Derdeyn, Colin P. MD*; Fiorella, David MD, PhD‡; Lynn, Michael J. MS§; Rumboldt, Zoran MD‖; Cloft, Harry J. MD, PhD¶; Gibson, Daniel MD*; Turan, Tanya N. MD#; Lane, Bethany F. RN§; Janis, L. Scott PhD**; Chimowitz, Marc I. MB, ChB#; for the Stenting and Aggressive Medical Management for Preventing Recurrent Stroke in Intracranial Stenosis Trial Investigators
BACKGROUND: Enrollment in the Stenting and Aggressive Medical Management for the Prevention of stroke in Intracranial Stenosis (SAMMPRIS) trial was halted owing to higher-than-expected 30-day stroke rates in the stenting arm. Improvement in periprocedural stroke rates from angioplasty and stenting for intracranial atherosclerotic disease (ICAD) requires an understanding of the mechanisms of these events.
OBJECTIVE: To identify the types and mechanisms of periprocedural stroke after angioplasty and stenting for ICAD.
METHODS: Patients who experienced a hemorrhagic or ischemic stroke or a cerebral infarct with temporary signs within 30 days of attempted angioplasty and stenting in SAMMPRIS were identified. Study records, including case report forms, procedure notes, and imaging were reviewed. Strokes were categorized as ischemic or hemorrhagic. Ischemic strokes were categorized as perforator territory, distal embolic, or delayed stent thrombosis. Hemorrhagic strokes were categorized as subarachnoid or intraparenchymal. Causes of hemorrhage (wire perforation, vessel rupture) were recorded.
RESULTS: Three patients had an ischemic stroke after diagnostic angiography. Two of these strokes were unrelated to the procedure. Twenty-one patients had an ischemic stroke (n = 19) or cerebral infarct with temporary signs (n = 2) within 30 days of angioplasty and stenting. Most (n = 15) were perforator territory and many of these occurred after angiographically successful angioplasty and stenting of the basilar artery (n = 8). Six patients experienced a subarachnoid hemorrhage (3 from wire perforation) and 7 had a delayed intraparenchymal hemorrhage.
CONCLUSION: Efforts at reducing complications from angioplasty and stenting for ICAD must focus on reducing the risks of regional perforator infarction, delayed intraparenchymal hemorrhage, and wire perforation.
ABBREVIATIONS: ACT, activated clotting time
CITS, cerebral infarction with temporary signs
ICAD, intracranial atherosclerotic disease
IPH, intraparenchymal hemorrhage
mRS, modified Rankin Score
PTAS, percutaneous transluminal angioplasty
SAH, subarachnoid hemorrhage
SAMMPRIS, Stenting and Aggressive Medical Management for the Prevention of Recurrent stroke in Intracranial Stenosis
TIA, transient ischemic attack
The efficacy of angioplasty and stenting for patients with symptomatic intracranial atherosclerotic disease was recently evaluated in the Stenting and Aggressive Medical Management for the Prevention of Recurrent stroke in Intracranial Stenosis (SAMMPRIS) trial.1 This trial is the largest prospective study to date in this population. Enrollment was stopped early owing to a higher rate of 30-day stroke and death in the stenting arm relative to aggressive medical management. Two hundred twenty-four patients were randomly assigned to the stenting arm, and 33 (14.7%) had a symptomatic stroke within 30 days of enrollment. An additional 4 patients experienced an intracranial hemorrhage with symptoms lasting less than 24 hours or a cerebral infarction with temporary signs (CITS) within 30 days of the stenting procedure.2
Detailed statistical analyses of the relationship between clinical, procedural, and operator variables and the risk of 30-day adverse events have already been published.2,3 The aims of the present study are to investigate the specific nature and mechanism of individual events, to describe the frequencies of the different mechanisms, and to describe the clinical and imaging features of each event to provide a more complete understanding of the periprocedural events in the trial. These data will be critical for developing an understanding of how patient selection or devices could be improved to reduce the risk of perioperative stroke from angioplasty and stenting for symptomatic intracranial atherosclerotic disease (ICAD).
PATIENTS AND METHODS
SAMMPRIS is an ongoing randomized, multicenter clinical trial funded by the National Institute of Neurological Disorders and Stroke.1,4 Enrollment and randomization were complete at the time of this writing, but medical treatment and follow-up of enrolled patients continued until March 2013. The study design has been published.1,4 Eligibility criteria included either transient ischemic attack (TIA) or nondisabling stroke within 30 days before enrollment attributable to an angiographically verified 70% to 99% stenosis of a major intracranial artery.
Percutaneous Transluminal Angioplasty Procedure
The Gateway PTA Balloon Catheter and Wingspan Stent System (Boston Scientific Corporation, Stryker Neurovascular, Fremont, California) was used for percutaneous transluminal angioplasty (PTAS) in the trial. Specific aspects of the study protocol for PTAS procedure, postprocedure care, and aggressive medical management (same in both arms of the trial) have been published.1,5 The PTAS procedure was mandated for within 3 business days of randomization. A 600-mg loading dose between 6 and 24 hours before PTAS was required if the patient was not on daily clopidogrel (75 mg) for 5 days before PTAS. Systemic heparinization during PTAS was required with a target activated clotting time (ACT) of between 250 and 300 seconds.
Central Adjudication of Outcome After PTAS
Clinical evaluations of treated patients were required at study entry and at 4 days (by study coordinator) and 30 days after enrollment. The patient was examined by a study neurologist, and brain imaging was typically performed if a periprocedural stroke was suspected. All potential study end points were adjudicated by central physician investigators blinded to treatment assignment.1,2
Ischemic stroke was defined as a new focal neurological deficit of sudden onset that lasted at least 24 hours and was not associated with a hemorrhage on brain imaging (computed tomography [CT] or magnetic resonance imaging [MRI]). If symptoms lasted for less than 24 hours and were associated with a new infarct on brain imaging, the event was classified as a CITS. Hemorrhagic stroke was defined as parenchymal, subarachnoid, or intraventricular hemorrhage detected by CT or MRI that was associated with new neurological signs or symptoms lasting ≥24 hours or a seizure. These were primary end points. Hemorrhagic stroke associated with symptoms or signs (excluding seizure) less than 24 hours in duration were not considered primary end points.
Subtype Classification of Events
The present study is a retrospective and post hoc analysis of data collected in the trial. Patients with centrally adjudicated 30-day ischemic stroke, symptomatic hemorrhagic stroke, asymptomatic hemorrhagic stroke, or CITS after randomization to the stenting arm were identified. Study records, including case report forms, scanned documents such as procedure and progress notes and discharge or death summaries, and records of central end-point adjudication were reviewed. In addition, electronically archived (iSite, Phillips, Eindhoven, Netherlands) baseline, procedural, and postprocedure brain and vascular images were reviewed.
All periprocedural (within 30 days after randomization) ischemic strokes, CITS, and hemorrhagic strokes were categorized by consensus of the 3 primary investigators (D.F., C.D., M.C.) based on an assessment of the available imaging and clinical data. Hemorrhagic strokes were classified as subarachnoid hemorrhages (SAHs) when the bleeding was predominantly subarachnoid and the presentations were evident immediately after the procedure, or as reperfusion hemorrhages when the bleeding was predominantly intraparenchymal (intracerebral hemorrhage) and within the vascular distribution of the stented vessel. Ischemic strokes were further categorized as local perforator territory (covered by the stent), distal embolic, and delayed stent thrombosis based on imaging findings and the clinical deficits. Ischemic strokes were categorized as perforator occlusions if the infarct(s) and symptoms could be localized to the distribution supplied by perforating vessels arising within the margins of the stent, or embolic if the infarct was in a territorial distribution distal to the treated lesion and the symptoms were explained by the distal infarct. If a patient had lesions on imaging in local perforator and distal territories, but the symptoms were consistent with perforator ischemia only, the event was classified as a perforator event. When more than 1 mechanism contributed to the clinical findings, the stroke was described as mixed. Delayed stent occlusion was diagnosed if there was imaging or other presumptive evidence of stent occlusion.
Images and procedure reports were carefully reviewed for any evidence of mechanical or procedural causes of the hemorrhagic or ischemic event, including wire perforation, vessel rupture for hemorrhage, and vessel dissection for ischemic stroke.
Tables and Figures
Tables of the data collected for each individual patient were created based on the results of these reviews (Tables 1-4). Tabulated data included age and sex, the nature of the qualifying event (stroke, TIA, and major symptoms), baseline imaging findings if available, location of the symptomatic stenosis, time from qualifying event to procedure, pertinent details of the procedure, nature and timing of the complication, presumed mechanism of the event, and the 30-day outcome (modified Rankin Score, mRS).
Figures (Figures 1 and 2) were constructed by using images submitted from the site: baseline qualifying events, pre- and postprocedural angiograms, and relevant representative images of the hemorrhage or infarction.
Two hundred twenty patients underwent attempted angioplasty and stenting. The procedure was aborted in 6 patients before any intervention owing to the findings on catheter angiography and, in 1 case, when attempts to cross the lesion with a wire were unsuccessful. Three of these 7 patients had an ischemic stroke (Table 1, patients 35-37, Figure 2). One stroke was a definite procedural embolic stroke (patient 35) in a patient randomly assigned to stenting based on previous imaging but found to have less than 50% stenosis at the time of the planned PTAS procedure. The remaining 2 patients had strokes days later (patients 36 and 37). Both of these patients had developed an interval complete occlusion of the target vessel between enrollment and the planned intervention.
Procedural Ischemic Strokes
Twenty-one ischemic events (19 ischemic strokes and 2 CITS) occurred in the remaining 213 patients (Table 2, patients 1-21, Figure 1). Of the 21 events, 14 were evident on emerging from general anesthesia (patients 1-14). Eleven of the 14 events primarily involved local perforators (and resulted in clinical syndromes attributable to the perforator infarction), 2 were embolic (patients 7 and 10), and 1 was mixed embolic and perforator territory owing to acute intraprocedural stent thrombosis (patient 11). Technical difficulties were noted in 2 of the 11 perforator territory strokes that were evident immediately after the procedure (patient 1 [small V4 dissection flap] and patient 8 [difficult vertebral artery access]). Postangioplasty angiographic images were unremarkable in all 11 cases of perforator infarction. Distal embolic occlusion was evident on the postangioplasty images in 1 case (patient 7, missing left superior cerebellar artery on postangioplasty angiogram). This patient also received no Plavix load, and ACTs were not recorded during the procedure.
Five patients had a delayed ischemic event (patients 15-19). All delayed events occurred within 6 days of the procedure. One of these events was a local perforator stroke only (patient 15, at 36 hours). One patient had a complete stent thrombosis at 4 days (patient 16), 1 had a probable stent thrombosis at 6 days (patient 17), 1 had extensive distal emboli at 4 days (patient 18), and 1 had mixed perforator and distal embolic strokes at 6 days (patient 19).
Both of the CITS events were related to local perforator or branch (jailed anterior inferior cerebellar artery) vessel occlusions (patients 20 and 21). One was in the early postoperative period, and the other occurred 3 weeks after the procedure.
Delayed Intraparenchymal Hemorrhage
Seven patients had primarily intraparenchymal hemorrhage (IPH) (Table 3, patients 22-28, Figure 2). Six were end-point events with symptoms lasting more than 24 hours: 1 was noted 2 hours after the procedure (patient 27) and 5 were noted when neurological signs developed several hours after PTAS. In the 7 patients with IPH, baseline brain imaging showed infarcts in 5 (2 presenting with ischemic strokes [patients 25 and 28] and 3 presenting with CITS [patients 23, 24, and 27]). The remaining 2 had either a normal CT (patient 22) or no imaging (patient 26) at baseline. All IPHs were distributed within the vascular territory of the treated artery. Of the 6 symptomatic IPHs, 4 were fatal, 1 resulted in a mRS of 5, and 1 resulted in a mRS of 2 at 90 days. One patient had a cerebellar hemorrhage with transient postoperative nausea but no symptoms at 24 hours (patient 28).
Procedural Subarachnoid Hemorrhage
SAH occurred in 6 patients (Table 4, patients 29-34, Figure 2). Three patients had wire perforations that were evident during the procedure (patients 29, 30, and 32). The clinically adjudicated endpoint for patient 32 was an ischemic stroke: the perforation was successfully treated with coil embolization of the injured arterial branch. This resulted in a clinical ischemic stroke (adjudicated and reported as ischemic stroke in the original primary analysis). A fourth patient (patient 33) had acute SAH during the procedure, but the etiology could not be ascertained. One patient with interval occlusion between randomization and the endovascular procedure was treated with angioplasty alone (patient 31, protocol violation). This resulted in a vessel rupture (postangioplasty angiogram showing active extravasation). One final patient (patient 34) had an asymptomatic SAH identified on postoperative CT. No cause was determined.
Angioplasty and stenting of intracranial arteries is an emerging, but as yet unproven, therapy for stroke risk reduction for patients with recently symptomatic ICAD. The SAMMPRIS study was the first randomized trial of this procedure for ICAD. Angioplasty and stenting in this trial was associated with a higher-than-expected rate of perioperative stroke. Reduction or prevention of these complications will be required for this procedure to be proven safe and effective. The purpose of this study was to perform a detailed, post hoc review of all complications that occurred in the stenting arm, in an effort to categorize and attribute the mechanism of stroke for each patient.
The most frequent types of stroke observed in the SAMMPRIS trial were local perforator ischemic strokes (n = 12), primary intraparenchymal hemorrhage (n = 7), and subarachnoid hemorrhage (n = 6). Distal symptomatic embolic stroke as an immediate complication of angioplasty and stenting was uncommon.
Local perforator stroke after angioplasty and/or stenting has been described in previous case series. Previous investigators have reported an association of a higher risk of procedural ischemic stroke with posterior vs anterior circulation lesions after angioplasty and stenting.6-9 Jiang and colleagues10 reported a 13% (9/69) 30-day risk for stroke after angioplasty and stenting of symptomatic basilar artery stenoses in a review of outcomes from a large single-institution series. However, this study did not categorize these strokes as either embolic or local perforator. Perforator occlusion by the displaced or disrupted atheromatous debris (snow-plowing) has been postulated as the mechanism for regional perforator stroke after stenting.11 Potential approaches to reduce the risk of this phenomenon may include performing angioplasty alone rather than angioplasty and stenting11 or using high-resolution MR vessel wall imaging for treatment planning or patient selection.2,12,13 Even if the risk of perforator stroke after stenting could be reduced, aggressive risk factor management for patients with evidence of unstable or ruptured plaques adjacent to perforator-rich vessel segments may remain more effective than mechanical intervention.
Parenchymal hemorrhage occurred with a higher-than-expected frequency in comparison with previous case series. In the US Wingspan Registry, Fiorella and colleagues14 reported 5 major events in 78 patients. Two were vessel perforations resulting in death, 1 was an IPH, and 2 were embolic ischemic strokes.9 In the National Institutes of Health wingspan registry, Zaidat and colleagues15 reported 2 IPHs in 129 patients. In SAMMPRIS, Fiorella et al reported that delayed IPH was independently associated with a higher baseline percentage of stenosis as well as the combination of a high procedural ACT (>300 seconds) and a loading dose of clopidogrel. The mechanism of IPH poststenting in SAMMPRIS patients is uncertain, but the relationship between severe stenosis and hemorrhage suggests the possibility of hyperperfusion or autoregulatory dysfunction as a mechanism.16 However, the time course and clinical features are different from the typical hyperperfusion syndrome seen after extracranial carotid revascularization.17
The etiology of the SAHs was clear in most of the cases. These could be attributed to wire perforation in 3 and vessel rupture in 1. The vessel rupture occurred in a patient with a completely occluded segment (interval occlusion between enrollment and the angioplasty procedure) and was a protocol violation. These events were potentially avoidable. The Wingspan system requires several exchanges of catheters over a 300-cm exchange wire. The wire tip may move into small distal branches and perforate for a number of technical reasons. One is lack of attention to detail by the operator. Another is related to inadequate guide catheter support leading to abrupt movement of the system. These complications could potentially be reduced with experience, although no relationship between hemorrhage and physician experience was found in the SAMMPRIS trial.3 These complications may also be reduced with angioplasty alone or angioplasty and stenting with devices that do not require exchanges.
The SAMMPRIS protocol did not include any tests of platelet function. The study policy disallowed resistance testing after randomization to avoid the use of antiplatelet agents or doses that were not specified by the protocol. It is unknown whether the patients with ischemic events were more resistant to aspirin or clopidogrel, or if the patients with hemorrhagic events were less resistant to the antiplatelet regimen.
This retrospective study is subject to a number of limitations, most significantly that of the attribution of stroke mechanism. This process was post hoc, based on review of available images and clinical data, and admittedly inexact. For ischemic stroke, stroke mechanism was based primarily on brain imaging and clinical symptoms. Many of the patients that were categorized as perforator stroke also had distal lesions on diffusion-weighted imaging. Although it is likely that many of these represent emboli from the procedure, the clinical relevance of asymptomatic diffusion-weighted imaging lesions is unclear.18 Parenchymal hemorrhage was separated from subarachnoid hemorrhage based on review of imaging and the timing of the clinical event. It is possible, however, that some of the parenchymal hemorrhages were related to wire perforation.
The most frequent causes of perioperative stroke in the SAMMPRIS trial were perforator-territory ischemic stroke, reperfusion hemorrhage, and SAH. Future trials of intracranial angioplasty and stenting will need to reduce these events to establish the safety and efficacy of this procedure.
The SAMMPRIS trial was funded by a research grant (U01 NS058728) from the US Public Health Service National Institute of Neurological Disorders and Stroke (NINDS). In addition, the following Clinical and Translational Science Awards, funded by the National Institutes of Health, provided local support for the evaluation of patients in the trial: Medical University of South Carolina (UL1RR029882), University of Florida (UL1RR029889), University of Cincinnati (UL1RR029890), and University of California, San Francisco (UL1RR024131). Stryker Neurovascular (formerly Boston Scientific Neurovascular) provided study devices and supplemental funding for third-party device distribution, site monitoring, and study auditing. This research was also supported by the Investigator-Sponsored Study Program of AstraZeneca that donates rosuvastatin (Crestor) to study patients. Drs Fiorella, Derdeyn, Turan, Janis, and Chimowitz, Michael Lynn, MS, and Bethany Lane, RN, serve on the Executive Committee of the SAMMPRIS trial that is funded by the NINDS (grant U01 NS058728). All receive salary support from the SAMMPRIS grant. All other authors were investigators in SAMMPRIS and were reimbursed from the SAMMPRIS grant for their effort. Dr Derdeyn receives grant support from the NINDS (P50 55977; R01 NS051631). He is also on the Scientific Advisory Board for W.L Gore and Associates and is the Chair of the Scientific Advisory Board for Pulse Therapeutics. Dr Fiorella has received institutional research support from Seimens Medical Imaging and Microvention, consulting fees from Codman/Johnson and Johnson, NFocus, W. L. Gore and Associates, and EV3/Covidien, and royalties from Codman/Johnson and Johnson. He has received honoraria from Scientia and has ownership interest in CVSL and Vascular Simulations. M. J. Lynn, MS, receives grant support from the National Eye Institute. He is the principal investigator of the Coordinating Center for Infant Aphakia Treatment Study (EY013287) and a coinvestigator on the Core Grant for Vision Research (EY006360). Dr Cloft has received research support for the SAPPHIRE Carotid Stent registry. B. F. Lane, RN, has received consulting fees from Microvention Terumo. Dr Turan is a past recipient of funding from the American Academy of Neurology (AAN) Foundation Clinical Research Training Fellowship and is the current recipient of a K23 grant from NIH/NINDS (1 K23 NS069668-01A1). She has also served as an expert witness in medical legal cases. Dr Janis is a program director at the NINDS. Dr Chimowitz has received research grants from NINDS to fund the WASID trial (1 R01 NS36643) and to fund other research on intracranial stenosis (1 K24 NS050307 and 1 R01 NS051688). He currently serves on the stroke adjudication committee of an industry-funded osteoporosis drug trial (Merck and Co, Inc) and on the DSMB of another industry-funded patent foramen ovale closure trial (W. L. Gore and Associates) and is compensated for those activities. He has also served as an expert witness in medical legal cases.
See SAMMPRIS Clinical Trial Sites and Principal Investigators, Supplemental Digital Content 1, http://links.lww.com/NEU/A519.
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The authors present a very straightforward analysis of the data acquired for the SAMMPRIS trial. Primarily a descriptive study, this analysis describes with some additional detail the potential etiologies for periprocedural complications in angioplasty and stenting. Interestingly, as previously described, the authors suggest that posterior circulation (in particular, basilar artery) procedures carry the majority of complication risk secondary to vessel perforation, perforator obstruction and hemorrhagic conversion. Thus, this retrospective analysis reiterates the significant risks incurred in posterior circulation atheromatous disease and emphasizes the need for proper patient education with a realistic discussion of risks and benefits to these patients and families. Unfortunately, there is no clear discussion as to potential modifications that should or could be made in techniques or in devices. The authors provide an excellent platform from which to begin the “deep dive” in data analysis of not only their own practice data, but also for future studies that will help practitioners in this field better understand patient selection and complication avoidance for patients with intracranial (specifically posterior circulation) atheromatous disease refractory to medical management.
Charles J. Prestigiacomo
Newark, New Jersey
This review is a detailed description of the strokes (occlusive and hemorrhagic) seen in the treatment cases of the SAMMPRIS Trial. The intent is to describe the events in an individual case format to better understand how these complications may be avoidable in future interventions. It appears that the basilar interventions carry a higher rate of procedural stroke.
The description of ischemic strokes (the majority of which were perforator territory), subarachnoid hemorrhages, and intra-cerebral hemorrhages gives the reader a much better sense of the mechanism and consequences of these events. This will improve our understanding of the risks associated with treatment of intracranial atherosclerotic disease. One hopes that this information will allow us to improve our tools, techniques, and patient selection to reduce the consequences of this intervention.
Sean D. Lavine
New York, New York