| |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
(Stroke. 2005;36:268.)
© 2005 American Heart Association, Inc.
Original Contributions |
Department of Neurology, Helsinki University Central Hospital, Neuroscience Program Biomedicum Helsinki, Helsinki, Finland
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
Elevated blood pressure (BP) in the typical presentation of stroke belongs to those few physiological variables that a physician truly has the power of controlling. Association of early elevated BP with poor outcome in observational studies1,2 has motivated some to recommend moderate BP reduction to improve outcome. Interventional randomized controlled studies focused on BP reduction have not been conducted, which would be necessary to prove a causal relationship between early BP elevation and unfavorable outcome. The nature of this relationship has been debated over decades,35 but surprisingly few randomized controlled studies have since been conducted with agents that reduce BP.
Cerebral blood flow in the human ischemic brain is passively dependent on the mean arterial pressure, because autoregulation is defective.6 Therefore, low BP or abrupt decreases in it are hazardous and risk enlargement of the initial infarction. Elevated BP, on the other hand, effects to maintain cerebral blood perfusion. This leads us to the 2 fundamental pathophysiological dogmas in considering therapeutics of acutely elevated BP. First, poststroke hypertension may be deleterious by facilitating edema and hemorrhage formation in the ischemic tissue where blood-brain barrier is damaged. Secondly, antihypertensive drugs may reduce the pressure-dependent cerebral blood flow in the ischemic penumbra with poor autoregulation.
The central question is, why does BP initially rise in the acute stroke? Hospitalization with paralysis is obviously a tremendous stress and has been viewed to explain BP elevation.7 However, because BP has been found to be elevated already during the first minutes after the onset of
Related Article:
Stroke 2005 36: 264-268.
This article has been cited by other articles:
![]() |
E. S. Prakash, Madanmohan, and P. J. Lindsberg What Causes the Acute Blood Pressure Elevation After Stroke? * Response: Stroke, October 1, 2005; 36(10): 2066 - 2066. [Full Text] [PDF] |
||||
|
Stroke Home | Subscriptions | Archives | Feedback | Authors | Help | AHA Journals Home | Search Copyright © 2005 American Heart Association, Inc. All rights reserved. Unauthorized use prohibited. |