engleski

Atherosclerosis and Inflamation

Atherosclerosis is a systemic disease characterized by deposits of lipid substances, cholesterol, cellular breakdown products, calcium and fibrin in the inner arterial wall. These deposits are known as plaques. Arterial wall involvement with the atherosclerotic process underlies a majority of stroke cases. There are numerous risk factors for the onset and development of atherosclerosis. Beside classical risk factors such as elevated blood pressure, high plasma lipids, diabetes mellitus, cigarette smoking, and excessive alcohol consumption, inflammation has recently been mentioned as an important factor in the genesis of atherosclerosis. The concept of association between inflammation and atherosclerosis is not a new one, as it was first proposed by William Osler in 1908. Although not accepted then, the role of chronic inflammation in the pathogenesis and progression of atherosclerosis has recently aroused interest. The current model of "response to injury" admits that endothelial damage may be initiated and perpetuated by inflammatory process. In this revival of the inflammatory theory of atherosclerosis, Chlamydia pneumoniae is the agent most frequently discussed, followed by cytomegalovirus and herpes simplex virus. The causative pathogen might exert a direct local inflammatory action on the arterial wall, including endothelial cell damage and/or dysfunction and smooth muscle cell proliferation. 'There may also be some indirect effects caused by chronic infection, circulating endotoxins, activation of inflammatory mediators, autoantibody production, or modifications of risk factors such as lipids, lipoproteins, C-reactive protein, fibrinogen, and other coagulation proteins. Chiamydia pneumoniae is a gram-negative, intracellular bacterium that causes respiratory infections such as sinusitis, pharyngitis and pneu monia. Chlamydia pneumoniae infection usually is subclinical and has a benign course. Epidemics due to Chlamydia pneumoniae occur every 5-7 years on an average, and particular individuals are certainly infected on several occasions, so that 50%-70% of adult population are seropositive for Chlamydia. The association between Chlamydia and atherosclerosis is supported by the association of elevated IgG and IgA antibody titers in patients with myocardial infarction and coronary disease. Antibodies to Chlamydia lipopolysaccharide were found in 68% of patients having suffered myocardial infarction versus only 3% in the control group. Chlamydia pneumoniae and its parts were detected by PCR techruque and immunohistochemical staining in aortic and coronary artery atheromas, but not in normal arteries. Circulating immunocomplexes contairung specific IgG antibodies to Chlamydia were more frequently found in patients with coronary disease and myocardial infarction than in the control group. Patients with carotid atherosclerosis and stroke are frequently seropositive to Chlamydia. Various authors report on positive Chlamydia findings in 17% to 79% samples of the material obtained on carotid endarterectomy. The association of Chlamydia and atherosclerotic lesions has also been confirmed on animal models. The animals infected with Chlamydia had significantly more atherosclerotic lesions. Indirect evidence on the association of Chlamydia and atherosclerosis has been provided by several published studies (in a small number of patients, though) of the effectiveness of macrolide antibiotics in secondary prevention of vascular accidents. Studies on the correlation between Chlamydia pneumoniae eradication with macrolide antibiotics and prevalence of atherosclerotic vascular accidents have just been in course. The causative relationship of inflammation due to Chlamydia pneumoniae cytomegalovirus or herpes simplex virus and atherosclerotic process has not yet been definitely demonstrated. These intracellular microorganisms may simply coincide with the process of atherosclerosis, which also includes an inflammatory reaction induced by arterial wall lesion.

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