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感染性心内膜炎的病理生理学。

Pathophysiology of infective endocarditis.

机构信息

Department of Internal Medicine, University of Manitoba, Winnipeg, Canada.

出版信息

Curr Infect Dis Rep. 2013 Aug;15(4):342-6. doi: 10.1007/s11908-013-0346-0.

Abstract

Infective endocarditis (IE) is an uncommon infection, occurring as a complication in varying percentages of bacteremic episodes. The ability of an organism to cause endocarditis is the result of an interplay between the predisposing structural abnormalities of the cardiac valve for bacterial adherence, the adhesion of circulating bacteria to the valvular surface, and the ability of the adherent bacteria to survive on the surface and propagate as vegetation or systemic emboli. Certain bacteria, if present in the bloodstream, may colonize the initially sterile vegetation composed of fibrin and platelets; bacterial growth enlarges the vegetation, further impeding blood flow and inciting inflammation that involves the vegetation and adjacent endothelium. The true incidence of endocarditis complicating each of the bacterial species causing IE is difficult to estimate. About 20 %-30 % of individuals with community-acquired staphylococcal bacteremia develop IE [1, 2].

摘要

感染性心内膜炎(IE)是一种罕见的感染,作为菌血症发作的各种百分比的并发症发生。生物体引起心内膜炎的能力是心脏瓣膜发生细菌黏附的易感性结构异常、循环细菌黏附在瓣膜表面以及黏附细菌在表面存活和繁殖为菌丛或全身栓塞的能力之间相互作用的结果。某些细菌如果存在于血液中,可能会定植在最初由纤维蛋白和血小板组成的无菌菌丛中;细菌生长会使菌丛增大,进一步阻碍血流并引发炎症,涉及菌丛和相邻的内皮。很难估计每种引起 IE 的细菌引起的心内膜炎并发症的真正发生率。约 20%-30%的社区获得性葡萄球菌菌血症患者发生 IE[1,2]。

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