Update on Infective Endocarditis

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Abstract

With infective endocarditis afflicting 15,000 patients each year and with a mortality rate that still hovers at almost 40%, the disease remains a very serious health problem. Surprisingly, the incidence has not declined over the last 30 years, and now with more health care interventions, such as pacer/defibrillators, and an increasingly elderly population with degenerative valvular heart disease, the number susceptible to endocarditis is actually increasing. Given the weak evidence for endocarditis prophylaxis, there remains a large population at risk.

Much has been learned recently about the pathogenesis of endocarditis, including the role of endothelial damage, platelet adhesion, and microbial adherence to the vegetation or intact valvular tissue. Three-fourths of patients have preexisting structural heart disease. Once infection is manifest, major cardiac complications include congestive heart failure, embolization, mycotic aneurysms, renal dysfunction, and abscess formation. The diagnosis of endocarditis has been enhanced recently by modifications in the Duke criteria to include the use of transesophageal echocardiography and microbial antibody titers. Surgery continues to play an important role, with criteria for emergency, urgent, and early surgery now defined.

The major organisms involved in infective endocarditis include streptococci and staphylococcus (representing 75% or so of all cases). Enterococcal infections account for many of the remaining cases, although small series and case reports suggest almost all organisms that infect humans can be implicated at times. A sizeable number of “culture-negative” cases still occur despite all the improvements in diagnostic methodology.

Recent guidelines for the diagnosis, treatment, and management of infective endocarditis from the American Heart Association are reviewed and the issues surrounding prophylaxis are summarized. International cooperative databases are now being developed that hold promise for a continual reexamination of the epidemiology of this highly aggressive disease and may help provide sorely needed prospective trial data that will enhance our understanding and treatment.

Section snippets

Historical Background and Introduction

Although Sir William Osler’s famed Gulstonian lectures of 18851 are often referred to as one of the earliest descriptions of infective endocarditis, Osler himself was quick to recognize the contribution of many previous investigators. The earliest description of the vegetative lesions of endocarditis has been attributed to Lazarus Riverius (1589-1655)2; later, Giovanni Lancisi (1654-1720) provided a more complete description of these pathologic lesions of the heart in “De Subitaneis Mortibus”

Epidemiology

The incidence of infective endocarditis (IE) is difficult to estimate because true population characteristics, including both cases and total population at risk, are difficult to obtain. Over the past 10 years, several well-designed epidemiologic studies have provided both data on the incidence of endocarditis and insight into populations at risk. In an urban setting, Hogevik and colleagues conducted an epidemiologic study of IE in Goteborg, Sweden from 1984 to 1988 and found, after adjusting

Pathogenesis of Endocarditis

The endothelial lining of the heart and valves is generally resistant to bacterial or fungal infection. A few highly virulent organisms are capable of infecting apparently normal heart valves, but this is the exception. The interactions that finally result in endocarditis involve a complex interaction between the host and the invading microorganisms that includes the vascular endothelium, the host immune system, hemostatic mechanisms, cardiac anatomical characteristics, the surface properties

Pathophysiology of Endocarditis

About three-fourths of all patients with endocarditis have a preexisting structural abnormality of the cardiac valve involved.25 While rheumatic disease was the most common lesion in the early 1900s, mitral prolapse is now reported in about a quarter of the cases.26 Aortic valve disease (either stenosis or regurgitation or both) appears to account for anywhere from 12 to 30% of cases,27 with from 10 to 20% of patients with endocarditis having preexisting congenital heart disease.

Endocarditis

Complications of Endocarditis

Despite improvements in our diagnostic tests and antibiotics, the incidence of complications in patients with endocarditis has not changed much over the last few decades.32 Table 1 provides a “ballpark estimate” of the incidence of clinical complications in the modern-day era.22

The Diagnosis of Infective Endocarditis

Historically, infective endocarditis has been defined as an infection of the valves and chordae within the cardiac chambers. In recent years this definition has been expanded to include an infection on any structure within the heart including normal endothelial surfaces (eg, myocardium and valvular structures), prosthetic heart valves (eg, mechanical, bioprosthetic, homografts, and autografts), and implanted devices (eg, pacemakers, implantable cardioverter defibrillators, and ventricular

General Approach to the Patient

A general approach to the evaluation and treatment of uncomplicated IE is outlined in Table 5. Most patients with IE become afebrile within several days of the initiation of antimicrobial therapy. Prolonged fever or recurrence of fever needs further evaluation. Some patients with S. aureus may remain febrile, though, for up to 2 weeks. When fever recurs, there should be concern that the antibiotics are ineffective, that there is an abscess or other infection somewhere that is not being

When to Operate in Infective Endocarditis

Based on the observation by Hasbun et al,68 medical therapy alone may be associated with an increase in mortality at 6 months compared to surgery. Vikram and colleagues78 used the same data to determine whether valve surgery reduced mortality in adults with complicated, left-sided, IE. In this study, propensity modeling was used to create a matched case-control study. The authors found that valve surgery was strongly associated with improved survival (OR 0.40, 95% CI 0.18 to 0.91) at 6 months

Streptococci

Streptococci and staphylococci account for 80 to 90% of IE cases in which identification is made. The streptococci have traditionally been the most common cause of IE,83 and many community hospitals still report viridans streptococci as the most common isolates among patients with IE.84 However, staphylococci have assumed increasing importance among isolates in community hospitals in recent years.85 Viridans streptococci remain the major cause of IE in children; IE in young women with isolated

Antimicrobial Treatment

While decisions regarding specific antibiotic therapy for patients with IE are always individualized, certain general therapeutic principles provide the framework for the current recommendations for treatment of endocarditis: (1) complete eradication takes weeks to achieve; (2) the infection exists in a sequestered area of impaired host defense; (3) the bacteria in valvular vegetations may exist in a state of reduced metabolic activity and cell division,155 rendering them less susceptible to

Prophylaxis and Prevention

Although definitive prophylaxis against IE is a challenging goal for patients at risk for its development, it remains an integral aspect of medical care. It is also an area of controversy because of the lack of evidence from well-designed human trials regarding its efficacy. However, it is generally accepted that certain groups of patients are at an increased risk for the acquisition of IE224: (1) High-risk group: prosthetic cardiac valves (eg, bioprosthetic xenograft, homograft, and mechanical

How to Study a Rare Disease

Definitive studies of IE have been difficult to perform due to the low incidence of disease, a limitation that is compounded by the heterogeneous nature of the populations at risk, variable underlying risk factors, and a wide array of infecting organisms. Out of necessity, most studies are derived from case reports or series of cases collected at a single clinical site. There have been few case-control studies or large prospective cohort studies, and even fewer randomized controlled trials.

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    The authors have no conflict of interests to disclose.

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