Hyperperfusion syndrome following carotid artery stenting: the largest single-operator series to date.

BACKGROUND Cerebral 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. METHODS A 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. RESULTS Seven 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%). CONCLUSIONS The 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.