Native and Prosthetic Valve Endocarditis

Pathology

Two conditions must be present for the development of almost all cases of NVE: endocardial injury causing a disruption of the valvular endocardial surface, and subsequent infiltration of the injured site by bloodborne microorganisms, typically bacteria. Endocardial trauma results from degenerative calcific changes, rheumatic disease, mitral valve prolapse, regurgitant jet flow, congenital abnormalities (e.g., bicuspid aortic valve), or iatrogenic causes (e.g., cardiac catheterization). Endocardial injury results in the deposition of platelet-fibrin products, which then serve as a nidus for the attachment of microorganisms. Organisms that cause NVE enter the bloodstream through compromise of the skin, mucosal surfaces, or other sites of focal infection. Common causes for bacteremia or fungemia that predispose to NVE include intravenous drug use, indwelling catheters, debilitated condition, medical procedures, and even simple events such as tooth brushing and mastication.

In all cases of NVE, complications and symptoms of the infection may be divided into two categories. Systemic manifestations of the disease result from sepsis and embolic phenomena, such as stroke, kidney failure, or fever. In addition, there are sequelae that are the direct results of infection and the location of the infection with respect to any critical myocardial anatomy.

In native aortic valve endocarditis, infection may spread into the aortic annulus, destroy the aortic valve, or result in paravalvular abscess formation. Conduction system pathology may result, including heart block, depending on the extent of the infection. Other complications include cardiac fistulas, coronary and systemic embolization of vegetations, stroke, cerebral infarction, and mycotic aneurysms. Large aortic valve vegetations can prolapse into the left ventricular cavity, contact the anterior leaflet of the mitral valve, and cause subsequent double-valve endocarditis. Typically, aortic insufficiency results from aortic valve endocarditis. Untreated cases can lead to destruction of the fibrous trigones and the tissue between the anterior mitral leaflet and the aorta. Heart failure may occur because of volume overload secondary to aortic insufficiency. Fistulas between the aorta and right atrium are also possible.

The most common site of vegetations in native mitral valve endocarditis is the mitral valve leaflet near the annulus on the atrial side. Vegetations may be located anywhere on the leaflets or the chordae, and they may occur on the ventricular side as well. Vegetations and debris may destroy part of the ventricular tissue. Complications include invasion into the atrioventricular (AV) groove proper and abscess formation, with severe cases leading to separation at the AV junction and complete destruction of the fibrous skeleton surrounding the valve.

Native tricuspid valve endocarditis usually affects the free margins of the leaflets with relatively infrequent involvement of the annular tissue. Complications of tricuspid NVE include cardiac and pulmonary sequelae as a consequence of valve destruction and embolism. Tricuspid regurgitation with chamber dilation and right heart failure can result, and local extension can cause abscess and fistula formation. Septic pulmonary emboli lead to pulmonary infarction, pulmonary abscess, empyema, and, in rare cases, mycotic aneurysms of the pulmonary arteries.

Microbiology

Endocarditis is caused principally by staphylococci and streptococci. The most common agents are Staphylococcus aureus (32%), viridans group streptococci (18%), enterococci (11%), coagulase-negative staphylococci (11%), and Streptococcus bovis (7%). Gram-negative bacteria can also cause NVE and are classified into either the HACEK group (fastidious gram-negative bacilli, including Haemophilus aphrophilus, Actinobacillus actinomycetemcomitans, Cardiobacterium hominis, Eikenella corrodens, and Kingella kingae ) or non-HACEK group, with each accounting for approximately 2% of all cases. These organisms require a prolonged incubation period before growth and are often resistant to many antibiotics. Fungal NVE, usually caused by Candida albicans or Aspergillus fumigatus, is rare but can lead to devastating complications.

The microbiology of NVE differs somewhat depending on specific individual risk factors and demographics. For example, viridans group streptococci is more prevalent in community-acquired endocarditis, whereas the more virulent S. aureus is more common in nosocomial cases. NVE of the right heart is predominantly a disease of intravenous drug users, and in this population native tricuspid valve endocarditis caused by S. aureus is the predominant form of the disease.

Approximately 2% to 7% of NVE cases are deemed “culture-negative endocarditis” when no microorganisms can be cultured from the blood or tissue samples. This occurs more frequently in developing countries, where fastidious or rare organisms are more likely to cause human infection. The most common reasons for culture-negative endocarditis in developed countries are administration of antimicrobial agents before cultures are taken, inadequate microbiological techniques, and infection with highly fastidious bacteria or nonbacterial pathogens (e.g., fungi). In all cases of culture-negative NVE, it is important to ascertain the absence of any underlying undiscovered infection and to initiate aggressive empiric treatment despite the negative culture data.

Diagnosis