Perivalvular Lesions of Infective Endocarditis Table

Extension of the valve infection into surrounding structures predicts a higher mortality, higher risk of significant heart failure, and the need for cardiac surgery [22]. In the early stage, perivalvular abscess is largely composed of inflammatory infiltrate, but at later stages necrosis and cavitation usually develop leading to destruction of perivalvular tissue [33]. Perivalvular abscess is not a static complication but is progressive and can evolve into serious perivalvular complications including perivalvu-lar leak, fistula and pseudoaneurysm. These perivalvular complications may develop in spite of early valve surgery. Perivalvular leak due to annular abscess may be seen with native valve IE

Perivalvular Abscess

(aortic more than mitral), but are especially common adjacent to infected valve prostheses [6]. Although a perivalvular leak may be technically related to poor tissues, suture unraveling, suture tissue cut-through, and other technical matters, it is important to keep the possibility of IE in mind with all perivalvular leaks. These leaks may cause clinically significant congestive heart failure and sometimes hemolysis.

Extension of an active valve infection to adjacent cardiac structures is common, including infected lesions where adjacent valves come in contact or are contiguous—such as from the aortic valve to the base of anterior mitral leaflet, from the posterior leaflet mitral valve to the left atrial endocardium, and from the aortic valve to the ascending aorta [34]. Jet lesions as a result of valvular insufficiency may cause infected endo-cardial lesions to form along the path of the regurgitant jet [9,34].

Infections may also extend from the mitral and aortic valves to the valve annuli (Figure 2.12) [35]. This complication is considerably more common in the aortic position as compared to the mitral. This may manifest as an aortic root abscess, or the mitral annulus or mitral annular calcification (MAC) may become infected. MAC is a common finding in the hearts of elderly patients [36]. It is considered to be an age-related finding, but it probably represents degenerative changes in the mitral annulus [37]. It is associated with mitral valve disease, especially mitral valve prolapse due to myxomatous/floppy

Gross Mitral Valve Prolapse
Figure 2.12. Gross photograph of opened aortic root and aortic valve at autopsy. The aortic valve is destroyed by vegetations (center) and to the right there is a large paravalular aortic root abscess. This root abscess contained infected laminated thrombus material.

mitral valve. Uncommonly the calcium extends onto the leaflet, producing a mass and the calcium may undergo liquefactive necrosis and grossly mimic IE [38-40]. MAC may ulcerate giving rise to thrombus deposition with potential for embolization and infection. If infected, there is usually leaflet perforation and myocar-dial abscess formation (Figure 2.13) [41]. If the infection spreads into the lateral atrioventricu-lar groove, the circumflex coronary artery may thrombose because of distortion from the local effects of the infection, and development of arteritis. Annular abscesses may also erode into to the pericardial surface, producing fibrinous or suppurative pericarditis and hemoperi-cardium with tamponade.

Aortic root abscesses may become a significant source of embolic material and they may compress adjacent structures around the aortic root. If the proximal coronary arteries are distorted, myocardial ischemic sequelae may result. The formation of annular abscess is not an end event. Rather these structures are progressive with potential formation of perforations or fistulas [33]. Due to the central position of the aortic valve, infection of this valve may form fistulas with practically any chamber (Figure 2.14) [42]. Each aortic cusp and sinus has its own pattern or

Fistulas Infective Endocarditis
Figure 2.13. Gross photograph of longitudinal section through the mitral valve, the mitral annulus, and left ventricle. There is mitral annular calcification (MAC) with large abscess formation in the calcific material.

Figure 2.14. Gross photograph of a heart opened to demonstrate the right atrium and tricuspid valve. Aortic valve fungal endocarditis had caused a fistula to the right atrium. This was closed with pledgets but the disease reoccurred. The metal probe is passed from the aortic region and the fistula is still infected and patent.This is the same patient as Figure 2.10 (aortic and mitral valve Aspergillus endocarditis).

Figure 2.14. Gross photograph of a heart opened to demonstrate the right atrium and tricuspid valve. Aortic valve fungal endocarditis had caused a fistula to the right atrium. This was closed with pledgets but the disease reoccurred. The metal probe is passed from the aortic region and the fistula is still infected and patent.This is the same patient as Figure 2.10 (aortic and mitral valve Aspergillus endocarditis).

Endocarditis Fistula

propensity for fistula formation and complication (Figure 2.15). Infection in the left aortic cusp or sinus may spread through the aortic wall and cause pericarditis or tamponade, or a fistula may extend into the left atrium. Infection of the posterior (non-coronary) aortic cusp or sinus may cause a fistula to either the left or right atrium. Infection of the right aortic cusp or sinus may cause a fistula to the right atrium, and the right ventricle or right ventricular outflow tract. An aorto-right ventricular fistula is possible due to the presence of the atrioventricular component of the interventricular septum. Extension into the myocardium and the conduction system may be found when the infection involves the valve ring or annulus. Fistulas and abscesses are important problems particularly with prosthetic IE, as discussed below.

Involvement of the coronary arteries may be due to distortion from an aortic root abscess or they may become directly infected by local extension through the coronary ostia or by formation of mycotic aneurysms. The latter may occur in normal arteries but also may be superimposed

Figure 2.15. Gross photograph of the base of the heart. The central aortic valve may form fistulas to nearly any chamber. Infections from the right cusp or sinus (R) may extend to the epicardium, the right atrium and the right ventricle outflow tract. Infection of the non-coronary cusp or sinus (NC) may form fistulas to both the right and left atria. Infections of the left cusp or sinus (L) may form fistulas to the epicardium,and the left atrium. Additional abbreviations: CS = coronary sinus; MV = mitral valve; PV= pulmonary valve; TV = tricuspid valve.

Figure 2.15. Gross photograph of the base of the heart. The central aortic valve may form fistulas to nearly any chamber. Infections from the right cusp or sinus (R) may extend to the epicardium, the right atrium and the right ventricle outflow tract. Infection of the non-coronary cusp or sinus (NC) may form fistulas to both the right and left atria. Infections of the left cusp or sinus (L) may form fistulas to the epicardium,and the left atrium. Additional abbreviations: CS = coronary sinus; MV = mitral valve; PV= pulmonary valve; TV = tricuspid valve.

Organic Tricuspid Valve DiseaseEndocarditis From Small Abscess

Figure 2.16. Gross photograph of longitudinal section of the left ventricle wall. The upper defect (CS) is the normal coronary sinus near the atrioventricular groove. The lower large intramyocardial defect (A) is an abscess cavity that contained purulent material.The patient had a floppy myxomatous mitral valve that became infected leading to coronary arteritis and myocardial abscesses.

Figure 2.16. Gross photograph of longitudinal section of the left ventricle wall. The upper defect (CS) is the normal coronary sinus near the atrioventricular groove. The lower large intramyocardial defect (A) is an abscess cavity that contained purulent material.The patient had a floppy myxomatous mitral valve that became infected leading to coronary arteritis and myocardial abscesses.

on an underlying atherosclerotic plaque. Mycotic aneurysms may thrombose and are a source of infected emboli that may seed the myocardium leading to myocardial abscesses. Myocardial abscesses may also form as a result of local valvular IE extension into the adjacent myocardium (Figure 2.16). Aortic root abscesses and myocar-dial abscesses may impinge upon or destroy the conduction system in the areas of the atrioven-tricular node and His bundle. Clinically this manifests as a progressively worsening degree of heart block and may be an important clinical sign that treatment is failing or disease is progressing.

Extension of infection to the pericardial space may lead to hemopericardium and tamponade or to pericarditis. Fibrinous pericarditis is a common finding with IE, but the pericardium may also become infected, leading to suppura-tive pericarditis.

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