristics are listed in Table 2. After the stenting procedures, all vessel segments showed satisfactory vasodilation and improved perfusion of the distal vasculature Figs. 2, 3. Three patients required further endovascular CVS treatment, but not for the stent-covered segments. No evidence of any luminal narrowing of the stented vessels was observed. No thromboembolic or spasm-related ischemic lesions were detectable in the supply area of the treated segments in control CT or MRI after stent implantation. Most patients (five of six, 83.3%) showed neurological improvement at discharge, and all patients showed neurological improvement at the 6-month follow-up. A good clinical outcome (mRS \u0026le; 2) was achieved in five of six patients Table 3.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eTable 2: Radiological and interventional findings of the patients in both groups.\u003c/strong\u003e\u003c/p\u003e\n\u003cdiv align=\"center\"\u003e\n \u003ctable border=\"0\" cellpadding=\"0\" cellspacing=\"0\" width=\"0\"\u003e\n \u003ctbody\u003e\n \u003ctr\u003e\n \u003ctd width=\"8.7018544935806%\"\u003e\n \u003cp\u003ePatients no.\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"6.704707560627675%\"\u003e\n \u003cp\u003eGroup\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"19.971469329529246%\"\u003e\n \u003cp\u003eLoading Medication\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"22.39657631954351%\"\u003e\n \u003cp\u003eStents\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"7.988587731811697%\"\u003e\n \u003cp\u003eVessels\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"11.269614835948644%\"\u003e\n \u003cp\u003eSegments\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"9.12981455064194%\"\u003e\n \u003cp\u003eIschemia after Stent\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"13.837375178316691%\"\u003e\n \u003cp\u003epostprocedural bleeding\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd width=\"8.7018544935806%\"\u003e\n \u003cp\u003e1\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"6.704707560627675%\"\u003e\n \u003cp\u003e1\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"19.971469329529246%\"\u003e\n \u003cp\u003e1 x 500 mg ASA \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; 1 x 75 mg Prasugrel \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"22.39657631954351%\"\u003e\n \u003cp\u003e1 x Solitaire 4/15\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"7.988587731811697%\"\u003e\n \u003cp\u003eACA ri\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"11.269614835948644%\"\u003e\n \u003cp\u003eA1-A2\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"9.12981455064194%\"\u003e\n \u003cp\u003eno\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"13.837375178316691%\"\u003e\n \u003cp\u003eno\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd width=\"8.7018544935806%\"\u003e\n \u003cp\u003e2\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"6.704707560627675%\"\u003e\n \u003cp\u003e1\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"19.971469329529246%\"\u003e\n \u003cp\u003e1 x 4 mg Eptifibatide \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp;2 x 500 mg ASA \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; 1 x 600 mg Clopidogrel \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"22.39657631954351%\"\u003e\n \u003cp\u003e1 x LVIS Jr. 2,5/24\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"7.988587731811697%\"\u003e\n \u003cp\u003eMCA ri\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"11.269614835948644%\"\u003e\n \u003cp\u003eCaro-bi-M1-M2\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"9.12981455064194%\"\u003e\n \u003cp\u003eno\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"13.837375178316691%\"\u003e\n \u003cp\u003eno\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd width=\"8.7018544935806%\"\u003e\n \u003cp\u003e3\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"6.704707560627675%\"\u003e\n \u003cp\u003e2\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"19.971469329529246%\"\u003e\n \u003cp\u003e1 x 500 mg ASA \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; 1 x 30 mg Prasugrel \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"22.39657631954351%\"\u003e\n \u003cp\u003e1 x Enterprise 4/39\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"7.988587731811697%\"\u003e\n \u003cp\u003eMCA ri\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"11.269614835948644%\"\u003e\n \u003cp\u003eM1-M2\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"9.12981455064194%\"\u003e\n \u003cp\u003eno\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"13.837375178316691%\"\u003e\n \u003cp\u003eno\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd width=\"8.7018544935806%\"\u003e\n \u003cp\u003e4\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"6.704707560627675%\"\u003e\n \u003cp\u003e2\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"19.971469329529246%\"\u003e\n \u003cp\u003e1 x 12.4 mg Eptifibatide \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp;1 x 500 mg ASA \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; 1 x 180 mg Ticagrelor \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"22.39657631954351%\"\u003e\n \u003cp\u003e1 x Enterprise 2 4/30\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"7.988587731811697%\"\u003e\n \u003cp\u003eMCA ri \u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"11.269614835948644%\"\u003e\n \u003cp\u003eM1-M2\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"9.12981455064194%\"\u003e\n \u003cp\u003eno\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"13.837375178316691%\"\u003e\n \u003cp\u003eno\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd width=\"8.7018544935806%\"\u003e\n \u003cp\u003e5\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"6.704707560627675%\"\u003e\n \u003cp\u003e2\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"19.971469329529246%\"\u003e\n \u003cp\u003e1 x 500 mg ASA \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; 1 x 10 mg Prasugrel \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"22.39657631954351%\"\u003e\n \u003cp\u003e1x Enterprise 4/16 \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp;1x Enterprise 4/23\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"7.988587731811697%\"\u003e\n \u003cp\u003eMCA ri \u0026nbsp; \u0026nbsp;ACA ri\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"11.269614835948644%\"\u003e\n \u003cp\u003eM1 \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp;A1-A2\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"9.12981455064194%\"\u003e\n \u003cp\u003eno\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"13.837375178316691%\"\u003e\n \u003cp\u003eno\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd width=\"8.7018544935806%\"\u003e\n \u003cp\u003e6\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"6.704707560627675%\"\u003e\n \u003cp\u003e2\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"19.971469329529246%\"\u003e\n \u003cp\u003e1 x 12.4 mg Eptifibatide \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp;1 x 500 mg ASA \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; 1 x 180 mg Ticagrelor \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"22.39657631954351%\"\u003e\n \u003cp\u003e1 x Neuroform Atlas 3/15 \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp;1 x Baby Leo 2/12 \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp;1 x Neuroform Atlas 4/24 \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; 1 x Neuroform Atlas 4,5/30\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"7.988587731811697%\"\u003e\n \u003cp\u003eACA ri \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp;ACA ri \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp;MCA le \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp;ACA le\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"11.269614835948644%\"\u003e\n \u003cp\u003eA2 \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; A1 \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; M1+Caro-bi \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp;A1-A2\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"9.12981455064194%\"\u003e\n \u003cp\u003eno\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"13.837375178316691%\"\u003e\n \u003cp\u003eno\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003c/tbody\u003e\n \u003c/table\u003e\n\u003c/div\u003e\n\u003cp\u003e\u003cbr\u003e\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eTable 3: Clinical and radiological findings of the patients in both groups.\u003c/strong\u003e\u003c/p\u003e\n\u003ctable border=\"0\" cellpadding=\"0\" cellspacing=\"0\" width=\"0\"\u003e\n \u003ctbody\u003e\n \u003ctr\u003e\n \u003ctd width=\"10.45045045045045%\"\u003e\n \u003cp\u003ePatients \u0026nbsp; \u0026nbsp; \u0026nbsp; no.\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"8.288288288288289%\"\u003e\n \u003cp\u003eGroup\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"13.693693693693694%\"\u003e\n \u003cp\u003eTCDD before \u0026nbsp; \u0026nbsp; the stenting\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"12.252252252252251%\"\u003e\n \u003cp\u003emRS before stenting\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"17.83783783783784%\"\u003e\n \u003cp\u003eTCDD 1 day after the stenting\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"12.072072072072071%\"\u003e\n \u003cp\u003emRS on discharge\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"8.468468468468469%\"\u003e\n \u003cp\u003emRS \u0026nbsp; \u0026nbsp; 90 days\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"9.90990990990991%\"\u003e\n \u003cp\u003emRS \u0026nbsp; \u0026nbsp; 180 days\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"7.027027027027027%\"\u003e\n \u003cp\u003elast mRS\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd width=\"10.45045045045045%\"\u003e\n \u003cp\u003e1\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"8.288288288288289%\"\u003e\n \u003cp\u003e1\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"13.693693693693694%\"\u003e\n \u003cp\u003e_\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"12.252252252252251%\"\u003e\n \u003cp\u003e2\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"17.83783783783784%\"\u003e\n \u003cp\u003e50\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"12.072072072072071%\"\u003e\n \u003cp\u003e1\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"8.468468468468469%\"\u003e\n \u003cp\u003e0\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"9.90990990990991%\"\u003e\n \u003cp\u003e0\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"7.027027027027027%\"\u003e\n \u003cp\u003e0\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd width=\"10.45045045045045%\"\u003e\n \u003cp\u003e2\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"8.288288288288289%\"\u003e\n \u003cp\u003e1\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"13.693693693693694%\"\u003e\n \u003cp\u003e160\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"12.252252252252251%\"\u003e\n \u003cp\u003e5\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"17.83783783783784%\"\u003e\n \u003cp\u003e90\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"12.072072072072071%\"\u003e\n \u003cp\u003e3\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"8.468468468468469%\"\u003e\n \u003cp\u003e2\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"9.90990990990991%\"\u003e\n \u003cp\u003e0\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"7.027027027027027%\"\u003e\n \u003cp\u003e0\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd width=\"10.45045045045045%\"\u003e\n \u003cp\u003e3\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"8.288288288288289%\"\u003e\n \u003cp\u003e2\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"13.693693693693694%\"\u003e\n \u003cp\u003e250\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"12.252252252252251%\"\u003e\n \u003cp\u003eintubated\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"17.83783783783784%\"\u003e\n \u003cp\u003e100\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"12.072072072072071%\"\u003e\n \u003cp\u003e4\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"8.468468468468469%\"\u003e\n \u003cp\u003e3\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"9.90990990990991%\"\u003e\n \u003cp\u003e3\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"7.027027027027027%\"\u003e\n \u003cp\u003e3\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd width=\"10.45045045045045%\"\u003e\n \u003cp\u003e4\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"8.288288288288289%\"\u003e\n \u003cp\u003e2\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"13.693693693693694%\"\u003e\n \u003cp\u003e240\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"12.252252252252251%\"\u003e\n \u003cp\u003e5\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"17.83783783783784%\"\u003e\n \u003cp\u003e95\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"12.072072072072071%\"\u003e\n \u003cp\u003e4\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"8.468468468468469%\"\u003e\n \u003cp\u003e3\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"9.90990990990991%\"\u003e\n \u003cp\u003e2\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"7.027027027027027%\"\u003e\n \u003cp\u003e2\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd width=\"10.45045045045045%\"\u003e\n \u003cp\u003e5\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"8.288288288288289%\"\u003e\n \u003cp\u003e2\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"13.693693693693694%\"\u003e\n \u003cp\u003e180\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"12.252252252252251%\"\u003e\n \u003cp\u003e5\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"17.83783783783784%\"\u003e\n \u003cp\u003e80\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"12.072072072072071%\"\u003e\n \u003cp\u003e3\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"8.468468468468469%\"\u003e\n \u003cp\u003e2\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"9.90990990990991%\"\u003e\n \u003cp\u003e2\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"7.027027027027027%\"\u003e\n \u003cp\u003e2\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd width=\"10.45045045045045%\"\u003e\n \u003cp\u003e6\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"8.288288288288289%\"\u003e\n \u003cp\u003e2\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"13.693693693693694%\"\u003e\n \u003cp\u003e160\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"12.252252252252251%\"\u003e\n \u003cp\u003e4\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"17.83783783783784%\"\u003e\n \u003cp\u003en.a.\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"12.072072072072071%\"\u003e\n \u003cp\u003e0\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"8.468468468468469%\"\u003e\n \u003cp\u003e0\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"9.90990990990991%\"\u003e\n \u003cp\u003e0\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"7.027027027027027%\"\u003e\n \u003cp\u003e0\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003c/tbody\u003e\n\u003c/table\u003e\n\u003cp\u003e\u003cbr\u003e\u003c/p\u003e\n\u003ch3\u003e\u003cstrong\u003eComplications\u003c/strong\u003e\u003c/h3\u003e\n\u003cp\u003eOne technical complication occurred. In the first group, one patient had an occlusion of the stent-covered MCA, but the thrombus formation resolved with the administration of eptifibatide IA (Integrilin, GlaxoSmithKline) Fig. 1. This complication did not lead to clinical consequences. The patient showed no associated ischemic lesions after the procedure. No complications occurred in the patients in group 2. No peri- or post-procedural hemorrhage or vascular injuries were encountered.\u003c/p\u003e"},{"header":"Discussion","content":"\u003cp\u003eAlthough the endovascular or microsurgical treatment of ruptured aneurysms has substantially improved during the past three decades, similar progress in the treatment of CVS is lacking. The past 20 years have seen a mindset shift from a fatalistic acceptance of poor outcomes due to CVS toward active attempts to address these outcomes. The search for a safe and efficacious treatment for CVS has been ongoing since the 1970s [\u003cspan citationid=\"CR23\" class=\"CitationRef\"\u003e23\u003c/span\u003e]. Balloon dilatation of proximal arteries (mainly the distal ICA and the proximal MCA) is an acceptable option, but the risk of vessel dissection and even rupture remains a concern. Intraarterial infusion of vasodilator drugs may work, but this treatment modality requires major logistic efforts and may fail. In recent years, endovascular mechanical vessel dilatation using stent retrievers (e.g., Solitaire, Medtronic; pRESET, or phenox) has been established [\u003cspan additionalcitationids=\"CR19 CR20 CR21\" citationid=\"CR18\" class=\"CitationRef\"\u003e18\u003c/span\u003e\u0026ndash;\u003cspan citationid=\"CR22\" class=\"CitationRef\"\u003e22\u003c/span\u003e]. The indications for this treatment are not yet well defined, particularly because the incidence of delayed cerebral ischemia (DCI) is approximately 30%. However, CVS is diagnosed in 70% of patients, and the areas of ischemia often do not correspond to vascular territories that demonstrate large proximal vessel vasospasm. This shift in interest away from targeting large vessel vasospasms has been supported by the failure of clazosentan, a potent vasodilator, to improve patient outcomes [\u003cspan additionalcitationids=\"CR25 CR26\" citationid=\"CR24\" class=\"CitationRef\"\u003e24\u003c/span\u003e\u0026ndash;\u003cspan citationid=\"CR27\" class=\"CitationRef\"\u003e27\u003c/span\u003e]. Nevertheless, evidence suggests that the treatment of CVS can improve clinical outcomes. Jabbar et al. [\u003cspan citationid=\"CR28\" class=\"CitationRef\"\u003e28\u003c/span\u003e] have compared two patient cohorts from two institutions treated between 2005 and 2012, including 1057 patients. All patients underwent daily TCD ultrasonography to detect CVS. Patients in group A were treated immediately after any suspicion of CVS, regardless of the TCD results. Patients in group B were treated by endovascular means only after persistent CVS despite induced hypertension for 2\u0026ndash;4 hours or when a mean flow velocity above 160 cm/sec was gradually exceeded for two consecutive days. In comparison, more patients were treated in group A. In group A, 24.4% of patients (n\u0026thinsp;=\u0026thinsp;121/495) underwent the first endovascular treatment on day 6\u0026thinsp;\u0026plusmn;\u0026thinsp;3.64, and in group B, 14.4% (n\u0026thinsp;=\u0026thinsp;81/562) underwent the first endovascular treatment on day 8.9\u0026thinsp;\u0026plusmn;\u0026thinsp;4.78; differences in the odds (p\u0026thinsp;\u0026lt;\u0026thinsp;0.0001, OR 1.92 95% CI 1.41\u0026ndash;2.63) were observed in the rate of treatment and the timing (p\u0026thinsp;\u0026lt;\u0026thinsp;0.0001). The rate of DCI was lower in cohort A (20.8% vs. 29%, p\u0026thinsp;=\u0026thinsp;0.0023, OR 0.64, 95% CI 0.48\u0026ndash;0.85), as confirmed by multivariate analysis (p\u0026thinsp;=\u0026thinsp;0.001, adjusted OR 0.59, 95% CI 0.44\u0026ndash;0.8). The rates of DCI were higher in patients undergoing endovascular treatment for delayed ischemic neurologic deficit than in those undergoing endovascular treatment solely because of TCD measurements (64% vs. 44.7%, p\u0026thinsp;=\u0026thinsp;0.0277). The rate of unfavorable outcomes after SAH was also lower in cohort A (44% vs. 56%, p\u0026thinsp;=\u0026thinsp;0.0404) and remained significant in multivariate analysis (p\u0026thinsp;\u0026lt;\u0026thinsp;0.0001, adjusted OR 0.55, 95% CI 0.4\u0026ndash;0.77). This study demonstrated that early identification and aggressive treatment might result in better functional outcomes.\u003c/p\u003e \u003cp\u003eNon-selective IA injection of vasodilators was one of the first endovascular treatments for CVS. Despite improving cerebral flow after the injection of vasodilators, this treatment can lead to an iatrogenic steal phenomenon due to more significantly improved inflow in the non-spastic arteries [\u003cspan citationid=\"CR29\" class=\"CitationRef\"\u003e29\u003c/span\u003e]. To avoid the iatrogenic steal phenomenon and improve outcomes in the distal vessels, distal vasospasm was suggested to be best treated with medication after initial mechanical treatment of the proximal vasospasm. Balloon angioplasty [\u003cspan additionalcitationids=\"CR14 CR15 CR16\" citationid=\"CR13\" class=\"CitationRef\"\u003e13\u003c/span\u003e\u0026ndash;\u003cspan citationid=\"CR17\" class=\"CitationRef\"\u003e17\u003c/span\u003e] and stentoplasty [\u003cspan additionalcitationids=\"CR19 CR20 CR21\" citationid=\"CR18\" class=\"CitationRef\"\u003e18\u003c/span\u003e\u0026ndash;\u003cspan citationid=\"CR22\" class=\"CitationRef\"\u003e22\u003c/span\u003e] have shown therapeutic efficacy and sustained improvement. Although balloon angioplasty was initially believed to damage the extracellular matrix, thus explaining angioplasty\u0026rsquo;s mechanism of action, evidence has indicated that balloon angioplasty of an arterial segment instead induces paralysis of the vessel without necessarily damaging the underlying extracellular matrix [\u003cspan citationid=\"CR20\" class=\"CitationRef\"\u003e20\u003c/span\u003e, \u003cspan citationid=\"CR30\" class=\"CitationRef\"\u003e30\u003c/span\u003e]. The induced vessel paralysis after angioplasty is affected by the contractile state of the vessel. Contracted vessels, such as vasospastic vessels, require less dilatation to become paralyzed; therefore, vessels with CVS are predisposed to paralysis after mechanical dilation and thus can be treated with devices with lower radial force [\u003cspan citationid=\"CR20\" class=\"CitationRef\"\u003e20\u003c/span\u003e]. The reason for this paralysis and the requirement for decreased dilatation to induce the same degree of paralysis in contracted vessels than in vessels in a relaxed state is not fully understood. Damage to the underlying contractile apparatus within the smooth muscle cells, which stiffen when contracted and may potentially be more prone to mechanical disruption, has been suggested to explain this phenomenon [\u003cspan citationid=\"CR31\" class=\"CitationRef\"\u003e31\u003c/span\u003e]. This finding suggests that mechanical angioplasty should be performed before chemical angioplasty, because it would be likely to have more significant effects. Simultaneously, lower forces might be required, thus potentially explaining why stentrievers have shown some success in treating CVS despite having much lower radial force than balloons. Kwon et al. [\u003cspan citationid=\"CR20\" class=\"CitationRef\"\u003e20\u003c/span\u003e], in a series of patients treated with both chemical angioplasty and stentoplasty, have compared patients in whom the stent was deployed initially followed by injection of a vasodilator (nicardipine) and those in whom a vasodilator was injected first, and stentoplasty was performed second. In the vasodilator-first group, 71.4% of treated vessel segments (10/14) showed vasodilation after stentoplasty, but 60% of patients (3/5) developed recurrent vasospasm requiring repeated angioplasty. In the stentriever-first group, 82.1% of segments (32/39) showed vasodilatation after stentoplasty, but none of the patients developed radiological or clinical evidence of recurrent vasospasm. This small clinical study corroborated the initial hypothesis suggested by Bhogal et al., building on the work of Fischell et al. [\u003cspan citationid=\"CR30\" class=\"CitationRef\"\u003e30\u003c/span\u003e, \u003cspan citationid=\"CR31\" class=\"CitationRef\"\u003e31\u003c/span\u003e]\u003c/p\u003e \u003cp\u003eThe use of permanently implanted stents has also been reported. Andic et al. [\u003cspan citationid=\"CR32\" class=\"CitationRef\"\u003e32\u003c/span\u003e] have analyzed data from 15 consecutive patients with 18 aneurysms, eight of whom underwent stent-assisted coiling. In most cases (n\u0026thinsp;=\u0026thinsp;6), an LVIS Jr (MicoVention) stent was implanted, with a Solitaire (Medtronic) or Acclino (Acandis) used in the remainder. In a single case, Y-stenting with the use of two LVIS Jr stents was used to treat an MCA bifurcation aneurysm. The authors observed moderate to complete dilatation in the spastic parent arteries after deployment of the stents in patients treated with stent-assisted coiling. In one case, refractory vasospasm occurred after the treatment of two aneurysms (a basilar bifurcation aneurysm and an MCA bifurcation aneurysm), and the authors found no evidence of recurrent vasospasm in the stented segments but observed widespread recurrent vasospasm in the segments previously treated with chemical angioplasty. Although these findings were based on only a small series, this article highlights the potential for braided and laser-cut stents to effectively treat and prevent recurrent CVS. Subsequently, Bhambri et al. [\u003cspan citationid=\"CR33\" class=\"CitationRef\"\u003e33\u003c/span\u003e] described a novel method of using drug-eluting stents to treat CVS. The authors developed polymer-coated laser-cut stents and used various methods to coat the stent: dip coating, spin coating, and electrospinning. The laser-cut and polymer-coated stents were also loaded with different doses of verapamil with varying drug release pharmacokinetics. In all cases, the combined stent demonstrated an initial burst phase of drug release followed by sustained drug release. Varying the concentration of the verapamil changed these different phases by altering the construction of the polymer coating. This preliminary in vitro study suggests the potential promise of further developing stents that release vasodilating drugs. However, to date, no further studies on this technology have been published.\u003c/p\u003e \u003cp\u003eDespite the development of endovascular techniques and their demonstrated effectiveness in treating recurrent vasospasm, some of these therapies remain unsuccessful. The possible reasons for the failure of endovascular treatment are as follows:\u003c/p\u003e \u003cp\u003e \u003cul\u003e \u003cli\u003e \u003cp\u003eSteal phenomenon, particularly with intra-arterial vasodilator treatment\u003c/p\u003e \u003c/li\u003e \u003cli\u003e \u003cp\u003eDistal location: difficult navigation and dilatation of CVS in distal vessel segments for endovascular mechanical treatments\u003c/p\u003e \u003c/li\u003e \u003cli\u003e \u003cp\u003eTortuosity and curved vessels: complex dilatation of spastic vessels in a curved course, such as the transition from the A1 to the A2 segment, particularly for balloon angioplasty\u003c/p\u003e \u003c/li\u003e \u003c/ul\u003e \u003c/p\u003e \u003cp\u003eSome endovascular treatments have a short-term maximal dilatation effect, but CVS is a dynamic and potentially long-term pathology during the first 3 weeks after SAH. Therefore, recurrent CVS may not be successfully treated in some cases despite multiple repeated endovascular treatments sessions. Consequently, the search for a therapeutic solution for refractory CVS continues. Intracranial stenting of vessels with vasospasm is an \u003cem\u003eultima ratio\u003c/em\u003e treatment in patients with severe recurrent vasospasm. We have attempted to induce permanent dilatation of vessels with resistant spasms by stent implantation. The implanted stents' relatively low and continuous radial force provides a good solution for distal and curved vessel segments. The implanted device is intended to avoid the steal phenomenon and enhance vasodilator drugs' effects, particularly on the peripheral vessels. By improving perfusion in the proximal vessels, we have also observed a reduction of CVS in the distal vessels.\u003c/p\u003e \u003cp\u003eThis level of improvement occurred only after stent implantation and therefore cannot be explained by the earlier IA administration of the vasodilator.\u003c/p\u003e \u003cp\u003eThe idea of treating CVS with intracranial stenting arose from incidental experience during the management of complications during aneurysm coil occlusion. During coiling, impaired perfusion of the parent vessel and the dependent vasculature was observed, owing to inadvertent displacement of the implanted coils. Stents were implanted to maintain the coils inside the aneurysm and restore normal blood flow. The vessels where the stents were implanted had shown CVS before and during the coiling despite the IA vasodilator administration. After stenting, we observed decreased vasospasms with similar perfusion improvement in the distal supply territory \u003cb\u003e(\u003c/b\u003eFig.\u0026nbsp;\u003cspan refid=\"Fig1\" class=\"InternalRef\"\u003e1\u003c/span\u003e\u003cb\u003e)\u003c/b\u003e. One of the two patients with incidental treatment was diagnosed with high-grade CVS after day 1, but not within or distal to the stented vessel. The stents used were not dedicated to treating CVS, but we believe that they may be valuable in extreme situations in which few choices are available. After our initial two incidental experiences and the excellent long-term outcome, we decided to perform this treatment in the four described cases after several unsuccessful chemical and mechanical treatments. In the first two patients, we implanted only one stent in the MCA in the M1-M2 junction. With experience, in the third patient, we implanted two stents in the middle and anterior cerebral artery ipsilaterally. In the last patient, four stents were implanted, two on each side. The stent implantations were always performed under dual antiplatelet therapy (DAPT). Overall, only one temporary thromboembolic occlusion occurred as a periprocedural complication. None of the patients showed postprocedural hemorrhage, in-stent stenosis, or DCI in the vascular territories of the stented vessels.\u003c/p\u003e \u003cp\u003eDetection and repetition of endovascular treatment of resistant spasms increase the risk of periprocedural complications and radiation exposure [\u003cspan citationid=\"CR34\" class=\"CitationRef\"\u003e34\u003c/span\u003e] Endovascular treatment may not always be feasible, owing to the complicated clinical management of patients with SAH, particularly respiratory and cardiovascular management. Intracranial stenting can be an unduly aggressive treatment for CVS, particularly because DAPT is required in the acute phase after SAH. Nonetheless, we believe that it is a viable treatment option as a last resort in refractory vasospasm to avoid life-threatening DCI after the failure of chemical and mechanical treatments. Of note, we observed that three of the used devices were Neuroform Atlas stents (Stryker). All sizes of this stent system can be implanted via a low profile 0.017 inch inner diameter microcatheter, thus making the navigation of distal vessel segments less traumatic and more manageable in patients with difficult probing conditions, particularly with associated CVS.\u003c/p\u003e \u003cp\u003eThis treatment method has several limitations. The need for DAPT during the acute phase after SAH is a reason for concern. Therefore, the ruptured aneurysm should be secured. All patients showed neurological improvement through intracranial stenting of recurrent CVS after the failure of various treatment methods. None of our patients showed postprocedural hemorrhage or any other persistent complication. This \u003cem\u003eultima ratio\u003c/em\u003e treatment has not been described in the English literature to our knowledge. Stenting, although not commonly used in this manner, is very effective over the long term and is safe if the medication is adjusted precisely.\u003c/p\u003e \u003cdiv id=\"Sec12\" class=\"Section2\"\u003e \u003ch2\u003eLimitations\u003c/h2\u003e \u003cp\u003eOur study has several limitations inherent to single-center retrospective data analyses. We present anecdotal experience in highly selected patients. The operator\u0026rsquo;s experience and skills influence the outcomes. The complexity of vasospasm and DCI poses a major logistic challenge for interventionists, intensivists, and neurosurgeons, far beyond the straightforward procedure of deploying a stent in a proximal brain artery. Stenting proximal arteries is only one piece in the armamentarium for the treatment of post-SAH vasospasm.\u003c/p\u003e \u003c/div\u003e"},{"header":"Conclusion","content":"\u003cp\u003eEndovascular treatment of post-SAH recurrent CVS with intracranial stenting is both practical and safe. This therapy is considered an \u003cem\u003eultima ratio\u003c/em\u003e after the failure of standard pharmacological and interventional measures. Peri- and post-procedural antiplatelet medication is essential to prevent thromboembolic complications.\u003c/p\u003e"},{"header":"Abbreviations","content":"\u003cp\u003eCT: computed tomography\u003c/p\u003e\n\u003cp\u003eCTA: computed tomography angiography\u003c/p\u003e\n\u003cp\u003eCTP: computed tomography perfusion\u003c/p\u003e\n\u003cp\u003eCVS: cerebral vasospasm\u003c/p\u003e\n\u003cp\u003eDAPT: dual antiplatelet therapy\u003c/p\u003e\n\u003cp\u003eDCI: delayed cerebral ischemia\u003c/p\u003e\n\u003cp\u003eDSA: digital subtraction angiography\u003c/p\u003e\n\u003cp\u003eIA: intra-arterial\u003c/p\u003e\n\u003cp\u003eICA: internal carotid artery\u003c/p\u003e\n\u003cp\u003eICA: internal carotid artery\u003c/p\u003e\n\u003cp\u003eMCA: middle cerebral artery\u003c/p\u003e\n\u003cp\u003eMRA: magnetic\u0026nbsp;resonance angiography\u003c/p\u003e\n\u003cp\u003eMRI: magnetic resonance imaging\u003c/p\u003e\n\u003cp\u003emRS: modified Rankin Scale\u003c/p\u003e\n\u003cp\u003eSAH: subarachnoid hemorrhage\u003c/p\u003e\n\u003cp\u003eTCCD: transcranial color-coded doppler\u003c/p\u003e\n\u003cp\u003eTCD: transcranial Doppler sonography\u003c/p\u003e"},{"header":"Declarations","content":"\u003cp\u003e\u003cstrong\u003eEthics approval and consent to participate\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eThis study was ethically approved by the Ethics Committee of the Landes\u0026auml;rztekammer Baden-W\u0026uuml;ttemberg (F-2016-128) Liebknechtstr. 33 . 70565 Stuttgart and adhered to the Declaration of Helsinki 2013.\u003cbr\u003e\u0026nbsp;For Germany there are currently no valid guidelines for the treatment of vasospasm available. The outdated guidelines (AWMF 030/073) were stating: \u0026ldquo;An endovascular therapy of ischemic deficit due to vasospasm may be considered and carried. Randomized trials are missing and therefore there is no general recommendation possible\u0026rdquo;.\u003cbr\u003e\u0026nbsp;The data presented in this manuscript have not be derived from a study protocol. There were generated through clinical routine and represent anecdotal observations.\u0026nbsp;\u003c/p\u003e\n\u003cp\u003eAll patients (or their legal representatives) provided written consent to the anonymized analysis and publication of the data.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eConsent for publication\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eNot applicable.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eAvailability of data and materials\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eThe datasets used and/or analysed during the current study available from the corresponding author on reasonable request.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eCompeting interests\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eThe authors have no conflict of interest in this regard.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eFunding\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eThis study was not funded.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eAuthors\u0026apos; contributions\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eA.K., P.B. and H.H. contributed to the conceptualization and design of the study, A.K. and A.C. organized the data curation, A.K., P.B. and H.B. analyzed and interpreted the patient data, A.K., P.B. and H.H. organized the methodology, H.H. and H.B. were the project administrators, H.H.,P.B. and O.G. performed the supervision, A.K. wrote the original draft, H.H., A.K., P.B. and A.C. reviewed and edited the manuscript. All authors have read and agreed to the published version of the manuscript.\u0026nbsp;\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eAcknowledgements\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eNot applicable.\u003c/p\u003e"},{"header":"References","content":"\u003col\u003e\n\u003cli\u003eKeyrouz SG, Diringer MN. Clinical review: Prevention and therapy of vasospasm in subarachnoid hemorrhage. Crit Care. 2007;11:220.\u003c/li\u003e\n\u003cli\u003eEsmaeeli S, Hrdlicka CM, Bastos AB, Wang J, Gomez-Paz S, Hanafy KA, et al. Robotically assisted transcranial Doppler with artificial intelligence for assessment of cerebral vasospasm after subarachnoid hemorrhage. J Neurocritical Care. 2020;13:32\u0026ndash;40.\u003c/li\u003e\n\u003cli\u003ePickard JD, Murray GD, Illingworth R, Shaw MD, Teasdale GM, Foy PM, et al. Effect of oral nimodipine on cerebral infarction and outcome after subarachnoid haemorrhage: British aneurysm nimodipine trial. BMJ. 1989;298:636\u0026ndash;42.\u003c/li\u003e\n\u003cli\u003eKassell NF, Torner JC, Jane JA, Haley EC, Adams HP. The International Cooperative Study on the Timing of Aneurysm Surgery: Part 2: Surgical results. J Neurosurg. 1990;73:37\u0026ndash;47.\u003c/li\u003e\n\u003cli\u003eStecco A, Fabbiano F, Amatuzzo P, Quagliozzi M, Soligo E, Divenuto I, et al. Computed tomography perfusion and computed tomography angiography in vasospasm after subarachnoid hemorrhage. J Neurosurg Sci. 2018;62:397\u0026ndash;405.\u003c/li\u003e\n\u003cli\u003eTamatani S, Sasaki O, Takeuchi S, Fujii Y, Koike T, Tanaka R. Detection of Delayed Cerebral Vasospasm, after Rupture of Intracranial Aneurysms, by Magnetic Resonance Angiography. Neurosurgery. 1997;40:748\u0026ndash;54.\u003c/li\u003e\n\u003cli\u003eFeigin VL, Rinkel GJ, Algra A, Vermeulen M, van Gijn J. Calcium antagonists in patients with aneurysmal subarachnoid hemorrhage: a systematic review. Neurology. 1998;50:876\u0026ndash;83.\u003c/li\u003e\n\u003cli\u003eCho W-S, Kang H-S, Kim JE, Kwon O-K, Oh CW, Son YJ, et al. Intra-Arterial Nimodipine Infusion for Cerebral Vasospasm in Patients with Aneurysmal Subarachnoid Hemorrhage. Interv Neuroradiol. 2011;17:169\u0026ndash;78.\u003c/li\u003e\n\u003cli\u003eShankar JJS, P. dos Santos M, Deus-Silva L, Lum C. Angiographic evaluation of the effect of intra-arterial milrinone therapy in patients with vasospasm from aneurysmal subarachnoid hemorrhage. Neuroradiology. 2011;53:123\u0026ndash;8.\u003c/li\u003e\n\u003cli\u003eDuman E, Karako\u0026ccedil; F, Pinar HU, Dogan R, Fırat A, Yıldırım E. Higher dose intra-arterial milrinone and intra-arterial combined milrinone-nimodipine infusion as a rescue therapy for refractory cerebral vasospasm. Interv Neuroradiol. 2017;23:636\u0026ndash;43.\u003c/li\u003e\n\u003cli\u003eStuart RM, Helbok R, Kurtz P, Schmidt M, Fernandez L, Lee K, et al. High-Dose Intra-arterial Verapamil for the Treatment of Cerebral Vasospasm After Subarachnoid Hemorrhage: Prolonged Effects on Hemodynamic Parameters and Brain Metabolism. Neurosurgery. 2011;68:337\u0026ndash;45.\u003c/li\u003e\n\u003cli\u003eOtt S, Jedlicka S, Wolf S, Peter M, Pudenz C, Merker P, et al. Continuous Selective Intra-Arterial Application of Nimodipine in Refractory Cerebral Vasospasm due to Aneurysmal Subarachnoid Hemorrhage. BioMed Res Int. 2014;2014:970741.\u003c/li\u003e\n\u003cli\u003eLabeyrie M-A, Gaugain S, Boulouis G, Zetchi A, Brami J, Saint-Maurice J-P, et al. Distal Balloon Angioplasty of Cerebral Vasospasm Decreases the Risk of Delayed Cerebral Infarction. AJNR Am J Neuroradiol. 2019;40:1342\u0026ndash;8.\u003c/li\u003e\n\u003cli\u003eBeck J, Raabe A, Lanfermann H, Berkefeld J, De Rochemont R du M, Zanella F, et al. Effects of balloon angioplasty on perfusion- and diffusion-weighted magnetic resonance imaging results and outcome in patients with cerebral vasospasm. J Neurosurg. 2006;105:220\u0026ndash;7.\u003c/li\u003e\n\u003cli\u003ePatel AS, Griessenauer CJ, Gupta R, Adeeb N, Foreman PM, Shallwani H, et al. Safety and Efficacy of Noncompliant Balloon Angioplasty for the Treatment of Subarachnoid Hemorrhage\u0026ndash;Induced Vasospasm: A Multicenter Study. World Neurosurg. 2017;98:189\u0026ndash;97.\u003c/li\u003e\n\u003cli\u003eChoi BJ, Lee TH, Lee JI, Ko JK, Park HS, Choi CH. Safety and Efficacy of Transluminal Balloon Angioplasty Using a Compliant Balloon for Severe Cerebral Vasospasm after an Aneurysmal Subarachnoid Hemorrhage. J Korean Neurosurg Soc. 2011;49:157\u0026ndash;62.\u003c/li\u003e\n\u003cli\u003eChen C-T, Chen C-C, Wang AY-C, Wu Y-M, Chin S-C, Hsieh P-C, et al. Early strategy of scepter XC balloon angioplasty and simultaneous Nimodipine infusion for vasospasm following ruptured aneurysm. BMC Neurol. 2020;20:271.\u003c/li\u003e\n\u003cli\u003eBhogal P, Paraskevopoulos D, Makalanda HL. The use of a stent-retriever to cause mechanical dilatation of a vasospasm secondary to iatrogenic subarachnoid haemorrhage. Interv Neuroradiol. 2017;23:330\u0026ndash;5.\u003c/li\u003e\n\u003cli\u003eBadger CA, Jankowitz BT, Shaikh HA. Treatment of cerebral vasospasm secondary to subarachnoid hemorrhage utilizing the Comaneci device. Interv Neuroradiol J Peritherapeutic Neuroradiol Surg Proced Relat Neurosci. 2020;:1591019920945554.\u003c/li\u003e\n\u003cli\u003eKwon H-J, Lim J-W, Koh H-S, Park B, Choi S-W, Kim S-H, et al. Stent-Retriever Angioplasty for Recurrent Post-Subarachnoid Hemorrhagic Vasospasm - A Single Center Experience with Long-Term Follow-Up. Clin Neuroradiol. 2019;29:751\u0026ndash;61.\u003c/li\u003e\n\u003cli\u003eBhogal P, Loh Y, Brouwer P, Andersson T, S\u0026ouml;derman M. Treatment of cerebral vasospasm with self-expandable retrievable stents: proof of concept. J Neurointerventional Surg. 2017;9:52\u0026ndash;9.\u003c/li\u003e\n\u003cli\u003eSu YS, Ali MS, Pukenas BA, Favilla CG, Zanaty M, Hasan DM, et al. Novel Treatment of Cerebral Vasospasm Using Solitaire Stent Retriever\u0026minus;Assisted Angioplasty: Case Series. World Neurosurg. 2020;135:e657\u0026ndash;63.\u003c/li\u003e\n\u003cli\u003eSen J, Belli A, Albon H, Morgan L, Petzold A, Kitchen N. Triple-H therapy in the management of aneurysmal subarachnoid haemorrhage. Lancet Neurol. 2003;2:614\u0026ndash;21.\u003c/li\u003e\n\u003cli\u003eMacdonald RL, Kassell NF, Mayer S, Ruefenacht D, Schmiedek P, Weidauer S, et al. Clazosentan to Overcome Neurological Ischemia and Infarction Occurring After Subarachnoid Hemorrhage (CONSCIOUS-1). Stroke. 2008;39:3015\u0026ndash;21.\u003c/li\u003e\n\u003cli\u003eMacdonald RL, Higashida RT, Keller E, Mayer SA, Molyneux A, Raabe A, et al. Clazosentan, an endothelin receptor antagonist, in patients with aneurysmal subarachnoid haemorrhage undergoing surgical clipping: a randomised, double-blind, placebo-controlled phase 3 trial (CONSCIOUS-2). Lancet Neurol. 2011;10:618\u0026ndash;25.\u003c/li\u003e\n\u003cli\u003eMacdonald RL, Higashida RT, Keller E, Mayer SA, Molyneux A, Raabe A, et al. Randomized Trial of Clazosentan in Patients With Aneurysmal Subarachnoid Hemorrhage Undergoing Endovascular Coiling. Stroke. 2012;43:1463\u0026ndash;9.\u003c/li\u003e\n\u003cli\u003eMacdonald RL, Higashida RT, Keller E, Mayer SA, Molyneux A, Raabe A, et al. Randomised trial of clazosentan, an endothelin receptor antagonist, in patients with aneurysmal subarachnoid hemorrhage undergoing surgical clipping (CONSCIOUS-2). Acta Neurochir Suppl. 2013;115:27\u0026ndash;31.\u003c/li\u003e\n\u003cli\u003eJabbarli R, Pierscianek D, R\u0026ouml;lz R, Darkwah Oppong M, Kaier K, Shah M, et al. Endovascular treatment of cerebral vasospasm after subarachnoid hemorrhage: More is more. Neurology. 2019;93:e458\u0026ndash;66.\u003c/li\u003e\n\u003cli\u003eLevitt MR, Morton RP, Haynor DR, Cohen W, Ghodke BV, Hallam DK, et al. Angiographic perfusion imaging: real-time assessment of endovascular treatment for cerebral vasospasm. J Neuroimaging Off J Am Soc Neuroimaging. 2014;24:387\u0026ndash;92.\u003c/li\u003e\n\u003cli\u003eFischell TA, Grant G, Johnson DE. Determinants of smooth muscle injury during balloon angioplasty. Circulation. 1990;82:2170\u0026ndash;84.\u003c/li\u003e\n\u003cli\u003eBhogal P, Pederzani G, Grytsan A, Loh Y, Brouwer PA, Andersson T, et al. The unexplained success of stentplasty vasospasm treatment - Insights using mechanistic mathematical modeling. Clin Neuroradiol. 2019;29:763\u0026ndash;74.\u003c/li\u003e\n\u003cli\u003eAndic C, Kardes O, Durdag E, Gedikoglu M, Akin S. Efficacy of endovascular treatment and feasibility of stent-assisted coiling in the presence of severe and symptomatic vasospasm. J NeuroInterventional Surg. 2017;9:1075\u0026ndash;80.\u003c/li\u003e\n\u003cli\u003eBhambri P, Sarvi A, Wong JH, Sundararaj U, Mitha AP. Verapamil eluting stents as a possible treatment for vasospasm after subarachnoid hemorrhage. J NeuroInterventional Surg. 2017;9:875\u0026ndash;9.\u003c/li\u003e\n\u003cli\u003eLoftus ML, Minkowitz S, Tsiouris AJ, Min RJ, Sanelli PC. Utilization Guidelines for Reducing Radiation Exposure in the Evaluation of Aneurysmal Subarachnoid Hemorrhage: A Practice Quality Improvement Project. AJR Am J Roentgenol. 2010;195:176\u0026ndash;80.\u003c/li\u003e\n\u003c/ol\u003e"}],"fulltextSource":"","fullText":"","funders":[],"hasAdminPriorityOnWorkflow":false,"hasManuscriptDocX":true,"hasOptedInToPreprint":true,"hasPassedJournalQc":"","hasAnyPriority":false,"hideJournal":false,"highlight":"","institution":"","isAcceptedByJournal":true,"isAuthorSuppliedPdf":false,"isDeskRejected":"","isHiddenFromSearch":false,"isInQc":false,"isInWorkflow":false,"isPdf":false,"isPdfUpToDate":true,"isWithdrawnOrRetracted":false,"journal":{"display":true,"email":"[email protected]","identity":"bmc-neurology","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":false,"externalIdentity":"nurl","sideBox":"Learn more about [BMC Neurology](http://bmcneurol.biomedcentral.com/)","snPcode":"","submissionUrl":"https://www.editorialmanager.com/nurl","title":"BMC Neurology","twitterHandle":"BMC_series","acdcEnabled":true,"dfaEnabled":false,"editorialSystem":"em","reportingPortfolio":"BMC Series","inReviewEnabled":true,"inReviewRevisionsEnabled":true},"keywords":"Subarachnoid hemorrhage, posthemorrhagic cerebral vasospasm, endovascular treatment, self-expanding stent","lastPublishedDoi":"10.21203/rs.3.rs-1801216/v1","lastPublishedDoiUrl":"https://doi.org/10.21203/rs.3.rs-1801216/v1","license":{"name":"CC BY 4.0","url":"https://creativecommons.org/licenses/by/4.0/"},"manuscriptAbstract":"\u003cp\u003e\u003cstrong\u003eBackground: \u003c/strong\u003eCerebral vasospasm is a leading cause of morbidity and mortality in patients after subarachnoid hemorrhage (SAH). Endovascular treatment, including intraarterial infusion of drugs with vasodilation effects, and balloon- and stentriever angioplasty, are helpful but can achieve only short-term effects in some patients. A need remains for long-lasting treatment of refractory recurrent vasospasm. We report our experience in stent implantation as a treatment for recurrent severe post-SAH vasospasm.\u003c/p\u003e\u003cp\u003e\u003cstrong\u003eMethods\u003c/strong\u003e\u003cem\u003e: \u003c/em\u003eA 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 or as a bail-out strategy after failed intraarterial drug infusion or mechanical treatment. All stented patients received dual antiplatelet therapy (DAPT).\u003c/p\u003e\u003cp\u003e\u003cstrong\u003eResults\u003c/strong\u003e\u003cem\u003e: \u003c/em\u003eNine 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 thromboembolic occlusion of the stented vessels was encountered. In long-term angiographic follow-up, neither in-stent stenosis nor stent occlusion was found.\u003c/p\u003e\u003cp\u003e\u003cstrong\u003eConclusions: \u003c/strong\u003eEndovascular implantation of self-expanding stents is a potential \u003cem\u003eultima ratio\u003c/em\u003e strategy for patients with severe refractory post-SAH cerebral vasospasm. Stents with reduced thrombogenicity (avoiding DAPT) and bioabsorbable self-expanding stents would further advance this concept.\u003c/p\u003e","manuscriptTitle":"Intracranial Stenting as a Bail-out Option for Posthemorrhagic Cerebral Vasospasm: A Single-Center Experience with Long-Term Follow-Up","msid":"","msnumber":"","nonDraftVersions":[{"code":1,"date":"2022-07-13 19:01:35","doi":"10.21203/rs.3.rs-1801216/v1","editorialEvents":[{"type":"communityComments","content":0},{"type":"decision","content":"Major revision","date":"2022-07-22T07:11:16+00:00","index":"","fulltext":""},{"type":"editorInvitedReview","content":"","date":"2022-07-20T01:25:38+00:00","index":"hide","fulltext":""},{"type":"reviewerAgreed","content":"6e7297b6-2bb4-45a5-8e89-cbd27207fd66","date":"2022-07-16T07:19:08+00:00","index":"hide","fulltext":""},{"type":"editorInvitedReview","content":"","date":"2022-07-14T08:19:14+00:00","index":"hide","fulltext":""},{"type":"reviewerAgreed","content":"4910477e-999b-400c-a5b1-5bec43c5d5bc","date":"2022-07-06T06:47:17+00:00","index":"hide","fulltext":""},{"type":"reviewersInvited","content":"","date":"2022-07-05T23:41:50+00:00","index":"","fulltext":""},{"type":"editorAssigned","content":"","date":"2022-07-05T23:35:44+00:00","index":"","fulltext":""},{"type":"editorInvited","content":"","date":"2022-07-05T18:22:08+00:00","index":"","fulltext":""},{"type":"checksComplete","content":"","date":"2022-07-05T18:18:14+00:00","index":"","fulltext":""},{"type":"submitted","content":"BMC Neurology","date":"2022-06-27T20:43:21+00:00","index":"","fulltext":""}],"status":"published","journal":{"display":true,"email":"[email protected]","identity":"bmc-neurology","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":false,"externalIdentity":"nurl","sideBox":"Learn more about [BMC Neurology](http://bmcneurol.biomedcentral.com/)","snPcode":"","submissionUrl":"https://www.editorialmanager.com/nurl","title":"BMC Neurology","twitterHandle":"BMC_series","acdcEnabled":true,"dfaEnabled":false,"editorialSystem":"em","reportingPortfolio":"BMC Series","inReviewEnabled":true,"inReviewRevisionsEnabled":true}}],"origin":"","ownerIdentity":"7c5c2ae7-80c4-40fc-8644-14fdc9cb5e85","owner":[],"postedDate":"July 13th, 2022","published":true,"recentEditorialEvents":[],"rejectedJournal":[],"revision":"","amendment":"","status":"under-review","subjectAreas":[],"tags":[],"updatedAt":"2022-08-29T12:59:43+00:00","versionOfRecord":[],"versionCreatedAt":"2022-07-13 19:01:35","video":"","vorDoi":"","vorDoiUrl":"","workflowStages":[]},"version":"v1","identity":"rs-1801216","journalConfig":"researchsquare"},"__N_SSP":true},"page":"/article/[identity]/[[...version]]","query":{"redirect":"/article/rs-1801216","identity":"rs-1801216","version":["v1"]},"buildId":"FbvkV6FR0MCFSLy54lSbu","isFallback":false,"isExperimentalCompile":false,"dynamicIds":[84888],"gssp":true,"scriptLoader":[]}