Time dependency of the acetazolamide effect on cerebral hemodynamics in patients with chronic occlusive cerebral arteries. Early steal phenomenon demonstrated by [15O]H2O positron emission tomography.
OBJECTIVE
The acetazolamide effect is thought to reach a maximum at 10 to 20 minutes after administration. However, we sometimes encountered patients who showed a transient deterioration of ischemic symptoms several minutes after acetazolamide administration. We therefore considered that a steal phenomenon may occur before the acetazolamide effect reaches a maximum. We evaluated the time dependency of the acetazolamide effect on cerebral hemodynamics in patients with severe stenosis or occlusion of the unilateral internal carotid artery.


METHODS
The subjects consisted of 13 patients with severe stenosis or occlusion of the unilateral internal carotid artery. Regional cerebral blood flow was measured at the resting state and at 5 and 20 minutes after the intravenous administration of 1 g acetazolamide by the use of the [15O]H2O bolus-injection method and positron emission tomography. The steal phenomenon was interpreted as positive when the regional cerebral blood flow values decreased by more than 10% after the administration of acetazolamide in more than one region of interest.


RESULTS
A steal phenomenon was observed in 5 of 13 patients at 5 minutes after acetazolamide administration on the occlusive side, whereas it was observed in only 1 patient at 20 minutes. Thus, this phenomenon was observed more frequently in the early phase of the acetazolamide test. It was also observed more frequently in patients with poorly developed collateral circulation.


CONCLUSIONS
Our acetazolamide [15O]H2O positron emission tomography study revealed an early steal phenomenon at 5 minutes after intravenous administration of acetazolamide, which may be a cause of the transient deterioration of ischemic symptoms during the acetazolamide test.
Kuwabara
Y
Y
Department of Radiology, Faculty of Medicine, Kyushu University, Fukuoka, Japan.
Ichiya
Y
Y
Sasaki
M
M
Yoshida
T
T
Masuda
K
K
D000086:Acetazolamide / Q000008:administration & dosage / Q000627:therapeutic use*; D000368:Aged; D001157:Arterial Occlusive Diseases / Q000000981:diagnostic imaging / Q000188:drug therapy* / Q000503:physiopathology; D001794:Blood Pressure; D002545:Brain Ischemia / Q000188:drug therapy / Q000503:physiopathology; D002343:Carotid Artery, Internal; D016893:Carotid Stenosis / Q000503:physiopathology; D002536:Cerebral Arteries / Q000000981:diagnostic imaging / Q000187:drug effects*; D002544:Cerebral Infarction / Q000188:drug therapy / Q000503:physiopathology; D002560:Cerebrovascular Circulation / Q000187:drug effects*; D002561:Cerebrovascular Disorders / Q000000981:diagnostic imaging / Q000188:drug therapy* / Q000503:physiopathology; D002908:Chronic Disease; D003097:Collateral Circulation; D005260:Female; D006439:Hemodynamics / Q000187:drug effects; D006801:Humans; D008297:Male; D008875:Middle Aged; D010104:Oxygen Radioisotopes; D013997:Time Factors; D014055:Tomography, Emission-Computed; D014665:Vasodilator Agents / Q000008:administration & dosage / Q000627:therapeutic use*; D014867:Water
D010104:Oxygen Radioisotopes; D014665:Vasodilator Agents; D014867:Water; D000086:Acetazolamide