Elsevier

Atherosclerosis

Volume 147, Issue 1, November 1999, Pages 49-53
Atherosclerosis

C-reactive protein (CRP) in cerebro-vascular events

https://doi.org/10.1016/S0021-9150(99)00162-8Get rights and content

Abstract

Background and purpose: C-reactive protein (CRP) is a useful prognostic factor in coronary heart disease. It has not been previously studied in acute cerebro-vascular events, which was the topic of the present study. Methods: Patients admitted to the hospital for an acute cerebro-vascular event were prospectively investigated. C-reactive protein was determined nephelometrically. Infection or inflammation were excluded clinically and with an erythrocyte sedimentation rate <30 mm/h. Computed tomography or nuclear magnetic resonance imaging of the brain was performed. Results: According to initial brain imaging and the clinical course the 138 patients were divided into five groups: 20 with transient ischemic attack, 20 with reversible neurological deficit lasting less than 2 weeks, 61 with completed stroke and restitution, 16 with stroke without restitution and 21 with cerebral hemorrhage. Median CRP values (range) were 3.2 (2.4–13.5), 3.3 (2.4–39.4), 4.2 (2.4–73.4), 3.4 (3.2–44.0) and 3.5 (2.4–104.0 mg/l), respectively with no significant differences between groups in a non-parametric test (Kruskal–Wallis). Risk factors for vascular disease in general and stroke in particular had no visible influence on CRP levels. No relationship was found between time interval since onset of symptoms and CRP measurement, suggesting that an acute cerebro-vascular event has little influence on CRP values. Conclusion: CRP is not a useful marker to predict the outcome of an acute cerebro-vascular event on hospital admission. This is in contrast to acute coronary events.

Introduction

In recent years it has become evident that an inflammatory process is involved in atherosclerosis. Coronary heart disease was found to be associated with chronic dental infections [1], helicobacter pylori and chlamydia pneumonia infections [2], [3], [4], [5], [6], [7], [8]; atherosclerosis of the carotid artery with chlamydia pneumonia and cytomegalovirus infections [9]. Atherosclerotic lesions show activation and proliferation of macrophages, cytokines and growth factors are produced, the complement system is activated and oxidized LDL, a proinflammatory modulator, is deposited [10], [11], [12]. Cytokines in turn, e.g. interleukin-6, induce an acute phase reaction, i.e. the production of acute phase proteins in the liver. The prototype acute phase protein is C-reactive protein (CRP). The physiological role of CRP is not fully understood. It has stimulatory functions such as complement activation [13] and induction of tissue factor synthesis in monocytes [14] as well as inhibitory effects, e.g. a reduction in neutrophil adhesion to the vessel wall [15].Recently the role of CRP in coronary heart disease has drawn much attention. In patients with chest pain an increased CRP value is a sensitive indicator of unstable angina and poor prognosis [13], [16], [17], [18], [19], [20], [21], [22], [23]. These elevated CRP values are not caused by the myocardial ischemia, but by the atherosclerotic process, since ischemia of vasospastic origin in variant angina of a similar degree is not associated with elevated CRP values [16].

Atherosclerosis of the carotid arteries was also found to be associated with CRP [19], [24]. However, CRP levels have not been measured in acute cerebro-vascular events so far. The aim of the present study was to measure CRP during acute cerebro-vascular events, to evaluate the role of inflammation and hence acute phase reaction in these conditions and to test the hypothesis that CRP might be a useful prognostic factor in stroke [24] as seen in unstable angina pectoris [16], [17].

Section snippets

Patients and methods

Patients with acute cerebro-vascular events admitted to the hospital were prospectively enrolled. At the time of hospital admission the medical history was taken (including the time interval between onset of symptoms and hospital admission) and a complete physical examination with special focus on neurological signs was performed. All patients underwent a computed tomography or a nuclear magnetic resonance imaging of the brain. Duplex ultrasonography of the extracranial carotid arteries was

Results

The final examination was on a total of 138 patients. Their age was 68.0±13.5 years (mean±S.D.). The group distribution was as follows: 20 patients (14.5%) became asymptomatic within 24 h (TIA); 20 patients (14.5%) had reversible ischemic neurological deficits resolving within 2 weeks (RIND); the majority, namely 61 patients (44.2%), improved partially over time (ischemic stroke with partial restitution); 16 patients (11.6%) had stroke without restitution or progressive stroke; and 21 patients

Discussion

The main topic of this work was to answer the question if CRP measured on admission for acute cerebro-vascular events would allow at least some prediction about the further development of the event, e.g. if a TIA without neurological sequelae or severe stroke with persistent disability was to be expected, which would have a clinical impact. The answer is no. There is a large scatter of the data and no significant relation between the CRP value and the severity of the clinical condition.

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