Chronic Infective Endocarditis Pathology Tables 21 and

With successful medical treatment of infective endocarditis the infected vegetations may organize and the thrombi may form calcific valve nodules. Destructive sequelae of the infection are common (Figure 2.11). The valve may have defects at the edges or central defects forming irregular perforations. Around the holes or perforation there may be brown nodules of organisms that eventually form fibrocalcific nodules. The destruction of the valve tissue may lead to defects at the margins resulting in poor valve coaptation. Distinguishing a post-IE perforation from a congenital accessory orifice may be difficult. In atrioventricular valves congenital orifices should have surrounding chordae, while a post-IE perforation would not. Fenestrations, an age-related finding, are also confused with perforations. These fenestrations are located laterally on the valve cusps near the commissures and always beyond the line of valve closure.

Chordae may rupture resulting in flail leaflets and valve regurgitation. The ruptured chords may knot and calcify along with the organizing

Table 2.2. Pathology of Perivalvular Sequelae of Infective Endocarditis

Perivalvular leaks

Prosthesis dehiscence

Annular and root abscess


Fistula or sinus formation

Conduction system destruction

Myocardial abscess



Coronary artery compression

Coronary artery erosion,thrombosis, or rupture

Figure 2.11. Gross photograph of an excised aortic valve with destructive sequelae of prior infective endocarditis.The right cusp has a defect surrounded by calcified material (old vegetation).Similar material is noted on the other two cusps.

infected thrombi. The valve itself may thicken and the chords may fuse. All these are significant contributors to chronic valve regurgitation.

Ventricular papillary muscles may rupture for multiple reasons due to IE. The infection may extend from an adjacent chord and cause myocardial necrosis and rupture. A coronary arterial embolus may cause a myocardial infarct with papillary muscle rupture, similar to any acute myocardial infarct. Finally an embolus may lead to a myocardial abscess with local tissue destruction.

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