C-reactive protein (CRP) in cerebro-vascular 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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