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.

 

 

Infective endocarditis is a bacterial infection of the inner lining of the heart muscle (endocardium).1

This inner lining also covers the heart valves, and it is these valves which are primarily affected by infective endocarditis.

I

There are several forms of infective endocarditis. Two types that have similar symptoms but are caused by different bacteria are acute bacterial endocarditis and subacute bacterial endocarditis. Acute bacterial endocarditis may affect normal heart valves, while subacute bacterial endocarditis more commonly affects heart valves which have been previously damaged by disease. A third type of infective endocarditis, prosthetic valvular endocarditis (PVE), may develop in patients who have previously had artificial (prosthetic) valve replacement or tissue valve replacement.

Signs & Symptoms

Infective endocarditis is infection of the endocardial surface of the heart and may involve one or more heart valves, a septal defect or an intracardiac device.

 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.

 

 

 

 

 

 

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Which of the following is accurate about the etiology of infective endocarditis?

Answer Overall, S aureus infection is the most common cause of infective endocarditis, including PVE, acute infective endocarditis, and IVDA infective endocarditis. Approximately 35%-60.5% of staphylococcal bacteremias are complicated by infective endocarditis. More than one half of all cases are not associated with underlying valvular disease.

The mortality rate of S aureus infective endocarditis is 40%-50%. S aureus infection is the second most common cause of nosocomial bloodstream infections, second only to coagulase-negative staphylococci infection.