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(Stroke. 2002;33:2732.)
© 2002 American Heart Association, Inc.
Editorials |
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.24 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
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