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INTRODUCTION AND EPIDEMIOLOGY

Endocarditis patients often have nonspecific signs and symptoms, but endocarditis has the potential for multiorgan involvement. The clinical course of endocarditis can be indolent or fulminant. The majority of endocarditis is infective; diagnosis relies on a set of explicit criteria (see later Tables 156-3 and 156-4 in “Diagnosis” section). Unrecognized endocarditis has frequent complications and high mortality.

In developed countries, the incidence of infective endocarditis ranges from 2 to 11.6 cases per 100,000 patient-years1-7 and is higher in urban settings (likely reflecting the impact of injection drug use). Pediatric endocarditis is uncommon and is primarily associated with structural heart disease, postoperative congenital heart disease, rheumatic heart disease, or catheter-related bacteremia.8 Overall, men are more commonly affected than women, and in-hospital mortality rate ranges from 18% to 32%.1,2,9 Short-term mortality in medically managed endocarditis increases with severe comorbid illnesses, abnormal mental status, congestive heart failure, or a bacterial etiology other than Streptococcus viridans.10

Most cases of endocarditis occur in those with a predisposing structural abnormality (congenital or acquired), prosthetic valve, or a risk factor for disease (e.g., injection drug use, intravascular device, poor dental hygiene, chronic hemodialysis, human immunodeficiency virus infection). Although the mitral valve is the most commonly affected site (followed by the aortic, tricuspid, and pulmonic valves), the incidence of tricuspid valve endocarditis has steadily increased, attributed principally to increased rates of injection drug use.11

For native valve endocarditis in the developed world, mitral valve prolapse is a common predisposing lesion. Other underlying structural factors include congenital defects (e.g., bicuspid aortic valve), degenerative cardiac lesions (calcific aortic stenosis), and rheumatic heart disease. In developing countries, rheumatic heart disease–related valvulopathy remains the leading risk factor.

The estimated risk in injection drug users is 2% to 5% per year, with a mean age of diagnosis of 30 years old. Injection drug use–associated endocarditis often involves the tricuspid valve, has an increased susceptibility to recurrence (approximately 40%), and has increased mortality in human immunodeficiency virus–positive patients with CD4+ count of <200/mm3. Large vegetation size and fungal organism are also associated with poor outcome.12

Indwelling vascular devices create increased risk that microorganisms will attach to valves during bacteremia. Healthcare-associated endocarditis occurs when diagnosis is made >72 hours after admission without evidence of endocarditis on admission, endocarditis develops within 6 months after hospital discharge, or endocarditis develops within 6 months of cardiovascular manipulations including central venous catheter use, arteriovenous fistula for hemodialysis, invasive intravascular techniques, or intracardiac devices such as pacemakers and left ventricular assist devices.13,14

Prosthetic valve endocarditis occurs in 1% to 4% of recipients during the first year following replacement and in approximately 1% per year thereafter. There is no difference in infection risk between mechanical or bioprosthetic valves. Cases with onset within 60 days after surgery are termed ...

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