Chapter 22: Infective Endocarditis

Introduction

General Considerations

Infective endocarditis is one of several infections in which endothelium is the initial site of infection. Healthy endothelium possesses an effective system of defense against both hemostasis and infection. Infection of the endothelium of blood vessels occurs only at sites markedly altered by disease or surgery, such as the severely atherosclerotic aorta or the suture lines of vascular grafts. By contrast, infection of the cardiac valve leaflet endothelium (endocardium) is not rare and occurs even in the absence of identifiable preexisting valve disease.

Pathophysiology & Etiology

A. Cardiac Infection—Vegetations

1. Precursor lesion and bacteremia

Valve infection probably begins when minor trauma, with or without accompanying valve disease, impairs the antihemostatic function of valve endocardium. Infection usually first appears along the coapting surface of the leaflets, suggesting a role for valve opening and closing. This hypothesis is supported by the observation that the ranking of valves in order of frequency of infection corresponds to the ranking of valves according to the force acting to close the valve (mitral > aortic > tricuspid > pulmonic).

This minor trauma may cause the formation of a microscopic thrombus on the leaflet surface. A small noninfected thrombus on the leaflet is called nonbacterial thrombotic endocarditis (NBTE). The next step is infection of the fibrin matrix of the thrombus by blood-borne organisms, which appear briefly in blood under many circumstances, such as toothbrushing, defecating, or other mucus membrane manipulation. When transient bacteremia coincides with the presence of an NBTE lesion, organisms may adhere to the valve leaflet and begin to proliferate.

This theory for the pathogenesis of endocarditis is supported by observations regarding the circumstances under which endocarditis occurs and the particular organisms involved. Patients with endocarditis sometimes tell of a preceding event that likely resulted in transient bacteremia. The common infecting organisms are those that gain entry to the blood because they colonize body surfaces and are adapted for attachment and proliferation in the NBTE lesion (see Clinical Syndromes).

2. Growth of vegetations

Vegetations begin near the coaptation line of the leaflet on the side that contacts the opposite leaflet during valve closure. Mitral valve vegetations are typically attached within 1–2 cm of the leaflet tip on the left atrial side and prolapse into the left atrium during systole. Aortic valve vegetations usually occur on the left ventricular (LV) side of the mid or distal portions of the aortic cusps and prolapse into the LV outflow tract during diastole. A similar distribution of lesions occurs on the tricuspid and pulmonic valves.

Although the course of ...