• Hutton P Brantley, Jennifer L Kiessling, Hugh B Milteer, and Farrell O Mendelsohn.
• Baptist Health System, Inc., Birmingham, AL 35211, USA. hbrantley@gmail.com
• J Invasive Cardiol. 2009 Jan 1;21(1):27-30.

BackgroundCerebral hyperperfusion syndrome (HPS) results from autoregulatory failure of cerebral blood flow following carotid endarterectomy (CEA) or carotid artery stenting (CAS) and encompasses a range of neurological findings including headache, seizure, intracranial hemorrhage (ICH), altered mental status and focal neurological changes. This report is the largest single-operator series evaluating the incidence and predictors of HPS following CAS.MethodsA retrospective review was conducted on 482 consecutive patients who underwent CAS between August 1999 and December 2007 at Baptist Medical Center--Princeton, Birmingham, Alabama. All interventions were performed by a single operator (FM). The mean patient age was 70.4 +/- 10.3 years and 36% were symptomatic. All patients were high-risk for CEA. After cerebral protection catheters were routinely available, they were used in all but 6 cases (98.1%) where the anatomy precluded delivery. Brain computed tomography (CT) was performed immediately for any neurological change or significant headache following CAS. After neurological consultation and imaging, HPS was diagnosed if: 1) a neurological change occurred (not simply a headache); 2) CT revealed ipsilateral sulcal effacement/cerebral edema; and 3) stroke or transient ischemic attack (TIA) was excluded.ResultsSeven patients (1.45%) developed HPS following CAS. All patients achieved complete neurological recovery 6-24 hours following the procedure. Patients who developed HPS were significantly more likely to have had recent transient ischemic attack (TIA) symptoms than patients without HPS (p = 0.04). Unlike previous reports, there were no significant differences in procedural details, lesion characteristics and post-procedure blood pressure between the HPS and non-HPS patients, although the number of cases was small. Overall, the HPS cohort had a higher prevalence of comorbidities, though these differences did not reach statistical significance. Hypertension was present in all 7 HPS patients. Other complications in the series were death (0.83%), stroke (1.87%) and TIA (1.45%).ConclusionsThe incidence of HPS is low (1.45%) following CAS, but it is an important complication to distinguish from stroke and TIA. Patients with a recent TIA may be predisposed to HPS. This report may underestimate the incidence of HPS, since patients with an isolated headache did not meet our diagnostic criteria and routine post-procedure brain CT imaging was not performed. The clinical predictors of HPS and its optimum management remain to be determined.

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