DEFINITION AND PATHOGENESIS

The term infective endocarditis (IE) denotes an infection of the endothelial surface of the heart. This is usually a valvular surface, but nonvalvular extracardiac endothelium can also be infected.

In the past, IE was classified as acute or subacute, depending on the severity of clinical presentation. Since the advent of antibiotics, classification and therefore therapeutic decisions are based on the bacteriology and the valvular tissue involved, that is, native valve versus prosthetic valve.

The animal model of endocarditis has improved the understanding of the in vivo aspect of the pathogenesis of this disease. Any structural abnormalities that cause turbulent blood flow across a high to low pressure gradient denude epithelium from surfaces impacted on by the turbulence. Such damaged areas (most commonly valvular surfaces) are predisposed to platelet and fibrin deposition and eventually to the formation of sterile vegetation, also known as nonbacterial thrombotic endocarditis (NBTE).

When transient bacteremia occurs after injury to mucosal surfaces in the oropharynx, genitourinary tract, or gastrointestinal tract, organisms are deposited onto the NBTE, where they adhere firmly, multiply, and stimulate further deposition of platelets and fibrin. The infected site is sustained by inaccessibility of the organisms to host defenses. Enlargement of the lesion into a mature vegetation may result in destruction of valves and may cause complications through local bacterial spread or through embolization of fragments of the vegetation.