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Endocarditis, inflammation of the endocardial surface of the heart, can have numerous etiologies including mechanical irritation, neoplastic, autoimmune, or infectious diseases.14 This chapter will focus on the infectious causes that are typically bacteria, mycobacteria, and fungi. Although the cardiac valves are most commonly involved, the mural endocardium, septal defects, chordae tendineae, and even intracardiac medical equipment (pacemaker/defibrillator leads or septal occluder devices) can also be sites of infection.16 Infectious endocarditis (IE) has an incidence of 3.6/100,000 per year and accounts for 1/1,000 hospital admissions in the United States. There is a 2:1 male to female ratio with current overall in-patient mortality between 11% and 26%, although this figure may be drastically different for the various subsets of IE patients.1,3,7

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The first published description of the valvular cardiac lesions due to IE was over 300 years ago by Lazarus Riverius, while about 200 years ago Jean Baptiste Boulaud defined the anatomy of the endocardium; 150 years ago, the association of preexisting rheumatic valvular damage and bicuspid aortic valves with IE was noted by Sir James Paget.8,9 In 1905 when blood cultures came into clinical practice, the antemortem diagnostic rate for IE was approximately 50%.9 IE has had numerous classification schemes over the last century starting with Sir William Osler who divided IE into “simple” and “malignant” categories based on the length of time from symptom onset to death along with the associated complications. These categories evolved into the following IE classification in the preantibiotic era: (1) acute (onset of symptoms to death <6 weeks, caused by a highly virulent organism capable of infecting a normal heart); (2) subacute (onset of symptoms to death 6 weeks to 3 months, caused by a less virulent organism that infects hearts with preexisting endocardial damage); (3) chronic (>3 months from symptom onset to death, caused by an indolent microbe capable of infecting only abnormal hearts or immunosuppressed patients).9,10 Current classifications include diagnostic status (definite or probable), anatomic site (right- or left-sided cardiac valves), valve type (native or prosthetic), microbe (bacterial or fungal species), and patient population (intravenous [IV] drug abusers [IVDA], elderly, nosocomial infection). Prosthetic valve IE is further divided into early (<2 months after surgery), intermediate (2 months to 1 year), and late (>1 year after surgery) cases; the early cases are typically nosocomial while the intermediate and late cases are community acquired.1012 Another classification that reflects the early description by Osler is simple (infection limited to valve cusps and leaflets) or advanced (deep tissue infection including perivalvular structures, cardiac abscess or pseudoaneurysm formation, and systemic infectious emboli). These various categories of IE differ in incidence, presentation, microbial etiology, and outcome.1,3,10,13

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The disease process of IE and vegetation formation requires multiple steps (see Figure 38-1) starting with endothelial damage from high-velocity jets of blood due to congenital or acquired cardiac abnormalities, or mechanical damage from intracardiac devices or blood-borne debris.1,10 Platelets and fibrin then form a sterile thrombus at the site of endothelial damage; certain disease states, such as malignancy, uremia, and autoimmune diseases, can form sterile cardiac vegetations without overt endothelial damage. The initially ...

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