Course of cerebrovascular reactivity in patients with carotid artery occlusions.
OBJECTIVE
Patients with internal carotid artery occlusions and highly impaired cerebrovascular reactivity have been identified as having an increased risk of stroke. It is still unclear, however, whether cerebral hemodynamics may be restored in the course of time by the development of collaterals.


METHODS
During a 5-year period we assessed cerebrovascular reactivity in 452 carotid occlusions by transcranial Doppler CO2 testing. Ninety-eight patients could be reinvestigated at least once after 2 to 58 months (mean follow-up time, 26 months).


RESULTS
On admission, patients with recent transient ischemic attack or stroke (< or = 3 months) as well as patients with contralateral carotid stenoses of 80% diameter reduction or greater and occlusions revealed a significantly higher incidence of impaired CO2 reactivity (P < .0001 and P < .01, respectively). During follow-up, 64% of the patients with no or minor contralateral carotid stenoses, but only 22% of the patients with bilateral carotid occlusions, showed a spontaneous improvement in cerebrovascular reactivity (P < .001), mainly during the first few months. In six of eight patients cerebral hemodynamics on the occluded side improved after endarterectomy of a contralateral high-grade carotid stenosis. Five of the patients who did not undergo surgery developed a stroke during follow-up, with three of them occurring in patients with permanently exhausted cerebrovascular reactivity.


CONCLUSIONS
In the majority of patients with carotid occlusions an initially impaired cerebrovascular reactivity improves spontaneously with time. This could influence therapeutic decisions: During the first few months antihypertensive treatment may be avoided in such cases until a reestablished reactivity can be demonstrated. If cerebral hemodynamics remain depleted, extracranial-intracranial bypass surgery or endarterectomy of an asymptomatic contralateral high-grade carotid stenosis could be helpful.
Widder
B
B
Department of Neurology, University of Ulm, Germany.
Kleiser
B
B
Krapf
H
H
D000368:Aged; D000369:Aged, 80 and over; D001157:Arterial Occlusive Diseases / Q000000981:diagnostic imaging / Q000503:physiopathology*; D001783:Blood Flow Velocity / Q000502:physiology; D002245:Carbon Dioxide; D002340:Carotid Artery Diseases / Q000000981:diagnostic imaging / Q000503:physiopathology*; D002343:Carotid Artery, Internal / Q000000981:diagnostic imaging / Q000503:physiopathology; D002536:Cerebral Arteries / Q000000981:diagnostic imaging / Q000503:physiopathology; D002560:Cerebrovascular Circulation / Q000502:physiology*; D002561:Cerebrovascular Disorders / Q000503:physiopathology; D003097:Collateral Circulation / Q000502:physiology; D003251:Constriction, Pathologic / Q000000981:diagnostic imaging / Q000503:physiopathology; D005260:Female; D005500:Follow-Up Studies; D006439:Hemodynamics / Q000502:physiology; D006801:Humans; D006935:Hypercapnia / Q000503:physiopathology; D016857:Hypocapnia / Q000503:physiopathology; D002546:Ischemic Attack, Transient / Q000503:physiopathology; D008297:Male; D008875:Middle Aged; D017585:Ultrasonography, Doppler, Transcranial; D014711:Vertebral Artery / Q000503:physiopathology
D002245:Carbon Dioxide