- Blood cultures positive for bacteria or fungi.
- Cardiac lesions on echocardiography.
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.
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 brushing
one’s teeth. 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 often 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).
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
Although the course of cardiac lesions in endocarditis varies, in a typical sequence of events (without treatment), the infection
progresses by enlargement of the vegetation and extension of its
region of attachment toward the base of the leaflet. Valve regurgitation
almost always develops, as a result of either destruction of the ...