Stroke and Proinflammatory Markers

Abstract

Possible infectious origin of atherosclerosis has received attention because the development of atherosclerotic process cannot always be explained by classical risk factors alone. 1 For instance, hyperlipoproteinaemia is only being detected in half of the patients with coronary heart disease. Inflammation of the vessel wall plays a crucial part in the initiation and progression of the atherosclerotic process, and it is also implicated in erosion, fissuring, or even rupture of the plaque. 2 Chronic infection and the atherosclerotic process have some features in common (eg, activation of lymphocytes and macrophages with enhanced production of cytokines). Increased levels of the biochemical parameters of inflammation can be detected in the bloodstream of some patients, and these levels correlate with the incidence of complications in patients with the acute coronary syndrome. 3 Infections with Chlamydia pneumoniae, cytomegalovirus, and Helicobacter pylori are found in patients with various forms of coronary heart disease. Antibiotic therapy in some studies reduced the risk for relapse of acute myocardial infarction. 4 Few studies focused on parameters of inflammation in patients with stroke. Their short-term and long-term prognosis was correlated with levels of different parameters of inflammation. 5 Nevertheless, markers of inflammation have not been studied yet in patients with stroke in light of possible infectious origin of atherosclerosis. Etiological diagnosis is crucial for therapy of patients with stroke. Some clinical signs (atrial fibrillation demonstrated by ECG and prothrombotic condition demonstrable by echocardiography) are suggestive of the embolic etiology of stroke. The thrombotic etiology is associated mainly with the risk factors for atherosclerosis: diabetes mellitus, smoking, hypertension, and history of atherosclerosis in family. The aim of this study was to find out possible association between the parameters of inflammation and etiology of stroke that could be suggestive of the role of inflammation in the etiology of thrombotic stroke, and at the same time could be helpful in differential diagnosis of the etiology of ischaemic stroke.