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Infective endocarditis is a disease in which a microorganism colonizes a focus in the heart, producing fever, heart murmur, splenomegaly, embolic manifestations, and bacteremia or fungemia. Early diagnosis of this condition is extremely important because it almost invariably leads to devastating complications and death if not treated with antibiotics, combined or not with surgery. Infective endocarditis is defined as community-acquired or health care–associated infection. The latter can be nosocomial or non–nosocomial health care associated.
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Predisposing factors for infective endocarditis are cardiac abnormalities that disrupt the endocardium by means of a jet injury, as well as the presence of blood-borne microorganisms that colonize these abnormal surfaces. Among patients with aortic valve endocarditis, congenitally bicuspid aortic valve is the most common predisposing lesion.1 Other congenital abnormalities of the aortic valve, degenerative calcific aortic stenosis, aortic insufficiency secondary to connective tissue disorders, and rheumatic aortic valve disease, are also predisposing lesions for infection. Depending on the virulence of the offending microorganism, normal aortic valves can also be affected. Patients with prosthetic heart valves have a constant risk of developing infective endocarditis.
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It is difficult to determine the incidence and prevalence of native aortic valve endocarditis in the general population because this disease is continuously changing.2 The annual incidence of infective endocarditis is estimated to range from 1.7 to 7.0 episodes per 100,000 person-years in North America.3–5
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Patients with prosthetic aortic valves are reported to have an incidence of infective endocarditis of 0.2 to 1.4 episodes per 100 patient-years, which varies with the type of aortic valve.6–12 Approximately 1.4% of patients undergoing aortic valve replacement develop prosthetic valve endocarditis during the first postoperative year.13
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The incidence of nosocomial endocarditis is increasing because more patients undergo invasive procedures. Infective endocarditis in hemodialysis patients is relatively infrequent, but it is associated with high mortality.14 Dental extractions have been demonstrated to produce bacteremia. Dental flossing can produce bacteremia in periodontally healthy and periodontally diseased individuals at a rate comparable with that caused by some dental treatments, for which antibiotic prophylaxis is usually given to prevent endocarditis.15 Endoscopic procedures may also produce bacteremia. Intravenous drug users are particularly susceptible to infective endocarditis, which often occurs in structurally normal heart valves. (Please see Prophylaxis of Infective Endocarditis elsewhere in this chapter.)
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In 1928, Grant and colleagues16 theorized that platelet-fibrin thrombi on the heart valve served as a nidus for bacteria adherence. In 1963, Angrist and Oka17 introduced the term nonbacterial thrombotic endocarditis to describe sterile vegetations on a heart valve and provided experimental animal evidence supporting the role of these vegetations in the pathogenesis of endocarditis. Experimental inoculation in animals with preexisting nonbacterial thrombotic endocarditis produced by mechanical abrasion of the endothelial covering of heart valves causes a prompt leukocytic infiltration of the thrombi.18 As the microorganism multiplies, more leukocytes and thrombotic material accumulate in the area and a verrucous vegetation ...