Donate Help Contact The AHA Sign In Home
American Heart Association
Stroke
Search: search_blue_button Advanced Search
Stroke. 2002;33:2732-2733
Published online before print October 31, 2002, doi: 10.1161/01.STR.0000041034.33647.41
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
33/12/2732    most recent
01.STR.0000041034.33647.41v1
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 HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Muir, K. W.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Muir, K. W.
Right arrowPubmed/NCBI databases
*Compound via MeSH
*Substance via MeSH
Hazardous Substances DB
*CHOLESTEROL
Medline Plus Health Information
*Stroke

(Stroke. 2002;33:2732.)
© 2002 American Heart Association, Inc.


Editorials

Inflammation, Blood Pressure, and Stroke: An Opportunity to Target Primary Prevention?

Keith W. Muir, MD, FRCP

From the University Department of Neurology, Institute of Neurological Sciences, Southern General Hospital, Glasgow, Scotland, UK.

Correspondence to Keith W. Muir, MD, MRCP, South Glasgow University Hospital NHS Trust, University Department of Neurology, Institute of Neurological Sciences, 1345 Govan Road, Glasgow G51 4TF, Scotland. E-mail k.muir@clinmed.gla.ac.uk


Key Words: blood pressure • inflammation • prevention • stroke


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

The weight of evidence supporting a link between the inflammatory response and vascular disease has grown considerably in recent years, driven to a large extent by the development of highly sensitive and standardized assays for the acute phase reactant C-reactive protein (CRP), and has led to the current view of atherosclerosis as a systemic inflammatory disease rather than simply a process of intravascular lipid deposition.1 Most evidence hitherto has looked at coronary heart disease and in particular has sought to relate inflammatory markers to existing biochemical risk factors, such as cholesterol and homocysteine.

Case-control studies conducted within several large clinical trials indicate that elevated CRP concentration increases the risk of coronary, and vascular, events, with a relative risk of 1.7 to 4.4, independent of conventional risk factors.2–4 Inflammation interacts with cholesterol concentrations in prediction of coronary events, and adding CRP to conventional lipid measurement may transform the unfavorable economics of primary prevention with statins, with an order of magnitude difference in numbers needed to treat.5 Similar relationships with cytokines, adhesion molecules, or serum amyloid A protein have been found.6 Ischemic stroke has been included as an end point in some of these case-control studies,2 and an independent predictive value of CRP has been confirmed recently in a prospective cohort study of elderly subjects from the Framingham population, with follow-up averaging 13 years.7

In this issue of Stroke, Engström and colleagues report further results from a prospective cohort of 6071 healthy middle-aged men in Malmö, Sweden, followed up for nearly . . . [Full Text of this Article]




This article has been cited by other articles:


Home page
StrokeHome page
M. Di Napoli, M. Schwaninger, R. Cappelli, E. Ceccarelli, G. Di Gianfilippo, C. Donati, H. C.A. Emsley, S. Forconi, S. J. Hopkins, L. Masotti, et al.
Evaluation of C-Reactive Protein Measurement for Assessing the Risk and Prognosis in Ischemic Stroke: A Statement for Health Care Professionals From the CRP Pooling Project Members
Stroke, June 1, 2005; 36(6): 1316 - 1329.
[Abstract] [Full Text] [PDF]