Pathophysiology of Infective Endocarditis

Abstract

Infective endocarditis is a life-threatening disease whose pathophysiology is based on unique host-pathogen interaction. Pathogenesis includes pre-existing endocardial lesions or inflammation that leads to endothelial cells and platelets activation, coagulation and thrombus formation. When bacteraemia occur and are repeated, pathogens can adhere to endocardial thrombus thanks to adhesins. After adhesion, the subsequent colonization and invasion of the endocardium maintain both the inflammation and the coagulation processes, resulting in a vicious circle with the formation of infective vegetation in which the pathogens persist, multiply and escape from the host defenses. Consequently, the vegetation will grow and the valve tissue will be destroyed, resulting ultimately in embolic events, abscess formation and valve dysfunction. Moreover, the excessive host response can be responsible to the aggravation of the lesions by secondary autoimmune effects.