CEREBRAL BLOOD-FLOW RESERVE ASSESSMENT IN SYMPTOMATIC VERSUS ASYMPTOMATIC HIGH-GRADE INTERNAL CAROTID-ARTERY STENOSIS

Background and Purpose Thromboembolic stroke is likely to occur in pat ients with a restricted cerebral blood flow reserve. Our aims were to determine (1) whether symptomatic patients had any significant hemodyn amic restriction ipsilateral to carotid occlusive disease compared wit h patients whose carotid stenosis is asymptomatic and (2) whether pati ents with carotid occlusive disease have impaired cerebral perfusion r eserve compared with control subjects. Methods We compared cerebral bl ood flow and collateral capacity using the Xe-133 inhalation method an d acetazolamide test in symptomatic (n=10) and asymptomatic (n=10) pat ients who had a high-grade internal carotid artery stenosis (range, 70 % to 99%). Results were compared with those from 10 healthy control su bjects. Results Mean baseline cerebral blood flow was 40.29+/-1.38 mL/ 100 g per minute on the symptomatic side in symptomatic patients versu s 45.20+/-2.53 mL/100 g per minute on the lesion side in asymptomatic patients (control subjects, 46.91+/-2.11 mL/100 g per minute in the ri ght hemisphere versus 46.17+/-1.93 mL/100 g per minute in the left). T here was no statistical difference between patients in symptomatic and asymptomatic groups versus control subjects (P>.10). Mean cerebral bl ood flow increase after acetazolamide was in the same range in symptom atic (52.89+/-2.54 mL/100 g per minute) and asymptomatic (56.22+/-3.35 mL/100 g per minute) patients (P>.10), and no difference was observed regarding control subjects (54.25+/-2.94 mL/100 g per minute; P>.10). Three asymptomatic and two symptomatic patients and three control sub jects had no significant cerebral blood flow increase after acetazolam ide. Conclusions An additional hemodynamic factor in thromboembolic is chemia related to severe unilateral carotid stenosis might be an unusu al finding in patients without apparent hemodynamic induction of sympt oms. The lack of significant variation in postacetazolamide cerebral b lood flow in some patients and control subjects implies that this proc edure may be inconsistent in assessing the cerebral perfusion reserve in the individual case.