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INTRODUCTION

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Mitral valve infective endocarditis (IE) is one of the more devastating complications of mitral valve disease, and if left untreated, it is universally fatal, like any other form of IE. In surgical practice, mitral valve endocarditis is usually less common than aortic valve endocarditis, with most infections occurring in native mitral valves. Although the distribution of causes of mitral valve dysfunction has changed in recent years, the overall incidence of IE has increased during the past 3 decades.1-6 Rheumatic valve disease, which was a frequent predisposing factor to IE in the 1980s, is now rare in industrialized nations.6-7 Predisposing factors more frequently encountered today, several of which are consequences of advances that characterize modern medicine,1-7 include degenerative valvular disease, prosthetic valves, other intravascular prostheses and devices, hemodialysis, nosocomial infections, intravenous drug abuse, and immunosuppression. Repaired valves have a low risk of endocarditis compared with prosthetic valves. (To learn more about the epidemiology of IE, see Chapter 31.)

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More effective antimicrobial agents have improved the early and long-term outcomes of patients treated for endocarditis. However, endocarditis is still associated with high rates of complications, morbidity, and mortality and frequently requires an operation for cure.1-13 Increased experience and advances in surgical techniques have improved the success of these challenging operations.

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PATHOLOGY

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Native Mitral Valve Endocarditis

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Native valve endocarditis (NVE) begins with endocardial injury, which allows deposition of fibrin and platelets with subsequent attachment of bacteria.6,14 Endocardial injury may be secondary to rheumatic valvulitis or other leaflet disease, or valvular or annular calcification. Although vegetations may be seen anywhere on the leaflets or chordae, the usual site at which infective NVE of the mitral valve causes valvular destruction and invasion is the base of the atrial aspect of the mitral valve leaflets. Annular or subanular invasion is more likely to cause atrioventricular (AV) separation when the invasion site is underneath the leaflet and is exposed to high ventricular pressure. Invasion into the AV groove fat with abscess formation is more serious and difficult to radically debride and sterilize (Fig. 38-1).15 Fortunately, mitral annular invasion more often opens toward the atrium and is therefore shallow in most cases; invasion is generally more common and deeper in aortic valve IE.16

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FIGURE 38-1

A case of very advanced invasive mitral valve endocarditis. (A) Transesophageal echocardiogram showing circumferential pericardial effusion with fibrin stranding posteriorly. (B) Severe hemorrhagic pericarditis. Patient was septic and not responding to adequate antibiotic therapy. (C) After peeling fibrinous capsule off heart, these multiple necrotic spots, suggesting abscesses along the AV groove, became apparent. (D) Vegetations were found on the base of P3 scallops of posterior leaflet. (E) After debridement, multiple abscess cavities in the AV groove were seen to communicate with both the left atrium and pericardium. Intact coronary vessels bridge the infected groove. (F) Annulus ...

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