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(Stroke. 2003;34:945.)
© 2003 American Heart Association, Inc.

Original Contributions

Monitoring of Cerebral Vasodilatory Capacity With Transcranial Doppler Carbon Dioxide Inhalation in Patients With Severe Carotid Artery Disease

Randolph S. Marshall, MD; Tanja Rundek, MD; Douglas M. Sproule, AB; Brian-Fred M. Fitzsimmons, MD; Shauna Schwartz, AB Ronald M. Lazar, PhD

From The Neurological Institute, Columbia University College of Physicians and Surgeons, New York, NY.

Correspondence to Randolph S. Marshall, MD, The Neurological Institute, Columbia University, College of Physicians and Surgeons, 710 W 168th St, New York, NY 10032. E-mail rsm2{at}columbia.edu

Background and Purpose— Cerebral vasodilatory capacity (CVC) testing with transcranial Doppler has been shown to be useful in the assessment of stroke risk in patients with symptomatic and asymptomatic internal carotid artery (ICA) stenosis and occlusion, but whether hemodynamic status improves, deteriorates, or remains the same over time is uncertain.

Methods— Thirty-five patients with 80% carotid artery stenosis or complete occlusion underwent CVC testing at baseline and 6 months later. CVC was assessed by measuring the increase in ipsilateral middle cerebral artery mean flow velocity in response to 5% inhaled CO₂. Continuous tracings of left and right middle cerebral artery flow velocity, heart rate, respiratory rate, and PCO₂ were recorded and then analyzed offline. One-way analysis of variance was used to compare baseline CVC in symptomatic and asymptomatic patients with control subjects. A paired t test was used to compare CVC before and after revascularization. Also, ² analysis was used to compare rates of cerebrovascular events in patients with low compared with normal CVC over the 6-month period and in 14 patients whose ICAs were revascularized.

Results— Patients with high-grade stenosis or occlusion of the ICA who had ICA disease had an average CVC of 2.4±1.9%/mm Hg PCO₂; control subjects averaged 4.2±1.1%/mm Hg PCO₂. (P=0.01). In the revascularization group, CVC increased from an average of 1.4±1.7%/mm Hg PCO₂ at baseline to an average of 2.8±1.0%/mm Hg PCO₂ after revascularization, significantly different from the spontaneous change in the natural history group over 6 months (P=0.003). Over the 6-month follow-up period, in the natural history group and in the treatment group after revascularization, 4 ischemic events occurred, all in patients with abnormal CVCs; abnormal CVC was associated with ischemic events (Fisher’s exact test, P=0.03).

Conclusions— In a timeframe pertinent to clinical decision making and clinical trial outcomes, cerebral hemodynamic status may not be constant. A higher ischemic risk may be present in patients with severe carotid artery disease whose CVC is poor at baseline, becomes poor over 6 months, or fails to normalize after revascularization.

Key Words: autoregulation • cerebral blood flow • cerebrovascular reactivity • ultrasonography, Doppler, transcranial

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