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感染性心内膜炎时赘生物的形成机制

Author
Daniel J Sexton, MD
Section Editor
Stephen B Calderwood, MD
Deputy Editor
Elinor L Baron, MD, DTMH
Translators
邵一兵, 主任医师

引言

感染性心内膜炎是指心内膜血小板-纤维蛋白附着灶的继发感染并伴赘生物形成；这些赘生物反过来又会直接损害心内膜组织和/或瓣膜。本专题将总结感染性心内膜炎的发病机制。

感染性心内膜炎的其他方面内容，包括赘生物形成的临床结局，将单独讨论。 (参见“感染性心内膜炎的流行病学、危险因素及微生物学”和“人工瓣膜心内膜炎的流行病学、临床表现及诊断”和“静脉药瘾者的感染性心内膜炎”和“儿童感染性心内膜炎”和“成人疑似自体瓣膜心内膜炎的临床表现与评估”和“自体瓣膜心内膜炎的抗菌治疗”和“人工瓣膜心内膜炎的抗生素治疗”和“自体瓣膜心内膜炎的外科手术”和“感染性心内膜炎的并发症与转归”)

发病机制

赘生物形成 — 心脏及心脏瓣膜的内皮层正常情况下能够抵挡细菌和真菌感染。动物模型实验证实，必须经过一系列互相关联的事件，微生物才会在心内膜上形成感染性病灶或赘生物：

●赘生物形成的第一步是心内膜损伤，然后是血小板和纤维蛋白的局灶性附着。一些高毒力的微生物，如金黄色葡萄球菌(Staphylococcus aureus)，能够感染正常的人体心脏瓣膜。

●最初无菌的血小板-纤维蛋白灶受到血液中循环微生物的继发性感染；这些微生物可能来源于远处局灶性感染，也可能来源于黏膜或皮肤感染引起的一过性菌血症[1,2]。

         

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Literature review current through: 2017-06 . | This topic last updated: 2017-07-21.
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