We found that patients who underwent intracranial angioplasty and stenting for symptomatic intracranial stenosis of 50–99% had a significantly higher risk of the primary endpoint (any stroke or death within 30 days of stenting or ischemic stroke in the territory of the stented artery beyond 30 days) if they had a posterior circulation stenosis, were treated at low volume sites, were stented soon after a qualifying event, or had a stroke as the qualifying event rather than a TIA. As seen on the Kaplan-Meier curves, patients with any of these risk factors appeared to have an elevated risk of the primary endpoint beginning within the first week after intracranial stenting.
Several case series have previously reported clinical outcomes in patients who underwent intracranial angioplasty and stenting of the posterior circulation.6,13,15,18,19
In one early case series, any stroke or death within 30 days was reported in 4 of 11 patients treated with a coronary stent.6
A more recent and larger case series from China included 79 patients treated with a coronary or intracranial stent and reported a 30-day stroke or death rate of 4.6%.15
The Stenting of Symptomatic Atherosclerotic Lesions in the Vertebral or Intracranial Arteries study, a multicenter nonrandomized prospective study using the NEUROLINK system, reported a 30-day risk of stroke in 6.6% (4/61) of patients, including three ischemic strokes in the posterior circulation and one subarachnoid hemorrhage.20
Some authors have suggested that there may be an increased risk of perforator strokes associated with stenting of the basilar artery due to compression of plaque into perforator ostia.21
In our patient registry, we found that patients who underwent stenting of their basilar arteries had a trend toward higher rates of the primary endpoint than patients who underwent vertebral artery stenting, although this did not reach significance (basilar artery 30%, vertebral artery 14%; logrank p
Patients treated at low enrollment sites also had significantly higher rates of the primary endpoint than patients treated at high enrollment sites, with the majority (51%) of events at low enrollment sites occurring within 24 hours of the procedure. Mean pre-stenting percent stenosis was higher at low volume sites compared with high volume sites, suggesting that the patients at low volume sites may have been at a higher risk. It is important to note, however, that the number of patients with pre-stenting stenosis of ≥70% was similar between the two groups. Other potential differences in baseline features of patients at low vs high enrolling sites that were not measured in this study could have contributed to the differences in outcomes of these two groups.
Differences in periprocedural adverse events between low and high enrollment sites in our study may represent differences in the procedural experience of interventionalists at the various sites before enrollment in the registry. Interventionalists at high enrollment sites likely performed more intracranial angioplasty and stenting procedures before enrollment in the registry than interventionalists at low enrollment sites. A similar procedural learning curve has previously been demonstrated to influence clinical outcomes in carotid endarterectomy22–24
and carotid stenting25,26
with a decrease in periprocedural complications associated with more procedural experience. If this learning curve is not achieved with stenting for intracranial arterial stenosis, the high rate of periprocedural complications may outweigh any potential benefit of stenting.
Intracranial angioplasty and stenting within 10 days of the qualifying event and stroke as the qualifying event were both found to be risk factors for the primary endpoint with trends toward significance. While angioplasty and stenting soon after a stroke may be associated with poststroke cerebrovascular hemodynamic changes, the trend toward a higher risk of major cerebrovascular complications in stenting soon after the qualifying event persisted even after adjusting for stroke as the qualifying event. It is possible that recent events (stroke or TIA) may be associated with unstable atherosclerotic plaque that increases the risk of stenting. Notably, patients with recent ischemic symptoms and stroke as the qualifying event are also at a high risk of recurrent ischemic events on medical therapy.5
Therefore, optimizing the time of stenting to minimize the risk of stroke should be a focus of research in this area.
Limitations of our study include the lack of central adjudication of events and cerebral angiograms and the lack of prospective follow-up of study patients. Because in-person follow-up was not required and relied on patient self-report, the risk of stroke may have been underestimated. In addition, since the main focus of the registry was to collect preliminary data on the periprocedural complications of intracranial stenting, detailed information on medical comorbidities, the number of intracranial stenting procedures performed by interventionalists at the various sites before inclusion into the registry, and violations of the recommended protocol were not collected. This limits our ability to correlate medical comorbidities, previous stenting experience, and protocol violations with outcome following stenting. Finally, because we did not obtain data on patients treated with stents other than Wingspan, it is possible that low enrollment sites may have performed an equivalent number of stenting procedures utilizing coronary stents and only utilized Wingspan stents for more technically challenging cases, resulting in higher rates of periprocedural complications than high enrollment sites.
Nevertheless, our results suggest that adverse events after intracranial angioplasty and stenting may be associated with posterior circulation stenosis, low volume sites, stenting soon after a qualifying event, and stroke as the qualifying event. These factors will need to be monitored in future trials of intracranial stenting.