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C-Reactive protein: a novel and promising marker in ischemic stroke
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Mario Di Napoli, Consultant Neurologist Casa di Cura Villa Pini d'Abruzzo, 66100-Chieti, Italy
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mariodinapoli{at}katamail.com Mario Di Napoli
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To The Editor:
The article by Drs. Rifai and Ridker(1) provides an overview of C-reactive protein (CRP) as a marker of coronary heart disease. Higher CRP levels indicate increased risk of coronary and cerebrovascular events in otherwise healthy individuals and predict worse prognosis in myocardial infarction and stroke. It is not clear whether this reflects a causal relation and, although inflammatory response is an integral part of the atherosclerotic process, we still do not know why.(2)
From this point of view, I refer to the results of my group on CRP in ischemic stroke(3,4)that provided additional evidence that the associations between CRP and coronary heart disease apply to cerebral vascular disease. In patients with first-ever ischemic stroke, plasma CRP increases, and may remain elevated, and is independently associated with increased risk of death and/or new cardiovascular events, including cerebral vascular events. The prognostic significance of CRP value in ischemic stroke could be partly related to extent of the necrosis and partly to unknown individual determinants of the intensity of the acute phase response and reflect inflammation related to the pathobiology of ischemic stroke.(5) The most intriguing question is if CRP levels can predict the extent of necrosis earlier than neuroradiological findings. To shed some light on this point, I reviewed the data of two patients with multiple and very early determinations of CRP during the first 12 hours after stroke with previous known CRP levels and an embolic stroke in the middle cerebral artery. The Canadian Neurological Stroke Scale Scores were equal (3.0) and similar treatments were performed. CRP increased during the first 12 hours after stroke in both patients but this increase was slower in the patient with a successful opening of the infarct- related artery. (Plots of the data for CRP and other relevant tests are available from the author.) A low CRP value within 3 hours of stroke might help to identify patients with a high probability to have an early opening and it could be used in future studies of interventions in ischemic stroke to help refine the choice of the intravenous thrombolytic therapy. At the same time, higher levels could identify patients with unfavorable outcome where thrombolytic treatment is inappropriate and dangerous. Acute stroke intervention is entering its infancy. More ideas, time, effort and trials of agents designed to inhibit coagulation and inflammation raise the hope that there may someday be additional options for the successful treatment of ischemic stroke. CRP could provide a window on the inflammatory response of the individuals and might represent an extraordinary opportunity to afford a solution to current challenges posed in the therapy of acute ischemic stroke.
Mario Di Napoli, MD
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