OBJECTIVE:

In 10% of patients undergoing carotid endarterectomy (CEA), the cognitive function declines postoperatively, primarily in association with postoperative cerebral hyperperfusion. In contrast, in the majority of patients undergoing CEA, long-term cognitive outcomes remain unclear. Furthermore, it is not known whether the decline in cognition due to cerebral hyperperfusion recovers on a long-term basis. This study aimed to understand how postoperative cerebral hyperperfusion affects the cognitive outcomes of patients who undergo CEA.

METHODS:

The participants in this prospective observational study were patients with internal carotid artery stenosis who underwent CEA. Cerebral hyperperfusion syndrome or asymptomatic cerebral hyperperfusion following CEA was determined based on brain perfusion SPECT scans and symptomatology before and after surgery. Neuropsychological testing was performed preoperatively, at 1-2 months postoperatively, and at 2 years postoperatively to investigate cognitive decline.

RESULTS:

A logistic regression analysis revealed that asymptomatic cerebral hyperperfusion (95% CI 13.0-84.5, p < 0.0001) and cerebral hyperperfusion syndrome (95% CI 449.7-14,237.4, p < 0.0001) were significantly associated with cognitive decline at 1-2 months postoperatively. The incidence of cognitive decline was significantly decreased at 2 years postoperatively (7%) in comparison to 1-2 months postoperatively (11%) (p = 0.0461). A logistic regression analysis also revealed that asymptomatic cerebral hyperperfusion (95% CI 3.7-36.7, p < 0.0001), cerebral hyperperfusion syndrome (95% CI 128.0-6183.6, p < 0.0001), and further strokes during the 2-year follow-up period (95% CI 1.5-78.7, p = 0.0167) were significantly associated with cognitive decline at 2 years postoperatively. The incidence of cognitive decline at 1-2 months postoperatively was significantly higher in patients with cerebral hyperperfusion syndrome (100%) than in those with asymptomatic cerebral hyperperfusion (44%) (p < 0.0001). No significant difference in incidence was observed in the former patients at 2 years postoperatively (88%), but significant reduction was found in patients with asymptomatic cerebral hyperperfusion and cognitive decline between the timepoints of 1-2 months postoperatively (100%) and 2 years postoperatively (39%) (p = 0.0001).

CONCLUSIONS:

Postoperative cerebral hyperperfusion causes prolonged cognitive decline at 2 years postoperatively in patients undergoing CEA.