Donate Help Contact The AHA Sign In Home
American Heart Association
Stroke
Search: search_blue_button Advanced Search
Stroke. 1997;28:2479-2482

This Article
Right arrow Full Text
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow Request Permissions
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Szabo, S.
Right arrow Articles by Ficzere, A.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Szabo, S.
Right arrow Articles by Ficzere, A.
Right arrowPubmed/NCBI databases
*Compound via MeSH
*Substance via MeSH
Hazardous Substances DB
*ACETAZOLAMIDE
Medline Plus Health Information
*Transient Ischemic Attack

(Stroke. 1997;28:2479-2482.)
© 1997 American Heart Association, Inc.


Articles

Cerebrovascular Reserve Capacity Many Years After Vasospasm Due to Aneurysmal Subarachnoid Hemorrhage

A Transcranial Doppler Study With Acetazolamide Test

Sandor Szabo, MD; Rishi N. Sheth; Laszlo Novak, MD; Laszlo Rozsa, MD, PhD; Andrea Ficzere, MD

From the Departments of Neurosurgery (S.S., L.N., L.R.) and Neurology (A.F.), Medical School University of Debrecen (Hungary).

Background and Purpose Vasospasm in aneurysmal subarachnoid hemorrhage results in proliferative vasculopathy. Systemic hypertension also causes vascular hypertrophy. Both of these histological changes can lead to rigidity of the cerebrovascular system, reducing its autoregulatory capacity.

Methods Blood flow velocity (BFV) in the middle cerebral artery at rest and cerebrovascular reserve capacity (CVRC) (percent rise in BFV after acetazolamide stimulation) measured by means of transcranial Doppler sonography were studied many years after aneurysmal subarachnoid hemorrhage in patients with proven cerebral vasospasm (mean BFV >160 cm/s). The BFV under resting conditions and the CVRC values of the ipsilateral and the contralateral hemispheres were measured in 29 patients (mean age, 43 years; mean follow-up, 4.6 years) and compared with those of control subjects.

Results Persistent high BFV (>120 cm/s) was found in three patients in the peripheral branch of the ipsilateral middle cerebral artery. In the main trunks of the arteries of the anterior circle of Willis, BFV was normal in all cases. CVRC was normal in all patients (ipsilateral, 52±21%; contralateral, 56±17%); values did not differ significantly from each other or from the control value (45±18%). The higher value of CVRC on the contralateral side was found to be statistically significant in selected groups (hypertensive patients and patients with residual infarct on late CT).

Conclusions Proliferative vasculopathy developed at the time of vasospasm must have resolved and did not reduce late vasoreactivity. Comorbidity with hypertension also did not seem to influence the late vasoreactivity toward normalization.


Key Words: acetazolamide • Doppler • subarachnoid hemorrhage • vasospasm