Morrish et al (1) incorrectly state there has been no report to date in the literature regarding the incidence of postprocedural intracerebral hemorrhage after extracranial carotid artery angioplasty and stent placement. Authors working at the University of California, San Francisco, were the first to publish a series report examining the incidence of intracranial hemorrhage and cerebral hyperperfusion syndrome after craniocervical stent placement (2). In our series of 140 patients, the incidence of intracranial hemorrhage was only 1.4% compared with 4.4% in the current report. Moreover, we encountered 0% mortality, whereas the current authors report a rate of 3.3%. We also reported on patients with clinical or radiologic manifestations of cerebral hyperperfusion syndrome without intracerebral hemorrhage, something the current authors did not attempt. Indeed, we observed the major contribution to the 5% incidence of cerebral hyperperfusion syndrome were these cases.
Although it is true that the incidence of intracranial hemorrhage after surgical carotid endarterectomy is approximately 0.6%, Morrish and colleagues fail to indicate that reports examining the incidence of cerebral hyperperfusion syndrome by means of perioperative transcranial Doppler studies have reported rates of up to 9% (3, 4). Because the clinical findings in cerebral hyperperfusion syndrome may be subtle, and ancillary investigations examining postprocedural cerebral blood flow such as brain perfusion CT, nuclear medicine single-photon emission CT, xenon CT, and transcranial Doppler sonography are not often performed, one may expect a significant reporting bias that can skew the published data. We would be interested to know if any of these patients had postprocedural headaches before their hemorrhage, particularly if severe and unilateral; something the authors have not mentioned. Furthermore, what was the preprocedural status of the collateral flow pathways in the patients with intracranial hemorrhage? Although the authors mention in their Discussion that this represents a risk factor for the development of cerebral hyperperfusion syndrome, they have only provided data on the patency of the contralateral carotid artery.
Finally, in any such report, it should be clearly elucidated if the technique in any of these procedures involved placing a guidewire either deliberately or inadvertently intracranially, particularly as multiple centers were involved. The authors have stated this in the legend accompanying the Figure illustrating findings in patient 4, but they have not done so for the other three patients.
References
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