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Infective endocarditis (IE) is a disease caused by microbial infection of the endothelial lining of intracardiac structures and is invariably fatal if untreated. Infection most commonly resides on one or more heart valve leaflets, but may involve mural endocardium, chordal structures, myocardium, and pericardium. The presence of an intracardiac or endovascular device provides a nidus for infection, as well as a barrier to eradication. Despite significant advances in the diagnosis and treatment of IE, 6-month mortality rates still approach 25%.1,2 Changes in both patient demographics and microbial biology have challenged conventional wisdom. Prompt recognition, triggered by a high index of clinical suspicion in susceptible patients, early diagnosis, and aggressive treatment, are the critical components of a successful management strategy. Combined medical and surgical interventions can lead to improved outcomes for selected patients. Patient education, attention to general oral-mucosal hygiene, and the appropriate use of prophylactic antibiotics are the mainstays of prevention.


The earliest description of the vegetative lesion of IE has been attributed to Lazarus Riverius (1589-1655).3 During his tenure as Vatican physician to Pope Clement XI, Giovanni Lancisi (1654-1720) recorded additional observations in De Subitaneis Mortibus (1709).4 Despite these descriptions, it was not until the mid-19th century that a connection was made between vegetative lesions, systemic inflammation (Boulllard, 1841), and embolic phenomena (Virchow, 1847; Kirkes, 1852).5 Sir William Osler made several important advances in the understanding of IE, as summarized in his famed Gulstonian lectures of 1885.6 He defined IE as a primary "mycotic" process and provided the first formal description of two clinical variants of the disease—an acute and fulminating form versus a chronic and insidious form. Despite his extensive knowledge of the disease, Osler was also the first to acknowledge the reality of diagnostic uncertainty in many cases.


In the first half of the 20th century, IE was predominantly a complication of rheumatic heart disease and poor dentition. In developing countries, rheumatic heart disease remains the most frequent predisposing cardiac condition.7 However, the epidemiologic features of IE in developed countries have changed considerably. The aging of the population has been paralleled by increases in the prevalence of degenerative heart valve disease and in the use of implanted heart valve substitutes and intracardiac devices. The numbers of patients with chronic, predisposing medical comorbidities, such as diabetes, HIV infection, and end-stage renal disease, have also increased, as has the commensurate risk of exposure to nosocomial bacteremia, often with antibiotic resistance.8-10 A recent prospective study of 2781 adults with IE found that 25% of cases were associated with recent health care exposure.2 These changing demographics are reflected in two observations: First, the median age of patients with IE has gradually increased from 30 to 40 years in the pre-antibiotic era to 47 to 69 years in the late 20th century.2,11,12 Second, the incidence of IE in developed countries has remained unchanged, despite the dramatic reduction in the incidence of ...

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