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Infective endocarditis (IE) is uncommon. The yearly incidence reported in developed countries ranges between 1.8 and 6.2 per 100 000 of the population [1–5]. However, these estimates may be imprecise for a variety of reasons. Although it affects neonates [6,7], infants , children [9,10], young adults, and pregnant women , the incidence increases after 30 years of age and exceeds 10 per 100 000 for people aged over 50 years . It is a life-threatening disease with a substantial in-hospital morbidity and mortality (approximately 20%) despite improved techniques to aid diagnosis and modern antibiotics and surgical therapies . One-year mortality approaches 40% . Prosthetic valve endocarditis (PVE), although uncommon (0.1–2.3% per patient year) carries an even higher mortality rate [15–17] and prevention of IE is therefore extremely important .
ETIOLOGY AND PATHOGENESIS
Infective endocarditis predominantly affects individuals with underlying structural cardiac defects who develop bacteremia with microorganisms likely to cause endocarditis .The incidence and risk of IE in such patients following cardiac surgical and interventional procedures has been reviewed in the literature [20,21]. Experimental studies suggest that endothelial damage leads to platelet and fibrin deposition and thus a nonbacterial thrombotic endocardial lesion [22,23]. If bacteremia then occurs, for example as a result of a surgical or dental procedure or instrumentation involving mucosal surfaces contaminated by microorganisms, bacteria settle on the damaged or abnormal heart valves or on the endocardium close to anatomic defects resulting in endocarditis or endarteritis. Valvular and congenital cardiac abnormalities, especially those that result in abnormal high-velocity jets, can damage the endothelial surface and predispose to the formation of a potential site for an infective endocardial lesion [24,25] and the pathologic hallmark of endocarditis— infective vegetations (Figure 1.1), which are composed of masses of organisms enmeshed with fibrin, platelets, and variable inflammatory cell infiltrate (Figures 1.2–1.4) . Thus, in patent ductus arteriosus, vegetations usually occur on the pulmonary artery, at the site where the jet of blood from the aorta hits the pulmonary artery through the ductus. In mitral regurgitation, vegetations occur on the atrial aspect of the mitral valve and in aortic regurgitation on the ventricular aspect of the aortic valve. Progressive, uncontrolled infection leads to intracardiac abscess formation, valvular perforation, destruction, and dehiscence causing regurgitation, fistula, and false aneurysm formation as well as devastating embolic and vasculitic complications.