Inflammatory Response in Infective Endocarditis

نویسنده

  • E. DEVIRI
چکیده

In 1885 Osler described the clinical course of infective endocarditis (1). Until the introduction of antibiotics the course of the disease was mostly fatal. The introduction of penicillin in 1941 made the disease treatable. However the mortality was considerable, mainly due to heart failure secondary to valve destruction.(2). In 1960 Kay was the first one to report surgical treatment for a valve lesion caused by infective endocarditis(3). In the USA infective endocarditis has an annual incidence of 5-7 cases per 100,000 persons (4). Despite the progress in diagnosis, antimicrobial treatment and surgical techniques, the mortality varies from 5% in uncomplicated cases to 59% in complicated cases (5), and in 2-31% etiologic diagnoses cannot be obtained (6). The pathogenesis of infective endocarditis is not fully understood. The disease involves a complex interaction of bacteria, endocardium and blood components. Heart failure is sometimes out of proportion to the valve incompetence. Bacteria of low virulence can induce severe disease when present in vegetations. Extracardiac manifestations such as renal lesions, arthritis, vasculitis, splenomegaly, splenic infarcts cutaneous and ocular signs cannot be explained alone by the presence of circulating bacteria (7). Understanding the inflammatory response and the interaction between the bacterium, white blood cells, platelets and endothelial cells and the role of various cytokines may explain some of the pathophysiological findings associated with infective endocarditis. In addition, a better understanding of the inflammatory response to infective endocarditis may improve the diagnosis rate (especially in cases of culture negative endocardi), the follow up of the activity of the disease, the treatment, and above all the survival and cure rate.

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تاریخ انتشار 2007