From 2010 to the present, there have been numerous observational (nonrandomized) reports regarding the effect of anesthetic management on the outcome of patients undergoing emergency endovascular thrombectomy to treat acute ischemic stroke. With some recent exceptions,1,2 nearly all observational reports have suggested that outcomes were more favorable when endovascular thrombectomy was conducted with local anesthesia (with or without IV sedation—hereafter collectively referred to as “sedation”) instead of general anesthesia. Based on these reports, currently, many in the interventional community strongly favor sedation for endovascular thrombectomy “whenever possible.”3
In April 2014, the Society for Neuroscience in Anesthesia and Critical Care published an expert consensus statement regarding anesthetic management of endovascular thrombectomy.4 The statement was based on a literature review through August 2012 that included 5 of the first observational reports.5–9 Subsequently, in addition to many more observational reports, 3 single-center randomized clinical trials of sedation versus general anesthesia for endovascular thrombectomy have been completed: Sedation vs Intubation for Endovascular Stroke Treatment (SIESTA),10,11 Anesthesia during Stroke (AnStroke),12 and General or Local Anesthesia in Intra Arterial Therapy (GOLIATH).13,14 There is now a much greater fund of evidence on which to base the anesthetic management of patients undergoing endovascular thrombectomy. The best current evidence indicates that when accomplished with rapid workflow and maintenance of blood pressure, general anesthesia is a reasonable option for patients treated with endovascular thrombectomy; see part 2 of this review.15
The aim of this 2-part review is to provide a practical perspective on the clinical literature regarding anesthesia care of patients treated with endovascular thrombectomy. Part 1 (this article) reviews the development of endovascular thrombectomy and the determinants of endovascular thrombectomy effectiveness irrespective of method of anesthesia. A major aim is to explain why rapid workflow and maintenance of blood pressure are critical to maintain the viability of the ischemic brain until reperfusion is accomplished. Understanding the nonanesthesia factors determining endovascular thrombectomy effectiveness is essential to put the literature regarding anesthesia for endovascular thrombectomy into context and to apply it, which is the aim of part 2 (the companion article).15 In part 2, the observational literature is briefly reviewed; greater emphasis is placed on recent randomized controlled trials of anesthesia for endovascular thrombectomy. Part 2 concludes with a pragmatic approach to anesthesia decision making and management of patients treated with endovascular thrombectomy.
Epidemiology, Rationale, and Development
Stroke is a major public health burden. Each year in the United States, approximately 795,000 adults experience a new or recurrent stroke, and 140,000 die as a result.16 In addition, stroke ranks fifth among all causes of death (behind heart disease, cancer, respiratory disease, and unintended injury/accident) and is the leading cause of serious long-term disability in the United States.16 The great majority (87%) of strokes are ischemic, with a minority due to intracranial hemorrhage (10%) or aneurysmal subarachnoid hemorrhage (3%).16
In 1995, IV tissue plasminogen activator administered within 3 hours of stroke symptom onset was shown to improve the long-term (3 months) functional outcome of patients with acute ischemic stroke, odds ratio = 1.7 (95% CI, 1.1–2.6; P = .019).17 A subsequent study showed IV tissue plasminogen activator also improved outcome when administered between 3 and 4.5 hours of symptom onset, odds ratio = 1.42 (95% CI, 1.02–1.99; P = .04).18 Timely administration of tissue plasminogen activator continues to be the standard of care of patients with acute ischemic stroke.19 However, many patients with ischemic stroke are not eligible to receive tissue plasminogen activator, either because of late presentation or by having one or more tissue plasminogen activator exclusion criteria such as intracranial hemorrhage, recent major surgery or trauma, some forms of preexisting anticoagulation or coagulopathy, and/or a very large or severe stroke.19 Even when tissue plasminogen activator is administered within its efficacy window, complete clot lysis and restoration of cerebral perfusion do not occur in many patients. In a meta-analysis, the 24-hour recanalization rate in patients who received tissue plasminogen activator was 2-fold greater than the spontaneous recanalization rate (46% vs 24%, respectively), but still, recanalization had occurred in less than half of the tissue plasminogen activator patients.20 Incomplete recanalization is the primary reason that tissue plasminogen activator is estimated to confer benefit in only about one-third of all patients who receive it.21 In particular, tissue plasminogen activator is not effective in clot lysis and restoration of perfusion with occlusions of larger (more proximal) cerebral arteries.22 In a meta-analysis of studies reporting recanalization within 3 hours of tissue plasminogen activator, rates of complete recanalization were 38% for the distal middle cerebral artery, 21% for the proximal middle cerebral artery, but only 4% for both the intracranial carotid and basilar arteries.23 The limited effectiveness of IV tissue plasminogen activator in restoring cerebral perfusion, especially with large vessel occlusion, was the impetus for the development of mechanical (ie, endovascular) methods to rapidly remove thrombi from the cerebral circulation.
In 2013, 3 randomized clinical trials showed first-generation thrombectomy devices did not significantly improve outcomes of patients with acute ischemic stroke when compared to standard medical therapy with IV tissue plasminogen activator.24–26 However, in 2015, 5 randomized clinical trials established endovascular thrombectomy with a new generation of thrombectomy devices (most commonly, retrievable stents) combined with rapid workflow improved functional outcomes of patients with acute ischemic stroke due to large vessel thrombotic occlusion in the anterior circulation: Multicenter Randomized Clinical Trial of Endovascular Treatment for Acute Ischemic Stroke in the Netherlands (MR CLEAN),27 Extending the Time for Thrombolysis in Emergency Neurological Deficits—Intra-Arterial (EXTEND-IA),28 Endovascular Treatment for Small Core and Anterior Circulation Proximal Occlusion with Emphasis on Minimizing CT to Recanalization Times (ESCAPE),29 Solitaire with the Intention for Thrombectomy as Primary Endovascular Treatment (SWIFT PRIME),30 and Randomized Trial of Revascularization with Solitaire FR Device versus Best Medical Therapy in the Treatment of Acute Stroke Due to Anterior Circulation Large Vessel Occlusion Presenting within Eight Hours of Symptom Onset (REVASCAT).31 Compared with patients who received standard medical therapy (most often tissue plasminogen activator), endovascular thrombectomy doubled the percentage of patients who recovered with little or no long-term (90 days) functional impairment, quantified as a modified Rankin Scale score of 0, 1, or 2.32–34 However, these 5 randomized clinical trials showed that endovascular thrombectomy effectiveness rapidly decreased as the time between stroke onset and reperfusion increased. Specifically, among the 390 of 563 (70%) of patients treated with endovascular thrombectomy who achieved adequate reperfusion, each hour between stroke onset and reperfusion decreased the likelihood of functional independence (odds ratio, 0.85; 95% CI, 0.77–0.95).35 There was no demonstrable benefit with endovascular thrombectomy over medical therapy unless adequate reperfusion was established within 6–7 hours of symptom onset (Figure 1).35 In 2018, 2 randomized clinical trials demonstrated that in selected patients, endovascular thrombectomy improved the outcomes of patients who were treated between 6 and 16 hours (Diffusion-weighted imaging or computerized tomography perfusion assessment with clinical mismatch in the triage of wake up and late presenting strokes undergoing neurointervention with Trevo [DAWN])36 or 6–24 hours (Endovascular Therapy Following Imaging Evaluation for Ischemic Stroke 3 [DEFUSE 3])37 after symptom onset. In both trials, computed tomography perfusion or magnetic resonance imaging was used to identify and treat only patients who had both an ischemic core (infarct) that was small and a relatively large penumbral region that, although moderately ischemic and dysfunctional, was still potentially viable. Accordingly, the 2018 American Heart Association stroke care guidelines consider endovascular thrombectomy to be the standard of care for patients who have acute ischemic stroke in the anterior circulation when arterial puncture can be made within 6 hours of symptom onset or within 6–24 hours of symptom onset, but only when DAWN or DEFUSE 3 eligibility criteria are satisfied.19 “Late” endovascular thrombectomy (6–24 hours after symptom onset) provides a previously unavailable treatment option for patients who present with stroke on awakening or who experience a perioperative stroke38 in which symptoms are often recognized relatively late39 and/or tissue plasminogen activator would be contraindicated because of recent surgery.
The effectiveness of endovascular thrombectomy in patients who have acute ischemic strokes in the posterior circulation (ie, the basilar artery) has not yet been formally established. At least 2 randomized clinical trials are in progress: the Basilar Artery International Cooperation Study (BASICS) trial (NCT01717755)40 and the Acute Basilar Artery Occlusion: Endovascular Interventions vs Standard Medical Treatment (BEST) trial (NCT02441556).41 A meta-analysis of observational studies using different methods to achieve basilar artery reperfusion showed that recanalization significantly improved outcomes.42 A subsequent meta-analysis of observational studies utilizing endovascular thrombectomy reported a basilar artery reperfusion rate of 81% (95% CI, 73%–87%).43 Therefore, it seems likely that endovascular thrombectomy will be shown to be effective in the treatment of posterior circulation (basilar artery) stroke in the near future.
In the United States, endovascular thrombectomy is most commonly performed in the 163 medical centers designated by the Joint Commission as comprehensive stroke centers, although some centers designed as primary stroke centers also perform endovascular thrombectomy.44 Recommended performance characteristics of centers performing endovascular thrombectomy have been proposed by the Society of Vascular and Interventional Neurology,45 the Society of NeuroInterventional Surgery,3 and, in 2018, by a consensus of multiple societies.46 In addition to immediate availability of complete range of acute stroke diagnostic and therapeutic services, medical centers must have a sufficient case volume (>30 endovascular thrombectomies per year) and achieve endovascular thrombectomy workflow targets: (1) arrival to diagnostic imaging <30 minutes; (2) diagnostic imaging to arterial puncture <60 minutes; and (3) arterial puncture to first thrombectomy attempt <30 minutes45 or even faster!3,46
The emphasis on rapid workflow is because, as discussed above, endovascular thrombectomy effectiveness progressively decreases as the time between stroke onset and reperfusion increases.35 The DAWN and DEFUSE 3 trials suggest that in patients who have good collateral perfusion to the ischemic hemisphere, endovascular thrombectomy effectiveness may be less time sensitive.36,37 Nevertheless, in both DAWN and DEFUSE 3, rapid workflow, compatible with the above guidelines, was accomplished. Thus, within the bounds of safety, the time between the decision to perform endovascular thrombectomy and starting the procedure (arterial puncture) and/or achieving reperfusion should be as brief as possible. This is a cardinal management principle.
Patients treated with endovascular thrombectomy present with signs and symptoms of acute ischemic stroke. Stroke severity is characterized by the National Institutes of Health Stroke Scale. The National Institutes of Health Stroke Scale assesses motor function in the limbs, level of consciousness, visual fields, dysarthria, and other signs. National Institutes of Health Stroke Scale scores range between 0 (no neurologic deficit) and 42, the maximum value. A patient with a complete hemiparesis, but with no other neurologic deficit, would have a National Institutes of Health Stroke Scale score of 8. By comparison, patients treated with endovascular thrombectomy typically have National Institutes of Health Stroke Scale scores ≥10–20.35,47 With National Institutes of Health Stroke Scale scores ≥15–20, swallowing dysfunction (dysphagia) is present in at least 30% of patients.48–50 Especially when the patient is supine, dysphagia may predispose the patient to airway obstruction (from secretions) and/or potentially increase aspiration risk. Difficulty speaking on the basis of motor dysfunction (dysarthria), which commonly coexists with dysphagia,49,51 is present in nearly 50% of patients treated with endovascular thrombectomy.52 Central language dysfunction (aphasia) is present in nearly 50% of patients treated with endovascular thrombectomy.5,52–54 Some aphasic patients cannot speak (nonfluent [“expressive”] aphasia) but can understand speech. Other aphasic patients may be able to speak (they are “fluent”) but cannot understand speech (“receptive” aphasia) and, consequently, cannot follow verbal commands. Pathologic breathing patterns (eg, Cheyne-Stokes) are present in nearly 25% of acute stroke patients and are associated with dysphagia and greater National Institutes of Health Stroke Scale scores.55
In observational reports of anesthesia for endovascular thrombectomy in which patients with both anterior and posterior circulation strokes underwent endovascular thrombectomy, anterior circulation strokes comprised 71%–98% (pooled average 87%) of the endovascular thrombectomy population, with 2%–29% of patients treated with endovascular thrombectomy (pooled average 13%) being treated for posterior circulation strokes.8,56–65 This distribution is consistent with the observation that approximately 15%–20% of all ischemic strokes occur in the posterior circulation.66,67 The majority of patients undergoing endovascular thrombectomy for posterior circulation stroke have an acute occlusion of the basilar artery. Because the posterior circulation is rich in collaterals, the signs and symptoms of basilar ischemia are highly variable and may include quadriplegia, hemiplegia, dysarthria, dysphagia, and cranial nerve palsies.67 Because the reticular activating system is supplied by branches of the basilar artery, the hallmark of basilar ischemia is impaired consciousness.67 In a prospective multicenter observational report of patients with acute basilar artery occlusion, more than half presented with coma, quadriplegia, or locked-in state, and the group median National Institutes of Health Stroke Scale score was 22.68 Because of the nature and severity of these symptoms, with only a few exceptions69 virtually all patients with basilar occlusions have been intubated for endovascular thrombectomy70–74; see part 2 of this review.15
Patients treated with endovascular thrombectomy are typically elderly, with a mean age 66 ± 13 years.35,47 Most patients treated with endovascular thrombectomy have one or more comorbidities including: (1) chronic hypertension (≥60%); (2) atrial fibrillation (≥33%); (3) diabetes mellitus (≥20%); (4) coronary artery disease (approximately 25%); and/or (5) previous stroke (10%–15%).35 Mild hyperglycemia at presentation (glucose = 135–145 mg/dL) is common.35 Many patients treated with endovascular thrombectomy will have received IV tissue plasminogen activator (administered as an initial bolus followed by a 1-hour infusion) within a few minutes or hours before endovascular thrombectomy. Accordingly, many patients treated with endovascular thrombectomy are acutely coagulopathic when they arrive in the interventional suite. Most patients treated with endovascular thrombectomy will be at least moderately hypertensive at presentation. Systolic blood pressure (SBP) is typically 140–150 mm Hg,27,29,31 but SBPs in the 160–180 range are common.14,75 Accordingly, at presentation, mean arterial pressure (MAP) is typically 100–110 mm Hg.12,14,75–77
Having both acute and chronic illness, the great majority of patients treated with endovascular thrombectomy will qualify as American Society of Anesthesiologists physical status score of IIIE or IVE.78 Many patients treated with endovascular thrombectomy will not be able to effectively communicate their medical history, allergies, medications, or even their fasting status. Hence, anesthetic management decisions are often made with limited patient-specific information, and are always made with minimal time for planning and preparation; see part 2 of this review.15
Based on imaging performed before the patient’s arrival in the interventional suite, the interventionist will usually know which cerebral arteries are occluded and are to be treated. This knowledge can help in anesthesia decision making. A single distal occlusion (eg, the proximal middle cerebral artery) may often be treated relatively “simply” and quickly (≤30 minutes). In contrast, a more complex proximal occlusion of the distal intracranial internal carotid artery (terminus) and one or more middle cerebral artery and anterior cerebral artery branches79 will require more time to restore perfusion (Supplemental Digital Content, Document, http://links.lww.com/AA/C720). The interventionist usually obtains arterial access via the right femoral artery, although access via a radial artery or direct carotid puncture are options. An initial selective digital subtraction angiogram is obtained to confirm the location of the occlusion(s). A digital subtraction angiogram “roadmap” is created, allowing subsequent live fluoroscopic images to be superimposed on the roadmap to guide the introduction of endovascular devices. After the roadmap is obtained, movement of the patient’s head and neck can potentially misalign the roadmap with subsequent fluoroscopic images, making the roadmap inaccurate. An inaccurate roadmap may increase the risk of cerebral arterial dissection or perforation from endovascular devices and/or increase the time to perform the procedure. That is why patient immobility during endovascular thrombectomy is very important. However, with variability among individual interventionists, tolerance for patient motion during endovascular thrombectomy procedures may be greater than during other neuroendovascular interventions, such as intracranial aneurysm embolization.
Various endovascular thrombectomy devices and their evolution are shown graphically in Figure 2.80 The following description pertains to endovascular thrombectomy devices that are currently in most common use, specifically, stent retrievers and suction catheters. Based on the preprocedural imaging, a large bore guide catheter is advanced into the ipsilateral arterial system. After the occlusion is angiographically confirmed, the guide catheter and/or suction catheter is advanced as close as possible proximal to the clot. If the interventionist decides to use a stent retriever, a soft microcatheter guidewire is advanced blindly through the body of the clot. A microcatheter is then advanced over the guidewire until the distal end of the microcatheter exits the clot and is positioned downstream in the lumen of the affected artery. Alternatively, the guidewire and microcatheter can be advanced blindly through the clot as a coaxial unit. The guidewire is removed and another angiogram is obtained by injecting contrast through the microcatheter to confirm the distal end of the microcatheter is intraluminal and downstream of the clot. The stent retriever is advanced inside the microcatheter until the distal end of the stent is placed beyond the distal end of the clot, but still within the catheter. Then the microcatheter is withdrawn and the self-expanding stent deploys. When the stent expands against the vessel wall, the clot is trapped within the stent mesh and perfusion is restored. After a few minutes, the stent is withdrawn, pulling the stent and the trapped clot into the cervical guide catheter or suction catheter. Stent retrieval requires suction to temporarily reverse arterial blood flow, preventing clot fragments from being washed out of the stent, resulting in distal emboli. Alternatively, during stent retrieval, brief flow arrest can be achieved by inflation of a proximal balloon catheter. Stent withdrawal places traction on the affected cerebral artery, causing the patient to experience temporary pain (headache), which can be marked. Stent withdrawal can also lead to intracranial hemorrhage from vessel injury.
Some new large bore catheters have such effective suction that when placed next to the clot they can sometimes be used to draw out the clot without the need for a stent retriever.81,82 When the interventionist decides to use primary suction thrombectomy, the microcatheter (distal to the clot) is removed and the large bore catheter (proximal to the clot) is attached to a suction device (syringe or pump) before withdrawal. One or 2 cycles of stent deployment/withdrawal and/or direct aspiration may be sufficient to remove the clot(s). However, sometimes several cycles are needed, particularly when multiple vessels are occluded. A final angiogram is performed to determine how well perfusion has been restored. From arterial puncture to final angiogram, endovascular thrombectomy typically takes 60–90 minutes, with some trials reporting reperfusion within 30 minutes of arterial puncture.83–85
Angioplasty and/or stenting of a diseased ipsilateral extracranial internal carotid artery is performed in conjunction with endovascular thrombectomy in approximately 9%–24% of patients.11,12,14,27,31 When a carotid stent is placed, patients will need to receive dual antiplatelet therapy during endovascular thrombectomy and/or shortly thereafter, raising some concern of an increased risk of post–endovascular thrombectomy hemorrhagic conversion in the ischemic brain.
Determinants of Endovascular Thrombectomy Effectiveness
It essential to understand the patient and procedural determinants of endovascular thrombectomy effectiveness to recognize the limitations (ie, biases) of observational reports of anesthetic management for endovascular thrombectomy; see part 2 of this review.15 In brief, the determinants of endovascular thrombectomy effectiveness include (1) patient age; (2) presentation National Institutes of Health Stroke Scale score; (3) time between stroke onset and reperfusion; (4) occlusion location; (5) collateral perfusion before reperfusion; and (6) achieving adequate reperfusion. For a complete discussion, the reader is referred to Supplemental Digital Content, Document, http://links.lww.com/AA/C720.
In virtually all studies, increasing patient age and increasing presentation National Institutes of Health Stroke Scale score are associated with less favorable outcome.47 Likewise, until recently, all studies showed a progressive—approximately linear—decrease in endovascular thrombectomy effectiveness with increasing time between stroke onset and endovascular thrombectomy, with no demonstrable benefit beyond 6–7 hours.83,86 However, as noted above, a subset of acute stroke patients who have a small ischemic core and large and relatively stable penumbra can benefit from endovascular thrombectomy when treated beyond the 6-hour window. Endovascular thrombectomy effectiveness in this subset of patients may be less time sensitive.36,37
Endovascular thrombectomy outcomes differ depending on the location of the occlusion. In general, patients who have occlusions limited to middle cerebral artery have more favorable outcomes than patients who have occlusions of the intracranial internal carotid artery87–90 or vertebrobasilar arteries.90 In anterior circulation strokes, these outcome differences are likely related to the adequacy of collateral perfusion. A key determinant of endovascular thrombectomy effectiveness is the adequacy of collateral perfusion to the ischemic brain before establishing reperfusion.91–93 Good collaterals maintain viability of the penumbra and afford greater time to achieve reperfusion.94 Finally, endovascular thrombectomy effectiveness depends on restoring adequate arterial perfusion throughout the territory of the affected vessels, achieving modified Thrombolysis in Cerebral Infarction classes of 2b, 2c, or 3 (hereafter denoted 2b–3)95 (Table). Newer-generation endovascular thrombectomy devices result in a greater percentage of patients who have adequate reperfusion and better functional outcomes than first-generation devices.96–99
Blood Pressure and Outcome in Acute Ischemic Stroke and Endovascular Thrombectomy
Patients with acute ischemic stroke are very commonly hypertensive, acutely,100 chronically,101 or both.100 For example, in patients with ischemic stroke, those who had a history of hypertension (n = 200, 68%) had greater SBP before their stroke (144 ± 21 mm Hg) and at stroke presentation (162 ± 30 mm Hg) than patients without a history of hypertension (n = 94, 32%), 134 ± 18 and 150 ± 28 mm Hg, respectively.100 Although highly variable among individuals, the mean increase in SBP with the onset of stroke (+16–18 mm Hg) did not differ between patients with and without chronic hypertension.100 Consistent with these observations, patients treated with endovascular thrombectomy are typically hypertensive at presentation. It has been suggested that the acute increase in blood pressure with stroke onset may be an adaptive response that increases collateral perfusion to the penumbra. If so, one might expect greater blood pressure at stroke presentation would be associated with better outcomes. However, paradoxically, the opposite is true—greater values for SBP at the time of stroke presentation are associated with less favorable outcome.
In the pre–endovascular thrombectomy era, several studies reported greater values for SBP at the time of stroke presentation were associated with less favorable outcome. The threshold SBP value above which outcomes were progressively less favorable varied among studies: SBP >130 mm Hg,102 SBP >150 mm Hg,103 or SBP >180 mm Hg.104 Recently, the same phenomenon and the same general SBP threshold have been observed in patients treated with endovascular thrombectomy. In the MR CLEAN trial, in both endovascular thrombectomy and control patients, 3-month functional outcome was progressively less favorable when presentation SBP exceeded approximately 130–140 mm Hg; see Figure 3.75 Consistent with this observation, 3 earlier endovascular thrombectomy studies also reported greater presentation blood pressure (SBP >140 mm Hg,105 SBP>150 mm Hg87,106) was associated with less favorable outcomes, either less successful reperfusion87 or less favorable 3-month functional outcome.105,106 A fourth endovascular thrombectomy study reported greater values for maximum SBP during endovascular thrombectomy were associated with less favorable 3-month functional outcome.89 The mechanism(s) that underlies these observations (greater presentation blood pressure associated with less favorable outcome) is not fully understood. Nevertheless, these observations—made in populations of patients treated with endovascular thrombectomy—must not be misinterpreted and must not be misapplied to individual patients treated with endovascular thrombectomy. The overwhelming weight of current evidence is that substantive decreases in blood pressure from values at presentation do not improve outcomes. In fact, the opposite is true—decreasing blood pressure (intended or not) in the setting of acute stroke is associated with less favorable outcome.
In the pre–endovascular thrombectomy era, several studies reported acute decreases in blood pressure (usually, decreases ≥20–30 mm Hg) within the first 24 hours of stroke were associated with less favorable outcome.104,107–111 This is consistent with the observation that collateral perfusion to the penumbra is blood pressure dependent, at least in some patients. In 1983, Olsen et al112 measured penumbral blood flow in 8 patients who had acute ischemic stroke in the middle cerebral artery distribution. Patients were studied at 46 ± 20 hours after stroke onset, and penumbral perfusion was angiographically proven to come from collaterals. Angiotensin was administered to increase MAP from 105 ± 14 to 139 ± 9 mm Hg. Compared with nonischemic/nonin-farcted brain, increases in blood flow in response to hypertension were greater in the penumbra, for both an absolute increase in cerebral blood flow: 4.0 ± 3.7 vs 8.5 ± 5.1 mL·100 g−1·minute−1, respectively (P = .016); and a relative increase in cerebral blood flow: 11 ± 11% vs 27 ± 11%, respectively (P = .008).a This study showed that in at least some stroke patients, collateral perfusion to the penumbra is blood pressure dependent. In other words, collateral-based perfusion to the penumbra is not governed by autoregulation. There are several case reports that demonstrate acute hypertension can cause radiographically demonstrable improvements in penumbral perfusion.113–115 More recent studies support the observation that autoregulation in the ischemic hemisphere is impaired in the acute phase of stroke.116 Because collateral perfusion to the penumbra is, at least in some patients, blood pressure dependent, hypotension has the potential to decrease collateral (penumbral) perfusion and, consequently, hasten the progression from ischemia to infarction.
In fact, in patients treated with endovascular thrombectomy, decreases in blood pressure during endovascular thrombectomy are associated with less favorable outcome. Two recent observational reports made remarkably similar observations. In a subset of 60 general anesthesia patients from the MR CLEAN trial, a decrease in intraendovascular thrombectomy mean MAP was associated with less favorable functional outcome (modified Rankin Scale): per 10 mm Hg decrease from presentation MAP (which was 100 mm Hg) odds ratio = 0.60 (95% CI, 0.43–0.90); P = .03.76 In a different study by Whalin et al,77 all patients underwent endovascular thrombectomy using dexmedetomidine sedation. Patients presented with a MAP = 109 ± 19 mm Hg. Functional outcome was associated with all indices of minimum MAP before reperfusion. Very similar to the MR CLEAN results, a decrease in minimum MAP to values <100 mm Hg was associated with less favorable functional outcome (modified Rankin Scale): per 10 mm Hg decrease, odds ratio = 0.78 (95% CI, 0.62–0.99); P = .043. Thus, irrespective of method of anesthesia, the effect of decreased blood pressure on endovascular thrombectomy outcome was quantitatively indistinguishable in these 2 different endovascular thrombectomy populations.
In principle, one might expect that patient sensitivity to decreased intraendovascular thrombectomy blood pressure would depend on the collateral status. Patients treated with endovascular thrombectomy with very good collaterals would be expected to have (1) a smaller volume of severely ischemic brain; (2) a lesser sensitivity to decreased blood pressure; and (3) the most favorable outcome. In contrast, patients treated with endovascular thrombectomy with poor collaterals would be expected to have (1) a greater volume of severely ischemic brain; (2) a greater sensitivity to decreased blood pressure; and (3) the least favorable outcome. Because National Institutes of Health Stroke Scale score at presentation correlates with collateral status,93,94,117–120 one might expect that sensitivity to decreased blood pressure might differ as a function of presentation National Institutes of Health Stroke Scale score. As shown in Figure 4, the observations of Whalin et al77 are entirely consistent with these expectations. In this observational report, the association between minimum MAP before successful reperfusion and functional outcome (90-day modified Rankin Scale score ≤2) appeared to depend on presentation National Institutes of Health Stroke Scale score. The group of patients treated with endovascular thrombectomy who presented with National Institutes of Health Stroke Scale scores <15 had the greatest percentage of patients with good outcome, and outcome appeared to be minimally affected by minimum MAP. Outcomes of patients treated with endovascular thrombectomy presenting with midrange National Institutes of Health Stroke Scale scores (15–20) did not appear to be affected by minimum MAP until it was <70 mm Hg. In the group of patients treated with endovascular thrombectomy who presented with the most severe strokes (National Institutes of Health Stroke Scale >20), minimum MAP <80 mm Hg before reperfusion appeared to be associated with less favorable outcome. Within each of 3 National Institutes of Health Stroke Scale groups, outcome appeared best in patients who had a prereperfusion minimum MAP >90 mm Hg. Thus, although some patients treated with endovascular thrombectomy may be relatively tolerant to decreases in blood pressure before reperfusion, the most prudent blood pressure management principle is to maintain blood pressure at pre–endovascular thrombectomy values until reperfusion is achieved. This is a cardinal management principle.
The 2018 American Heart Association acute stroke guidelines recommend that during and for 24 hours after tissue plasminogen activator or other acute reperfusion therapy (ie, endovascular thrombectomy), blood pressure should be ≤180/105 mm Hg.19 Therefore, at the present, American Heart Association guidelines are such that in patients treated with endovascular thrombectomy who have received tissue plasminogen activator, the maximum acceptable SBP is 180 mm Hg, and the maximum acceptable diastolic blood pressure is 105 mm Hg, implying a maximum acceptable MAP of 130 mm Hg. In patients treated with endovascular thrombectomy who have not received tissue plasminogen activator, 2018 guidelines suggest even greater blood pressure values may be reasonable, particularly before reperfusion.19 As discussed above, the minimum acceptable blood pressure value during endovascular thrombectomy (before reperfusion) likely varies among individuals but, in principle, attempting to maintain blood pressure close to preendovascular thrombectomy values appears reasonable. The 2014 Society for Neuroscience in Anesthesia and Critical Care guidelines for the anesthetic management of patients treated with endovascular thrombectomy4—SBP should be maintained at >140 and <180 mm Hg, and diastolic blood pressure at <105 mm Hg—are compatible with 2018 American Heart Association guidelines.
Although the majority of patients treated with endovascular thrombectomy are hypertensive at presentation, some are not. In the MR CLEAN trial 32 of 233 (14%) patients treated with endovascular thrombectomy presented with SBP <120 mm Hg.75 The percentage of patients treated with endovascular thrombectomy with 90-day modified Rankin Scale ≤2 did not differ between patients who presented with SBP <120 mm Hg versus those presenting with SBP ≥120 mm Hg; 13 of 32 (41%) vs 63 of 201 (31%), respectively (Fisher exact P = .31, calculated by the author of this review). Thus, at present, it is not known whether patients treated with endovascular thrombectomy who present with a relatively “low” to normal blood pressure should receive fluids or pressors to increase blood pressure to the 2014 Society for Neuroscience in Anesthesia and Critical Care guideline value of SBP >140 mm Hg.
The author thanks Drs Colin Derdeyn, Franklin Dexter, and Santiago Ortega-Gutiérrez for reviewing this review and for their helpful suggestions.
Name: Bradley J. Hindman, MD.
Contribution: This author is solely responsible for this study.
This manuscript was handled by: Gregory J. Crosby, MD.
1. Bracard S, Ducrocq X, Mas JL, et al.; THRACE investigators. Mechanical thrombectomy after intravenous alteplase versus alteplase alone after stroke (THRACE): a randomised controlled trial. Lancet Neurol. 2016;15:1138–1147.
2. Slezak A, Kurmann R, Oppliger L, et al. Impact of anesthesia on the outcome of acute ischemic stroke after endovascular treatment with the Solitaire stent retriever. AJNR Am J Neuroradiol. 2017;38:1362–1367.
3. McTaggart RA, Ansari SA, Goyal M, et al.; Standards and Guidelines Committee of the Society of NeuroInterventional Surgery (SNIS). Initial hospital management of patients with emergent large vessel occlusion (ELVO): report of the standards and guidelines committee of the Society of NeuroInterventional Surgery. J Neurointerv Surg. 2017;9:316–323.
4. Talke PO, Sharma D, Heyer EJ, Bergese SD, Blackham KA, Stevens RD. Society for Neuroscience in Anesthesiology and Critical Care Expert consensus statement: anesthetic management of endovascular treatment for acute ischemic stroke*: endorsed by the Society of NeuroInterventional Surgery and the Neurocritical Care Society. J Neurosurg Anesthesiol. 2014;26:95–108.
5. Nichols C, Carrozzella J, Yeatts S, Tomsick T, Broderick J, Khatri P. Is periprocedural sedation during acute stroke therapy associated with poorer functional outcomes? J Neurointerv Surg. 2010;2:67–70.
6. Abou-Chebl A, Lin R, Hussain MS, et al. Conscious sedation versus general anesthesia during endovascular therapy for acute anterior circulation stroke: preliminary results from a retrospective, multicenter study. Stroke. 2010;41:1175–1179.
7. Jumaa MA, Zhang F, Ruiz-Ares G, et al. Comparison of safety and clinical and radiographic outcomes in endovascular acute stroke therapy for proximal middle cerebral artery occlusion with intubation and general anesthesia versus the nonintubated state. Stroke. 2010;41:1180–1184.
8. Davis MJ, Menon BK, Baghirzada LB, et al.; Calgary Stroke Program. Anesthetic management and outcome in patients during endovascular therapy for acute stroke. Anesthesiology. 2012;116:396–405.
9. Hassan AE, Chaudhry SA, Zacharatos H, et al. Increased rate of aspiration pneumonia and poor discharge outcome among acute ischemic stroke patients following intubation for endovascular treatment. Neurocrit Care. 2012;16:246–250.
10. Schönenberger S, Möhlenbruch M, Pfaff J, et al. Sedation vs Intubation for Endovascular Stroke TreAtment (SIESTA) - a randomized monocentric trial. Int J Stroke. 2015;10:969–978.
11. Schönenberger S, Uhlmann L, Hacke W, et al. Effect of Conscious sedation versus general anesthesia on early neurological improvement among patients with ischemic stroke undergoing endovascular thrombectomy: a randomized clinical trial. JAMA. 2016;316:1986–1996.
12. Löwhagen Hendén P, Rentzos A, Karlsson JE, et al. General anesthesia versus conscious sedation for endovascular treatment of acute ischemic stroke: the AnStroke Trial (Anesthesia During Stroke). Stroke. 2017;48:1601–1607.
13. Simonsen CZ, Sørensen LH, Juul N, et al. Anesthetic strategy during endovascular therapy: general anesthesia or conscious sedation? (GOLIATH - General or Local Anesthesia in Intra Arterial Therapy) A single-center randomized trial. Int J Stroke. 2016;11:1045–1052.
14. Simonsen CZ, Yoo AJ, Sørensen LH, et al. Effect of general anesthesia and conscious sedation during endovascular therapy on infarct growth and clinical outcomes in acute ischemic stroke: a randomized clinical trial. JAMA Neurol. 2018;75:470–477.
15. Hindman BJ, Dexter F. Anesthetic management of emergency endovascular thrombectomy for acute ischemic stroke, part 2: integrating and applying observational reports and randomized clinical trials. Anesth Analg. 2019;128:706–717.
16. Benjamin EJ, Virani SS, Callaway CW, et al.; American Heart Association Council on Epidemiology and Prevention Statistics Committee and Stroke Statistics Subcommittee. Heart disease and stroke statistics-2018 update: a report from the American Heart Association. Circulation. 2018;137:e67–e492.
17. The National Institute of Neurological Disorder and Stroke rt-PA Stroke Study Group. Tissue plasminogen activator for acute ischemic stroke. N Engl J Med. 1995;333:1581–1587.
18. Hacke W, Kaste M, Bluhmki E, et al.; ECASS Investigators. Thrombolysis with alteplase 3 to 4.5 hours after acute ischemic stroke. N Engl J Med. 2008;359:1317–1329.
19. Powers WJ, Rabinstein AA, Ackerson T, et al.; American Heart Association Stroke Council. 2018 guidelines for the early management of patients with acute ischemic stroke: a guideline for healthcare professionals from the American Heart Association/American Stroke Association. Stroke. 2018;49:e46–e110.
20. Rha JH, Saver JL. The impact of recanalization on ischemic stroke outcome: a meta-analysis. Stroke. 2007;38:967–973.
21. Saver JL. Number needed to treat estimates incorporating effects over the entire range of clinical outcomes: novel derivation method and application to thrombolytic therapy for acute stroke. Arch Neurol. 2004;61:1066–1070.
22. Bhatia R, Hill MD, Shobha N, et al. Low rates of acute recanalization with intravenous recombinant tissue plasminogen activator in ischemic stroke: real-world experience and a call for action. Stroke. 2010;41:2254–2258.
23. Seners P, Turc G, Maïer B, Mas JL, Oppenheim C, Baron JC. Incidence and predictors of early recanalization after intravenous thrombolysis: a systematic review and meta-analysis. Stroke. 2016;47:2409–2412.
24. Broderick JP, Palesch YY, Demchuk AM, et al.; Interventional Management of Stroke (IMS) III Investigators. Endovascular therapy after intravenous t-PA versus t-PA alone for stroke. N Engl J Med. 2013;368:893–903.
25. Ciccone A, Valvassori L, Nichelatti M, et al.; SYNTHESIS Expansion Investigators. Endovascular treatment for acute ischemic stroke. N Engl J Med. 2013;368:904–913.
26. Kidwell CS, Jahan R, Gornbein J, et al.; MR RESCUE Investigators. A trial of imaging selection and endovascular treatment for ischemic stroke. N Engl J Med. 2013;368:914–923.
27. Berkhemer OA, Fransen PS, Beumer D, et al.; MR CLEAN Investigators. A randomized trial of intraarterial treatment for acute ischemic stroke. N Engl J Med. 2015;372:11–20.
28. Campbell BC, Mitchell PJ, Kleinig TJ, et al.; EXTEND-IA Investigators. Endovascular therapy for ischemic stroke with perfusion-imaging selection. N Engl J Med. 2015;372:1009–1018.
29. Goyal M, Demchuk AM, Menon BK, et al.; ESCAPE Trial Investigators. Randomized assessment of rapid endovascular treatment of ischemic stroke. N Engl J Med. 2015;372:1019–1030.
30. Saver JL, Goyal M, Bonafe A, et al.; SWIFT PRIME Investigators. Stent-retriever thrombectomy after intravenous t-PA vs t-PA alone in stroke. N Engl J Med. 2015;372:2285–2295.
31. Jovin TG, Chamorro A, Cobo E, et al.; REVASCAT Trial Investigators. Thrombectomy within 8 hours after symptom onset in ischemic stroke. N Engl J Med. 2015;372:2296–2306.
32. Yarbrough CK, Ong CJ, Beyer AB, Lipsey K, Derdeyn CP. Endovascular thrombectomy for anterior circulation stroke: systematic review and meta-analysis. Stroke. 2015;46:3177–3183.
33. Badhiwala JH, Nassiri F, Alhazzani W, et al. Endovascular thrombectomy for acute ischemic stroke: a meta-analysis. JAMA. 2015;314:1832–1843.
34. Ouyang F, Chen Y, Zhao Y, Dang G, Liang J, Zeng J. Selection of patients and anesthetic types for endovascular treatment in acute ischemic stroke: a meta-analysis of randomized controlled trials. PLoS One. 2016;11:e0151210.
35. Saver JL, Goyal M, van der Lugt A, et al.; HERMES Collaborators. Time to treatment with endovascular thrombectomy and outcomes from ischemic stroke: a meta-analysis. JAMA. 2016;316:1279–1288.
36. Nogueira RG, Jadhav AP, Haussen DC, et al.; DAWN Trial Investigators. Thrombectomy 6 to 24 hours after stroke with a mismatch between deficit and infarct. N Engl J Med. 2018;378:11–21.
37. Albers GW, Marks MP, Kemp S, et al.; DEFUSE 3 Investigators. Thrombectomy for stroke at 6 to 16 hours with selection by perfusion imaging. N Engl J Med. 2018;378:708–718.
38. Vlisides P, Mashour GA. Perioperative stroke. Can J Anaesth. 2016;63:193–204.
39. Vlisides PE, Mashour GA, Didier TJ, et al. Recognition and management of perioperative stroke in hospitalized patients. A A Case Rep. 2016;7:55–56.
40. van der Hoeven EJ, Schonewille WJ, Vos JA, et al.; BASICS Study Group. The Basilar Artery International Cooperation Study (BASICS): study protocol for a randomised controlled trial. Trials. 2013;14:200.
41. Liu X, Xu G, Liu Y, et al.; BEST Trial Investigators. Acute basilar artery occlusion: Endovascular Interventions versus Standard Medical Treatment (BEST) trial-design and protocol for a randomized, controlled, multicenter study. Int J Stroke. 2017;12:779–785.
42. Kumar G, Shahripour RB, Alexandrov AV. Recanalization of acute basilar artery occlusion improves outcomes: a meta-analysis. J Neurointerv Surg. 2015;7:868–874.
43. Gory B, Eldesouky I, Sivan-Hoffmann R, et al. Outcomes of stent retriever thrombectomy in basilar artery occlusion: an observational study and systematic review. J Neurol Neurosurg Psychiatry. 2016;87:520–525.
45. English JD, Yavagal DR, Gupta R, et al. Comprehensive stroke center requirements and endovascular stroke systems of care: recommendations from the endovascular stroke standards committee of the Society of Vascular and Interventional Neurology (SVIN). Intervent Neurol. 2016;4:138–150.
46. Sacks D, Baxter B, Campbell BCV, et al. Multisociety consensus quality improvement revised consensus statement for endovascular therapy of acute ischemic stroke: from the American Association of Neurological Surgeons (AANS), American Society of Neuroradiology (ASNR), Cardiovascular and Interventional Radiology Society of Europe (CIRSE), Canadian Interventional Radiology Association (CIRA), Congress of Neurological Surgeons (CNS), European Society of Minimally Invasive Neurological Therapy (ESMINT), European Society of Neuroradiology (ESNR), European Stroke Organization (ESO), Society for Cardiovascular Angiography and Interventions (SCAI), Society of Interventional Radiology (SIR), Society of NeuroInterventional Surgery (SNIS), and World Stroke Organization (WSO). J Vasc Interv Radiol. 2018;29:441–453.
47. Goyal M, Menon BK, van Zwam WH, et al.; HERMES collaborators. Endovascular thrombectomy after large-vessel ischaemic stroke: a meta-analysis of individual patient data from five randomised trials. Lancet. 2016;387:1723–1731.
48. Martino R, Foley N, Bhogal S, Diamant N, Speechley M, Teasell R. Dysphagia after stroke: incidence, diagnosis, and pulmonary complications. Stroke. 2005;36:2756–2763.
49. Kumar S, Doughty C, Doros G, et al. Recovery of swallowing after dysphagic stroke: an analysis of prognostic factors. J Stroke Cerebrovasc Dis. 2014;23:56–62.
50. Arnold M, Liesirova K, Broeg-Morvay A, et al. Dysphagia in acute stroke: incidence, burden and impact on clinical outcome. PLoS One. 2016;11:e0148424.
51. Flowers HL, Silver FL, Fang J, Rochon E, Martino R. The incidence, co-occurrence, and predictors of dysphagia, dysarthria, and aphasia after first-ever acute ischemic stroke. J Commun Disord. 2013;46:238–248.
52. Janssen H, Buchholz G, Killer M, Ertl L, Brückmann H, Lutz J. General anesthesia versus conscious sedation in acute stroke treatment: the importance of head immobilization. Cardiovasc Intervent Radiol. 2016;39:1239–1244.
53. Hassan AE, Adil MM, Zacharatos H, et al. Should ischemic stroke patients with aphasia or high National Institutes of Health stroke scale score undergo preprocedural intubation and endovascular treatment? J Stroke Cerebrovasc Dis. 2014;23:e299–e304.
54. Crijnen YS, Nouwens F, de Lau LM, et al.; MR CLEAN investigators. Early effect of intra-arterial treatment in ischemic stroke on aphasia recovery in MR CLEAN. Neurology. 2016;86:2049–2055.
55. Rowat AM, Dennis MS, Wardlaw JM. Central periodic breathing observed on hospital admission is associated with an adverse prognosis in conscious acute stroke patients. Cerebrovasc Dis. 2006;21:340–347.
56. Sugg RM, Jackson AS, Holloway W, Martin CO, Akhtar N, Rymer M. Is mechanical embolectomy performed in nonanesthetized patients effective? AJNR Am J Neuroradiol. 2010;31:1533–1535.
57. Langner S, Khaw AV, Fretwurst T, Angermaier A, Hosten N, Kirsch M. [Endovascular treatment of acute ischemic stroke under conscious sedation compared to general anesthesia - safety, feasibility and clinical and radiological outcome]. Rofo. 2013;185:320–327.
58. Soize S, Kadziolka K, Estrade L, Serre I, Bakchine S, Pierot L. Mechanical thrombectomy in acute stroke: prospective pilot trial of the Solitaire FR device while under conscious sedation. AJNR Am J Neuroradiol. 2013;34:360–365.
59. Li F, Deshaies EM, Singla A, et al. Impact of anesthesia on mortality during endovascular clot removal for acute ischemic stroke. J Neurosurg Anesthesiol. 2014;26:286–290.
60. Abou-Chebl A, Yeatts SD, Yan B, et al. Impact of general anesthesia on safety and outcomes in the endovascular arm of Interventional Management of Stroke (IMS) III Trial. Stroke. 2015;46:2142–2148.
61. Mundiyanapurath S, Schönenberger S, Rosales ML, et al. Circulatory and respiratory parameters during acute endovascular stroke therapy in conscious sedation or general anesthesia. J Stroke Cerebrovasc Dis. 2015;24:1244–1249.
62. Just C, Rizek P, Tryphonopoulos P, Pelz D, Arango M. Outcomes of general anesthesia and conscious sedation in endovascular treatment for stroke. Can J Neurol Sci. 2016;43:655–658.
63. Jagani M, Brinjikji W, Rabinstein AA, Pasternak JJ, Kallmes DF. Hemodynamics during anesthesia for intra-arterial therapy of acute ischemic stroke. J Neurointerv Surg. 2016;8:883–888.
64. Mundiyanapurath S, Stehr A, Wolf M, et al. Pulmonary and circulatory parameter guided anesthesia in patients with ischemic stroke undergoing endovascular recanalization. J Neurointerv Surg. 2016;8:335–341.
65. Athiraman U, Sultan-Qurraie A, Nair B, et al. Endovascular treatment of acute ischemic stroke under general anesthesia: predictors of good outcome. J Neurosurg Anesthesiol. 2018;30:223–230.
66. Libman RB, Kwiatkowski TG, Hansen MD, Clarke WR, Woolson RF, Adams HP. Differences between anterior and posterior circulation stroke in TOAST. Cerebrovasc Dis. 2001;11:311–316.
67. Mattle HP, Arnold M, Lindsberg PJ, Schonewille WJ, Schroth G. Basilar artery occlusion. Lancet Neurol. 2011;10:1002–1014.
68. Schonewille WJ, Wijman CA, Michel P, et al.; BASICS study group. Treatment and outcomes of acute basilar artery occlusion in the Basilar Artery International Cooperation Study (BASICS): a prospective registry study. Lancet Neurol. 2009;8:724–730.
69. Jadhav AP, Bouslama M, Aghaebrahim A, et al. Monitored anesthesia care vs intubation for vertebrobasilar stroke endovascular therapy. JAMA Neurol. 2017;74:704–709.
70. Möhlenbruch M, Stampfl S, Behrens L, et al. Mechanical thrombectomy with stent retrievers in acute basilar artery occlusion. AJNR Am J Neuroradiol. 2014;35:959–964.
71. van Houwelingen RC, Luijckx GJ, Mazuri A, Bokkers RP, Eshghi OS, Uyttenboogaart M. Safety and outcome of intra-arterial treatment for basilar artery occlusion. JAMA Neurol. 2016;73:1225–1230.
72. Fahed R, Di Maria F, Rosso C, et al. A leap forward in the endovascular management of acute basilar artery occlusion since the appearance of stent retrievers: a single-center comparative study. J Neurosurg. 2017;126:1578–1584.
73. Gory B, Mazighi M, Blanc R, et al. Mechanical thrombectomy in basilar artery occlusion: influence of reperfusion on clinical outcome and impact of the first-strategy (ADAPT vs stent retriever). J Neurosurg. 2018;129:1482–1491.
74. Rentzos A, Karlsson JE, Lundqvist C, Rosengren L, Hellström M, Wikholm G. Endovascular treatment of acute ischemic stroke in the posterior circulation. Interv Neuroradiol. 2018;24:405–411.
75. Mulder MJHL, Ergezen S, Lingsma HF, et al.; Multicenter Randomized Clinical Trial of Endovascular Treatment of Acute Ischemic Stroke in the Netherlands (MR CLEAN) Investigators. Baseline blood pressure effect on the benefit and safety of intra-arterial treatment in MR CLEAN (Multicenter Randomized Clinical Trial of Endovascular Treatment of Acute Ischemic Stroke in the Netherlands). Stroke. 2017;48:1869–1876.
76. Treurniet KM, Berkhemer OA, Immink RV, et al.; MR CLEAN investigators. A decrease in blood pressure is associated with unfavorable outcome in patients undergoing thrombectomy under general anesthesia. J Neurointerv Surg. 2018;10:107–111.
77. Whalin MK, Halenda KM, Haussen DC, et al. Even small decreases in blood pressure during conscious sedation affect clinical outcome after stroke thrombectomy: an analysis of hemodynamic thresholds. AJNR Am J Neuroradiol. 2017;38:294–298.
78. Sivasankar C, Stiefel M, Miano TA, et al. Anesthetic variation and potential impact of anesthetics used during endovascular management of acute ischemic stroke. J Neurointerv Surg. 2016;8:1101–1106.
79. Liebeskind DS, Flint AC, Budzik RF, et al.; MERCI and Multi-MERCI Investigators. Carotid I’s, L’s and T’s: collaterals shape the outcome of intracranial carotid occlusion in acute ischemic stroke. J Neurointerv Surg. 2015;7:402–407.
80. Spiotta AM, Chaudry MI, Hui FK, Turner RD, Kellogg RT, Turk AS. Evolution of thrombectomy approaches and devices for acute stroke: a technical review. J Neurointerv Surg. 2015;7:2–7.
81. Lapergue B, Blanc R, Gory B, et al.; ASTER Trial Investigators. Effect of endovascular contact aspiration vs stent retriever on revascularization in patients with acute ischemic stroke and large vessel occlusion: the ASTER randomized clinical trial. JAMA. 2017;318:443–452.
82. Stapleton CJ, Leslie-Mazwi TM, Torok CM, et al. A direct aspiration first-pass technique vs stentriever thrombectomy in emergent large vessel intracranial occlusions. J Neurosurg. 2018;128:567–574.
83. Goyal M, Jadhav AP, Bonafe A, et al.; SWIFT PRIME Investigators. Analysis of workflow and time to treatment and the effects on outcome in endovascular treatment of acute ischemic stroke: results from the SWIFT PRIME randomized controlled trial. Radiology. 2016;279:888–897.
84. Menon BK, Sajobi TT, Zhang Y, et al. Analysis of workflow and time to treatment on thrombectomy outcome in the Endovascular Treatment for Small Core and Proximal Occlusion Ischemic Stroke (ESCAPE) randomized, controlled trial. Circulation. 2016;133:2279–2286.
85. Menon BK, Almekhlafi MA, Pereira VM, et al.; STAR Study Investigators. Optimal workflow and process-based performance measures for endovascular therapy in acute ischemic stroke: analysis of the Solitaire FR thrombectomy for acute revascularization study. Stroke. 2014;45:2024–2029.
86. Fransen PS, Berkhemer OA, Lingsma HF, et al.; Multicenter Randomized Clinical Trial of Endovascular Treatment of Acute Ischemic Stroke in the Netherlands Investigators. Time to reperfusion and treatment effect for acute ischemic stroke: a randomized clinical trial. JAMA Neurol. 2016;73:190–196.
87. Nogueira RG, Liebeskind DS, Sung G, Duckwiler G, Smith WS; MERCI; Multi MERCI Writing Committee. Predictors of good clinical outcomes, mortality, and successful revascularization in patients with acute ischemic stroke undergoing thrombectomy: pooled analysis of the Mechanical Embolus Removal in Cerebral Ischemia (MERCI) and Multi MERCI Trials. Stroke. 2009;40:3777–3783.
88. Al-Ajlan FS, Goyal M, Demchuk AM, et al.; ESCAPE Trial Investigators. Intra-arterial therapy and post-treatment infarct volumes: insights from the ESCAPE randomized controlled trial. Stroke. 2016;47:777–781.
89. John S, Hazaa W, Uchino K, et al. Lower intraprocedural systolic blood pressure predicts good outcome in patients undergoing endovascular therapy for acute ischemic stroke. Interv Neurol. 2016;4:151–157.
90. Linfante I, Starosciak AK, Walker GR, et al. Predictors of poor outcome despite recanalization: a multiple regression analysis of the NASA registry. J Neurointerv Surg. 2016;8:224–229.
91. Leng X, Fang H, Leung TW, et al. Impact of collaterals on the efficacy and safety of endovascular treatment in acute ischaemic stroke: a systematic review and meta-analysis. J Neurol Neurosurg Psychiatry. 2016;87:537–544.
92. Leng X, Fang H, Leung TW, et al. Impact of collateral status on successful revascularization in endovascular treatment: a systematic review and meta-analysis. Cerebrovasc Dis. 2016;41:27–34.
93. Berkhemer OA, Jansen IG, Beumer D, et al.; MR CLEAN Investigators. Collateral status on baseline computed tomographic angiography and intra-arterial treatment effect in patients with proximal anterior circulation stroke. Stroke. 2016;47:768–776.
94. Kim BM, Baek JH, Heo JH, et al. Collateral status affects the onset-to-reperfusion time window for good outcome. J Neurol Neurosurg Psychiatry. 2018;89:903–909.
95. Zaidat OO, Yoo AJ, Khatri P, et al.; Cerebral Angiographic Revascularization Grading (CARG) Collaborators; STIR Revascularization Working Group; STIR Thrombolysis in Cerebral Infarction (TICI) Task Force. Recommendations on angiographic revascularization grading standards for acute ischemic stroke: a consensus statement. Stroke. 2013;44:2650–2663.
96. Nogueira RG, Lutsep HL, Gupta R, et al.; TREVO 2 Trialists. Trevo versus Merci retrievers for thrombectomy revascularisation of large vessel occlusions in acute ischaemic stroke (TREVO 2): a randomised trial. Lancet. 2012;380:1231–1240.
97. Saver JL, Jahan R, Levy EI, et al.; SWIFT Trialists. Solitaire flow restoration device versus the Merci Retriever in patients with acute ischaemic stroke (SWIFT): a randomised, parallel-group, non-inferiority trial. Lancet. 2012;380:1241–1249.
98. Broussalis E, Trinka E, Hitzl W, Wallner A, Chroust V, Killer-Oberpfalzer M. Comparison of stent-retriever devices versus the Merci retriever for endovascular treatment of acute stroke. AJNR Am J Neuroradiol. 2013;34:366–372.
99. Hentschel KA, Daou B, Chalouhi N, et al. Comparison of non-stent retriever and stent retriever mechanical thrombectomy devices for the endovascular treatment of acute ischemic stroke. J Neurosurg. 2017;126:1123–1130.
100. Fischer U, Cooney MT, Bull LM, et al. Acute post-stroke blood pressure relative to premorbid levels in intracerebral haemorrhage versus major ischaemic stroke: a population-based study. Lancet Neurol. 2014;13:374–384.
101. Gioia LC, Zewude RT, Kate MP, et al. Prehospital systolic blood pressure is higher in acute stroke compared with stroke mimics. Neurology. 2016;86:2146–2153.
102. Vemmos KN, Tsivgoulis G, Spengos K, et al. U-shaped relationship between mortality and admission blood pressure in patients with acute stroke. J Intern Med. 2004;255:257–265.
103. Leonardi-Bee J, Bath PM, Phillips SJ, Sandercock PA; IST Collaborative Group. Blood pressure and clinical outcomes in the International Stroke Trial. Stroke. 2002;33:1315–1320.
104. Castillo J, Leira R, García MM, Serena J, Blanco M, Dávalos A. Blood pressure decrease during the acute phase of ischemic stroke is associated with brain injury and poor stroke outcome. Stroke. 2004;35:520–526.
105. Whalin MK, Lopian S, Wyatt K, et al. Dexmedetomidine: a safe alternative to general anesthesia for endovascular stroke treatment. J Neurointerv Surg. 2014;6:270–275.
106. Goyal N, Tsivgoulis G, Iftikhar S, et al. Admission systolic blood pressure and outcomes in large vessel occlusion strokes treated with endovascular treatment. J Neurointerv Surg. 2017;9:451–454.
107. Ahmed N, Näsman P, Wahlgren NG. Effect of intravenous nimodipine on blood pressure and outcome after acute stroke. Stroke. 2000;31:1250–1255.
108. Boreas AM, Lodder J, Kessels F, de Leeuw PW, Troost J. Prognostic value of blood pressure in acute stroke. J Hum Hypertens. 2002;16:111–116.
109. Oliveira-Filho J, Silva SC, Trabuco CC, Pedreira BB, Sousa EU, Bacellar A. Detrimental effect of blood pressure reduction in the first 24 hours of acute stroke onset. Neurology. 2003;61:1047–1051.
110. Silver B, Lu M, Morris DC, Mitsias PD, Lewandowski C, Chopp M. Blood pressure declines and less favorable outcomes in the NINDS tPA stroke study. J Neurol Sci. 2008;271:61–67.
111. Sandset EC, Murray GD, Bath PM, Kjeldsen SE, Berge E; Scandinavian Candesartan Acute Stroke Trial (SCAST) Study Group. Relation between change in blood pressure in acute stroke and risk of early adverse events and poor outcome. Stroke. 2012;43:2108–2114.
112. Olsen TS, Larsen B, Herning M, Skriver EB, Lassen NA. Blood flow and vascular reactivity in collaterally perfused brain tissue. Evidence of an ischemic penumbra in patients with acute stroke. Stroke. 1983;14:332–341.
113. Chalela JA, Dunn B, Todd JW, Warach S. Induced hypertension improves cerebral blood flow in acute ischemic stroke. Neurology. 2005;64:1979.
114. Bogoslovsky T, Häppölä O, Salonen O, Lindsberg PJ. Induced hypertension for the treatment of acute MCA occlusion beyond the thrombolysis window: case report. BMC Neurol. 2006;6:46.
115. Georgiadis AL, Al-Kawi A, Janjua N, Kirmani JF, Ezzeddine MA, Qureshi AI. Cerebral angiography can demonstrate changes in collateral flow during induced hypertension. Radiol Case Rep. 2007;2:37.
116. Petersen NH, Ortega-Gutierrez S, Reccius A, Masurkar A, Huang A, Marshall RS. Dynamic cerebral autoregulation is transiently impaired for one week after large-vessel acute ischemic stroke. Cerebrovasc Dis. 2015;39:144–150.
117. Rusanen H, Saarinen JT, Sillanpää N. Collateral circulation predicts the size of the infarct core and the proportion of salvageable penumbra in hyperacute ischemic stroke patients treated with intravenous thrombolysis. Cerebrovasc Dis. 2015;40:182–190.
118. Marks MP, Lansberg MG, Mlynash M, et al.; Diffusion and Perfusion Imaging Evaluation for Understanding Stroke Evolution 2 Investigators. Effect of collateral blood flow on patients undergoing endovascular therapy for acute ischemic stroke. Stroke. 2014;45:1035–1039.
119. Lima FO, Furie KL, Silva GS, et al. The pattern of leptomeningeal collaterals on CT angiography is a strong predictor of long-term functional outcome in stroke patients with large vessel intracranial occlusion. Stroke. 2010;41:2316–2322.
120. Arsava EM, Vural A, Akpinar E, et al. The detrimental effect of aging on leptomeningeal collaterals in ischemic stroke. J Stroke Cerebrovasc Dis. 2014;23:421–426.