Despite all the progress made in antimicrobial therapy, bacterial endocarditis remains a “malignant disease,” as defined by Sir William Osler in the pre-antibiotic era. This is attributable to the difficulty of establishing its diagnosis as a result of its late presentation, the emergence of antibiotic-resistant organisms, and the increasing co-morbidity of affected patients. The term “endocarditis” suggests an infection of the endocardium. Although this condition can be observed in scattered cases, the lesions generally extend the entire thickness of valvular tissue. All cardiac valves can be involved, with in order of decreasing frequency aortic, mitral, tricuspid, and pulmonary valves. The infectious lesions affecting these valves may be destructive or proliferative. Destructive lesions include leaflet perforation, aorto-mitral separation, or chordae rupture. Proliferative lesions include vegetations and abscesses of the annulus or the leaflet tissue.
In recent years, the surgical treatment of bacterial endocarditis has benefited from two major advances: first, the recognition that early surgical intervention is preferable to prolonged preoperative antibiotic therapy, a strategy that actually promotes the extension of valvular lesions; and second, the development of reconstructive techniques that have proven to be feasible and effective in the majority of mitral and tricuspid cases with the advantage of preserving native tissues resilient to ongoing or recurrent infection.
CLINICAL PRESENTATION
Bacterial endocarditis presents with either acute or chronic manifestations. Acute manifestations include sepsis, heart failure, or systemic embolization. Sepsis is manifested by the abrupt onset of fever, chills, neurological disorders, and general signs of systemic toxicity, which may lead to death. The classic subacute form is more indolent with a prolonged history of low-grade fever, arthralgia, myalgia, and splenomegaly. Blood cultures are often negative when the patient has received nonspecific antibiotic therapy. In this setting, the association of preexisting valvular disease and an unexplained fever suggests the diagnosis of endocarditis, particularly in the context of a potential source of bacterial contamination. Modifications of a preexisting murmur or the appearance of a new murmur involving another valve makes the diagnosis even more probable. In the absence of preexisting valve pathology, the discovery of valve regurgitation is also highly suggestive of bacterial endocarditis in an infectious context. The diagnosis of endocarditis is more difficult in the setting of valve regurgitation without any signs of infection. A careful history, however, often finds episodic acute fever following dental care or subsequent to other infections treated by an incomplete course of antibiotic therapy. Whatever the clinical setting, the diagnosis of bacterial endocarditis in patients with the association of a cardiac murmur and acute or chronic fever can be established by two major or by one major and three minor simplified “Duke criterias” ( Table 28-1 ).
Major
|
Minor
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Echocardiography is an essential tool to confirm the diagnosis ( Fig. 28-1 ). In addition to occasional native valve pathology, characteristic lesions such as vegetations, abscesses (a) , leaflet perforations, or extensive chordae rupture (b) can be observed. In the setting of healed endocarditis, the diagnosis is more difficult because the lesions are less characteristic. Vegetations and abscesses are typically replaced by leaflet thickening, scattered calcifications, and leaflet adhesions to the ventricular wall or to the papillary muscles. The diagnosis of healed endocarditis, however, is likely in the presence of commissural prolapse caused by chordae rupture. Regardless of the lesions observed, functional and segmental valve analysis should be performed to guide valve reconstruction ( Table 28-2 ).
| Type | Function | Lesions |
|---|---|---|
| Type I | Normal leaflet motion | Vegetation |
| Leaflet perforation | ||
| Abscess | ||
| Type II | Leaflet prolapse | Chordae rupture |
| Type III | Restricted leaflet motion | Leaflet thickening |
| Leaflet adhesions | ||
| Calcifications |
BACTERIOLOGY
In patients without preexisting valve pathology but who have risk factors such as insulin-dependent diabetes or intravenous drug abuse, the most frequent causative organism is Staphylococcus aureus . During the last decade, however, Staphylococcus epidermidis has assumed an increasing role in patients with underlying degenerative mitral valve disease. In the subacute forms, which typically result from hematogenous seeding of a previously damaged mitral valve, the source of contamination is mostly oral with the various strains of Streptococcus viridans . Enterococci are a possible cause of endocarditis, particularly in patients with colorectal pathology or urinary tract infection. Candida or gram-negative organisms, particularly the HACEK group ( Haemophilus , Actinobacillus , Cardiobacterium , Eikenella , and Kingella ), are also potential, albeit rare, causes of endocarditis. When routine blood cultures remain negative, bacterial investigations should be pursued using special media and prolonged incubation periods.
PATHOLOGY
Aortic Valve Endocarditis
The usual lesions in the acute phase of aortic valve endocarditis include leaflet vegetations, leaflet destruction, and annular abscess. Vegetations, consisting of bacteria, altered polynuclear cells, and fibrin deposits, are indicators of an acute infectious process. They may be adherent or mobile with a sessile or pedicled base of insertion. Vegetations vary in size and rate of growth. Highly virulent organisms such as HACEK, MRSA (methicillinresistant Staphylococcus aureus ), and fungus cause particularly large vegetations that are at high risk for embolization. In the chronic phase, lesions include leaflet perforation, retraction and/or calcification.
Isolated Mitral Valve Endocarditis
Several types of lesions can be observed in mitral valve endocarditis ( Fig. 28-2 ), such as vegetations and leaflet perforation (a) , leaflet and annular abscess (b) , and chordae rupture (c) . Vegetations are commonly localized on the atrial side of the leaflets.
Valvular abscesses are typically seen within the body of a leaflet, most often the anterior leaflet. A leaflet abscess may form a true aneurysm, which is followed by leaflet perforation as the final stage in its evolution. A valvular abscess can also extend to the annulus and/or the aorto-mitral curtain, leading to anterior leaflet partial detachment. Annular abscess is the most deleterious lesion in mitral valve bacterial endocarditis since it can cause a false aneuyrsm of the left atrio-ventricular junction.
Associated Mitral and Aortic Endocarditis
Associated mitral and aortic endocarditis can occur because of the close anatomical relationship between these two valves. The infectious process can start from either the aortic or the mitral valve and extend towards the other. The extension from the aortic valve to the mitral valve may occur from two mechanisms: (1) an aortic annular abscess can extend to the aorto-mitral curtain and anterior leaflet, eventually causing partial or complete detachment from the annulus; (2) the diastolic jet of aortic regurgitation can produce an endothelial lesion on the anterior leaflet of the mitral valve, which then becomes secondarily infected. This so-called “kissing lesion” may occur in up to 10% to 15% of patients with aortic valve endocarditis.
Extension of endocarditis from the mitral valve to the aortic valve may also occur. This may result from direct extension of a mitral annular abscess or present as an isolated satellite lesion. The lesion is usually a small vegetation on the ventricular side of a leaflet that does not result in aortic valve regurgitation. Therefore a systematic analysis of the aortic valve is mandatory in mitral valve endocarditis.
Isolated Tricuspid Valve Endocarditis
Isolated tricuspid valve endocarditis usually occurs in patients who are intravenous drug users or in patients who have catheters or pacemaker leads that extend from the right atrium across the tricuspid valve.
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