Compromised cerebral blood flow reactivity is a predictor of stroke in patients with symptomatic carotid artery occlusive disease

• Published in: Journal of vascular surgery 1995-02, Vol.21 (2), p.338-345
• Main Authors: Webster, Marshall W., Makaroun, Michel S., Steed, David L., Smith, Holly A., Johnson, David W., Yonas, Howard
• Format: Article
• Language: English
• Subjects: Acetazolamide - pharmacology; Adult; Aged; Carotid Stenosis - complications; Carotid Stenosis - diagnostic imaging; Carotid Stenosis - physiopathology; Cerebral Arteries - drug effects; Cerebral Arteries - physiopathology; Cerebral Infarction - diagnostic imaging; Cerebral Infarction - etiology; Cerebral Infarction - physiopathology; Cerebrovascular Circulation - drug effects; Cerebrovascular Circulation - physiology; Cerebrovascular Disorders - diagnostic imaging; Cerebrovascular Disorders - etiology; Cerebrovascular Disorders - physiopathology; Disease-Free Survival; Female; Follow-Up Studies; Forecasting; Humans; Male; Middle Aged; Recurrence; Retrospective Studies; Risk Factors; Tomography, X-Ray Computed - methods; Vasodilator Agents - pharmacology; Xenon
• ISSN: 0741-5214; 1097-6809
• DOI: 10.1016/S0741-5214(95)70274-1

Purpose: The purpose of this study was to determine whether the hemodynamic consequences of extracranial carotid disease correlate with the risk of subsequent cerebral infarction. Methods: In 95 patients with symptoms who had greater than or equal to 70% stenosis (31 patients) or who had occlusion (64 patients) of the ipsilateral carotid artery, cerebral blood flow was measured by the stable xenon/computed tomography technique both at baseline and after vasodilatory challenge with intravenous acetazolamide. Patients were stratified into group 1, 43 patients with no more than a 5% decrease in flow in any vascular territory, and group 2, 52 patients with greater than a 5% decrease in one or more vascular territories after an acetazolamide challenge. Results: In group 2, 15 (28.9%) of 52 patients had a new stroke, but only one (2.3%) of 43 patients in group 1 did ( p = 0.0005). Of patients with total carotid occlusion 10 (26%) of 38 in group 2 and none (0%) of 26 in group 1 had a new stroke ( p = 0.003). Of patients with greater than or equal to 70% stenosis, five (36%) of 14 in group 2 and only one (6%) of 17 in group 1 had a stroke ( p = 0.067). Conclusion: The loss of cerebral reactivity in patients with symptoms who had greater than or equal to 70% carotid stenosis or occlusion is an important predictor of impending cerebral infarction. (J V ASC S URG 1995;21:338-45.)