Abstract
In the accompanying article, Arenillas and colleagues1 furnish new evidence that a persistently elevated level of CRP after a first cerebrovascular event (ischemic stroke or TIA) is associated with an increased risk of vascular events (both cerebral and cardiac) in a population of patients with documented intracranial large-artery occlusive disease. The evolving concept of using a high-sensitivity CRP assay as a marker of cerebrovascular risk is enticing, and the message suggested by the results of this study is both provocative and in accord with the increasing body of literature rapidly accumulating in the exciting field of stroke preventive medicine. The theory behind this association is fascinating: patients with high-risk lesions may be expected to manifest signs of increased inflammatory activity. Such inflammation appears to occur not only locally (in the affected vessel wall) but also systemically, as suggested by increased circulating levels of CRP. The use of an easily measurable systemic marker of inflammation (such as high-sensitivity CRP) may hold the key for determining which patients with intracranial large-artery occlusive disease are most at risk. In fact, the patients at highest risk manifest evidence of surprisingly widespread inflammatory response. Although the full relation between CRP elevation and cardiovascular risk is not yet completely known, the inflammatory status may be a marker for individuals with an exaggerated inflammatory response that may in turn accelerate atheroma progression and facilitate thrombogenesis. Studying the effect that a general inflammatory marker, such as CRP, has on cerebrovascular risk prediction is far from a simple task. Methodological problems are inherent in design, implementation, and analysis of any such study. The role of elevated high-sensitivity CRP as a risk marker for cardiovascular diseases, including coronary heart disease, …
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