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Epidemiology, clinical manifestations, and diagnosis of prosthetic valve endocarditis

Adolf W Karchmer, MD
Section Editor
Stephen B Calderwood, MD
Deputy Editor
Elinor L Baron, MD, DTMH


Prosthetic valve endocarditis (PVE) is a serious infection with potentially fatal consequences [1]. (See "Complications and outcome of infective endocarditis", section on 'Outcome'.)

The pathogenesis, epidemiology, microbiology, pathology, clinical manifestations, and diagnosis of PVE will be reviewed here. The antimicrobial and possible surgical treatment and prevention of PVE are discussed separately. (See "Antimicrobial therapy of prosthetic valve endocarditis" and "Surgery for prosthetic valve endocarditis".)


Prosthetic valve endocarditis (PVE) can arise early or late after surgery. The timing of the infection reflects different pathogenic mechanisms that, in turn, influence the epidemiology, microbiology, pathology, and clinical manifestations of the infection.

Early infection — Microorganisms can reach the valve prosthesis by direct contamination intraoperatively or via hematogenous spread during the initial days and weeks after surgery. The organisms have direct access to the prosthesis-annulus interface and to perivalvular tissue along suture pathways because the valve sewing ring, cardiac annulus, and anchoring sutures are not endothelialized early after valve implantation. These structures are coated with host proteins, such as fibronectin and fibrinogen, to which some organisms can adhere and initiate infection.

Late infection — As the sewing ring, sutures, and adjacent tissues become endothelialized over the months following valve replacement, sites for adherence of microorganisms and access to host tissues adjacent to the prosthesis are altered. The pathogenesis of late PVE has been postulated to resemble native valve endocarditis (NVE). (See "Pathogenesis of vegetation formation in infective endocarditis".)

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Literature review current through: Nov 2017. | This topic last updated: Jul 06, 2017.
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