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Table 6.3 Duke criteria for diagnosis of infective endocarditisa: two or one major + three minor or ve minor criteria are required

Major Minor Positive blood culture Predisposing heart condition

or intravenous drug use

Evidence of endocardial

Fever >38°

involvement – Positive echocardiogram Vascular phenomena – New valvular regurgitation Immunological phenomena

Microbiological evidence Echocardiogram

Consistent with infective endocarditis but not meeting major criteria

G. Thiene et al.

Fig. 6.11 (a) Annular abscess complicating infective endocarditis of aortic valve. (b) Right-sided heart: spread of the infection from the right anterior Valsalva sinus into the right atrial septum

Fig. 6.12 (a) Ulcero- vegetative infective

endocarditis of the aortic valve (b) “kiss” lesion to the anterior leaet of the mitral valve, with septic aneurysm and perforation

6 Infective Endocarditis

Fig. 6.13 Ulcero-vegetative endocarditis of mitral valve prolapse with cusp perforation and chordal rupture. (a) Drawing; (b) surgical pathology specimen. (c) Colonies of microorganisms at histology (Gram stain)

Fig. 6.14 (a) Healed endocarditis of the aortic valve: note a hole within a cusp with thickened borders; (b) valve repair with brosis and neovas- cularization at histology. Hematoxylin-eosin

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Cardiac Conditions/Patients at Risk (Table6.4)

Rheumatic valve disease (Fig.6.15) has been considered for years the major risk factor for IE, account in the rst 20–25% of cases. In the 1980s, this gure dropped to 7–10%. As previously mentioned, sterile thrombus formation on the surface of deformed valves, with altered blood ow dynamics and inammatory endothelial injury, is the main mechanism for both microbial settlement and valve disease progression. Although the frequency of rheumatic valve disease has

Table 6.4 Cardiac conditions at risk of infective endocarditis

Prosthetic heart valves, catheters Complex congenital cyanotic heart diseases Previous infective endocarditis Surgical systemic or pulmonary conduits Acquired valvular heart diseases Mitral valve prolapse with valvular regurgitation or severe valve

thickening Noncyanotic congenital heart diseases (except for secundum-type

atrial septal defect), including bicuspid aortic valves Hypertrophic cardiomyopathy

diminished in Europe and North America, it is still endemic in third world countries where it represents by far the leading predisposing factor, especially in children (Table6.5).

With increasing of life expectancy, currently acquired degenerative heart diseases are becoming the most common condition at risk for IE.

Mitral valve prolapse has emerged as predominant predisposing structural abnormality and accounts for 7–30% of cases of native valve IE in Western countries. The risk is almost entirely conned to patients with regurgitation (Figs.6.13 and

6.16), particularly those with valve redundancy and thickened

mucoid leaets. The incidence of IE in patients with mitral valve prolapse is ten times than in the general population. IE on a prolapsing mitral valve may lead to chordal rupture (Fig.6.13)

Table 6.5 Infective endocarditis: underlying predisposing heart disease in 186 Indian patients (Choudhury at al., 1992)

Rheumatic heart disease 79 (42%) Congenital heart disease Normal valve 17 (9%) Uncertain etiology 24 (13%) Floppy mitral valve 2 (1%) Prosthetic valve 2 (1%)

Bicuspid aortic valve in 25

62 (33%)

Fig. 6.15 (a) Rheumatic mitral valvulitis with commissural fusion and (b) verruca at histology. Hematoxylin-eosin

6 Infective Endocarditis

and only histologic evidence of microorganisms, inammatory inltrates, and/or neovascularization may allow to differentiate chordal rupture secondary to IE from spontaneous rupture complicating myxoid degeneration.

Dystrophic calcication of the mitral valve, a common nding at autopsy and surgery in elderly patients, usually presents with some degree of valve incompetence due to cusp and annular rigidity and impaired valve closure. Vegetations of infective endocarditis are found on the base of the posterior (mural) leaet (Fig.6.17) rather than related to its line of closure and are often associated with leaet ulceration.

The bicuspid aortic valve, which represents nowadays one of the main risk factors of IE, is the most common congenital defect, being present in 0.5–2% of the general population. IE may superimpose not only on a stenotic, symptomatic bicuspid valve in adult and elderly patients but also in the young subjects where this condition is clinically silent, the aortic valve is still normally functioning, and IE may represent the rst manifestation of the disease. Wear and tear mechanisms of the unnatural closing of the bicuspid valve account for predisposition to infection (Figs.6.18, 6.19 and 6.20).

Hypertrophic cardiomyopathy, an inherited heart muscle disease with gene mutations encoding defective sarcomeric proteins, may complicate with IE in 5–9% of cases, especially in patients with subaortic stenosis. Hemodynamic and anatomic alterations of the left ventricular outow tract, by contact between the ventricular septum bulging and the anterior leaet of the mitral valve due to systolic anterior motion, cause microtraumatisms with endocardial injury (plaques). The latter may represent the nidus for thrombus deposition and microbial seeding during bacteremia (Fig.6.21), involving both aortic and mitral valve leaets.

Other congenital heart diseases may be a predisposing risk factor of IE in children (75–90%), in the young (10– 20%), and in adults (8–10%). Ventricular septal defect,

tetralogy of Fallot (Fig. 6.22), discrete subaortic stenosis, patent ductus arteriosus, and coarctation of the aorta are the most common predisposing congenital defects. Secundum atrial septal defect is not associated with an increased risk of IE, probably because of the low-pressure, nontraumatic leftto- right shunt (Table6.4). Ventricular septal defect is at par-

Fig. 6.16 Ulcero-vegetative endocarditis of a mitral valve prolapse with perforation of the posterior leaet

Fig. 6.17 Vegetative infective endocarditis, complicating huge dystrophic calcication of the mitral annulus

Fig. 6.18 Infective endocarditis of bicuspid aortic valve with vegetations in a drug addict

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G. Thiene et al.

Fig. 6.19 (a) Infective endocarditis of bicuspid aortic valve. (b) Colonies of Gram-positive microorganisms at histology. Gram stain

Fig. 6.20 Healed infective endocarditis of bicuspid aortic valve with a chronic hole within one cusp

ticular risk if small or associated with aortic regurgitation. In case of isthmic coarctation and patent ductus arteriosus, infection may involve the great vessels with development of mycotic aneurysms. Bicuspid aortic valve and mitral valve prolapse have been identied in surgical pathology specimens as the most frequent predisposing factor in 23% and 18% of cases, respectively.

Finally, native valve IE may develop upon normal valves in up to 30% of cases (Fig.6.23). Whether such valves are indeed normal has been questioned. Risk factors, like intravenous drug use, alcoholism, and immunodeciencies, may play a major risk factor in otherwise normally structured hearts. Intravenous drug users can introduce several microorganisms of the skin ora, such as cocci and fungi. Right-sided heart structures are typically involved in this setting, particularly the tricuspid valve (Fig.6.24) and even the Eustachian valve. Hidden bicuspid aortic valve is particularly at risk in drug addicts (Fig.6.18). Among neonates, IE typically affects the tricuspid valve of a structurally normal heart as the consequence of infected intravenous feading right-sided catheters.

IE may complicate the implant of cardiac devices like endocardial pacemakers (Fig.6.25)or debrillators leads or valve prostheses.

Among the latter, IE may occur early (perioperative), mostly due to hospital infection, or late (postoperative), due to bacteremia risk factors, equal to those of native endocarditis.

In mechanical prostheses recipients, the substrate is represented by microthrombi on the sewing ring and suture lines. Infection can detach the annular stiches, creating perivalvular leaks with various degrees of prosthesis incompetence and hemolysis, according to the number and dimensions of the leaks (Fig.6.26). When the involvement of the annulus by IE is extensive, even complete detachment of the prosthesis and dislodgement may occur, presenting with acute, massive incompetence, and sudden death by pulmonary edema (Fig.6.27). Moreover, exuberant septic vegetations may embolize or interfere with the prosthetic valvedysfunction.

In bioprosthetic valve recipients, IE rarely presents with annular involvement. Usually, the microorganisms involve directly the biological tissue with cusp inltration, necrosis, and perforation, commissural dehiscence, and septic vegetations, features similar to those observed in native valve IE.Microorganisms may be detected either within the thrombotic vegetations or deep in the porcine (Fig.6.28) or bovine (Fig.6.29) pericardial leaets. Dissemination of IE with septic emboli, annular abscesses, and annular detachment may also occur. In case of fungal IE, obstruction of the bioprosthetic valve orice has been reported (Fig. 6.30). When infection spreads to the His bundle from an infected aortic prosthesis, complete atrioventricular block may ensue.

6 Infective Endocarditis

a b

Fig. 6.21 (a) Infective endocarditis complicating hypertrophic cardio- myopathy. The anterior mitral leaet shows perforation and vegetation. (b) View of the left ventricular outow track with asymmetric hypertro-

phy of the basal ventricular septum and anterolateral wall. Note the perforation of the anterior leaet of the mitral valve (“kissing lesion”)

Fig. 6.22 Infective endocarditis in tetralogy of Fallot. (a) Vegetations and disruption of the pulmonary valve. (b) The aortic valve is also involved

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G. Thiene et al.

Fig. 6.23 Infective aortic valve endocarditis over a normal aortic valve: gross view of huge vegetation

Fig. 6.24 Giant polypous septic vegetations of the anterior leaet of the tricuspid valve in a drug addict

Fig. 6.25 (a) Infective vegetative endocarditis upon pacemaker cathe- ter of the right ventricle. (b) Fungal (Candida) at histology

Fig. 6.26 Extensive leak of mechanical prosthetic aortic valve by endocarditis annulus

6 Infective Endocarditis

Fig. 6.27 Severe endocarditis of prosthetic mechanical aortic valve with total annular detachment of the device

101

Fig. 6.28 (a) Vegetative infective endocarditis of a porcine biopros- thetic valve explant. (b) Colonies of microorganisms, deep into the core of a cusp (Gram stain)

Fig. 6.29 (a) Histology of a bovine pericardial cusp with vegetative infective endocarditis. (b) Microorganisms within the vegetations (Gram stain)

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Fig. 6.30 (a, b) Vegetative infective endocarditis of bioprosthetic valve with orice occlusion. (c) Hyphae of aspergilli at histology (hematoxylin and eosin) and (d)at scanning electron microscopy

6 Infective Endocarditis

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