CHAPTER SUMMARY AND CENTRAL ILLUSTRATION
This chapter discusses the pathogenesis and epidemiology of infective endocarditis (IE), as well as the diagnosis and management of patients with this condition (see Fuster and Hurst’s Central Illustration). Cardiac endothelium is normally resistant to infection; endothelial damage, via hemodynamic or mechanical stress, is required for establishment of infection in most cases. The surface of an implanted cardiac device can also be a locus of infection. Bacteria circulating in the bloodstream due to remote infection or transient bacteremia interact with platelets, tissue factors, and endothelium to establish an infective site and form a macroscopic infective mass. Continuous high-grade bacteremia, fragmentation, and direct damage to underlying endocardial tissue and/or valves results. Risk for the development of IE is increased in older adults, persons who inject drugs, individuals with HIV, hemodialysis patients, individuals with cardiovascular implantable electronic devices, and people with prior history of endocarditis. In cases of IE, 6-month mortality is ~25%. Echocardiography should be obtained as soon as possible for any patient with suspected IE. Rapid diagnosis, staging, and careful collaboration between infectious disease, cardiology, and surgical teams to determine the best medical and surgical treatment are important to give the patient their best chance of recovery.
eFig 33-01 Chapter 33: Infective Endocarditis
Infection of intracardiac endothelial surfaces results in infective endocarditis (IE), a dreaded disease with many short- and long-term complications and a stubbornly high mortality that approaches 25% at 6 months.1,2,3 Without treatment, IE is fatal and can wreak havoc with heart valves, chordae, mural surfaces, or deeper myocardium and pericardium. The impact is systemic, with preferential effects on the central nervous system (CNS) and pulmonary systems. Implanted intracardiac devices (ICDs) such as prosthetic valves and rhythm devices amplify vulnerability to infections, which are often complicated and difficult to eradicate. The patient’s best chances for recovery result from rapid diagnosis, staging, and careful collaboration between infectious disease, cardiology, and surgical teams to determine the best medical and surgical treatment.3,4 Prevention of IE in patients at risk hinges on patient education, maintenance of good oral hygiene, and prophylactic antibiotics for a limited spectrum of procedures that may induce bacteremia with organisms known to be associated with endocarditis.
The natural cardiac endothelium is resistant to infection. In animal models of endocarditis, damage to the endothelium is required to establish infections, despite a large inoculum of bacteria.5 In most clinical endocarditis involving native tissues, an injury resulting from hemodynamic or mechanical stresses disrupts the endothelium, exposing underlying collagen and other matrix molecules. Fibrin and platelets adhere to these elements, creating a sterile vegetation. Bacteria circulating in the bloodstream due to remote infection or transient bacteremia may then bind to and replicate in this microthrombus, amplifying the ...