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Mitral valve infective endocarditis is one of the more devastating complications of heart valve disease, and, if left untreated, is universally fatal. Although the distribution of causes of mitral valve dysfunction has changed in recent years, the incidence of infective endocarditis has remained constant over the past several decades.1 Underlying rheumatic valvular disease, which was a frequent predisposing factor to infective endocarditis in the 1980s, is now rare in industrialized nations.2 Other predisposing factors more frequently encountered today include intravenous drug abuse, immunosuppression, degenerative valvular disease, intravascular prostheses and devices, hemodialysis catheters, and nosocomial infections. Several of these predisposing factors are consequences of advances that characterize modern medicine.3

Today, more effective antimicrobial agents have improved early and long-term outcomes of patients treated for endocarditis. However, endocarditis is still associated with high rates of morbidity and mortality and frequently requires operation for cure.4 Increased experience and improvements in surgical technique have improved success rates with these challenging operations.

Native Mitral Valve Endocarditis

Native valve endocarditis (NVE) refers to infectious endocarditis involving a patient's own (native) heart valve. Crude incidence of NVE is 6.2 per 100,000 people per year, and is highest in older age groups.5 The pathogenesis of NVE begins with endocardial trauma resulting in alteration of the valvular endocardial surface; this allows deposition of fibrin and platelets with subsequent attachment of bacteria. Endocardial injury may be secondary to rheumatic valvulitis or other leaflet disease, or valvular or annular calcification.5 Common reasons for bacteremia or fungemia predisposing to NVE include use of long-term indwelling catheters, intravenous drug abuse, and fungemia associated with prolonged antibiotic therapy.6,7 Although vegetations may be seen anywhere on the leaflets or the chordae, the usual site at which infective NVE of the mitral valve causes valvular destruction and invasion is at the base of the atrial aspect of the mitral valve leaflets. Annular or subannular invasion may cause separation at the atrioventricular (AV) junction. Fortunately, mitral annular invasion is shallow in most cases. Invasion into the AV groove fat with abscess formation is more serious and necessitates radical debridement. Destruction of the fibrous trigones and intervalvular fibrosa between the anterior mitral valve leaflet and the aorta is usually a consequence of aortic valve endocarditis with secondary mitral involvement. Occasionally “drop lesions” from an infected aortic valve seed the anterior mitral leaflet or the tensor apparatus of the mitral valve, resulting in double-valve endocarditis; the mechanism may be a large vegetation directly infecting the mitral leaflet or a jet lesion that becomes infected.

Prosthetic Mitral Valve Endocarditis

Prosthetic valve endocarditis (PVE) or replacement device endocarditis is infectious endocarditis involving a surgically implanted heart valve. The number of cases of PVE is on the rise as the number of patients with prosthetic heart valves continues to increase. In contradistinction to NVE, wherein the mitral valve is more likely ...

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