Donate Help Contact The AHA Sign In Home
American Heart Association
Circulation
Search: search_blue_button Advanced Search
Circulation. 2007;115:2907-2908
doi: 10.1161/CIRCULATIONAHA.107.707976
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
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 arrowRequest Permissions
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Messerli, F. H.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Messerli, F. H.
Related Collections
Right arrow Cerebrovascular disease/stroke

(Circulation. 2007;115:2907-2908.)
© 2007 American Heart Association, Inc.


Editorial

Cerebroprotection by Hypertension in Ischemic Stroke

The Crumbling of a Hypothesis

Franz H. Messerli, MD

From St Luke’s–Roosevelt Hospital Center, New York, NY.

Correspondence to Dr Franz H. Messerli, Division of Cardiology, St. Luke’s–Roosevelt Hospital Center, Columbia University, College of Physicians and Surgeons, 1000 Tenth Ave, New York, NY 10019. E-mail fmesserli@aol.com


Key Words: Editorials • blood pressure • cerebral infarction • hypertension • stroke


An extract of the first 250 words of the full text is provided, because this article has no abstract.
 

May not the elevation of systemic blood pressure be a natural response to guarantee a more normal circulation to the heart, brain and kidneys?"1 These words, taken from a renowned textbook of medicine, clearly illustrate that in the 1940s the teaching doctrine was to consider elevated blood pressure a compensatory mechanism serving to force blood through sclerotic arteries to the ischemic target organs. Hypertension was regarded as "essential" and therefore "should not be tampered with, even were it certain that we could control it."2 We have since learned that hypertension is a powerful risk factor for stroke, heart attacks, and renal failure and that lowering blood pressure dramatically reduces the risk of these events. The only clinical situation in which blood pressure elevation often still is considered protective is in the sequence of an acute ischemic stroke. Indeed, authoritative voices such as that of Adams and Victor3 have warned and continue to warn against lowering blood pressure in this setting with statements such as, "We agree with Britton and colleagues that it is prudent to avoid antihypertensive drugs in the first few days unless...the blood pressure is high enough to pose a risk to other organs."3 This statement can be found in the 1989 edition of this venerable neurology textbook and is repeated verbatim in every single subsequent edition until 2005. It thus has taught numerous neurologists that elevated blood pressure in the sequence of an ischemic stroke was a "noli me tangere" and that lowering blood pressure should be . . . [Full Text of this Article]