CHRONIC ENDOCARDITIS. 325 



of bead-like elevations on the ventricular surface, some little 

 distance from the margins of the cusps of the aortic (Figs. 

 143 and 144). These small warty elevations are less fre- 

 quently seen on the tricuspid and pulmonary valves, and on 

 the chordae tendinese and parts of the mural endocardium. 

 They crumble and can be easily detached by the finger, 

 leaving behind a slightly roughened surface, or possibly a 

 small ulcer the size of the base of the vegetation. The change 

 in the endocardium produced by the inflammatory process 

 and the extra irritation and friction at the line of contact of 

 the valves on closure, invite the deposition of fibrin ; there 

 is an active proliferation of the endothelial cells, which, 

 together with migrating leukocytes, infiltrate the layers of 

 fibrin and tend to bring about the organization of the clot 

 which has formed. 



In some cases the inflammatory process is especially severe 

 and there is a tendency to suppuration and ulceration. Small 

 collections of pus may be seen at the base of the valves. The 

 masses of fibrinous deposit are more abundant and irregular, 

 occurring indiscriminately over the endocardial surface of the 

 valves and heart-wall. Where there has been actual destruc- 

 tion of tissue there will be noted on section, microscopically, 

 at the bases of these vegetations, typical granulation-tissue, 

 to which the clot is firmly adherent. If the section is prop- 

 erly stained, micro-organisms may usually be seen in the 

 superficial layers of the endocardium. The vegetations are 

 liable to be broken off and carried in the circulation, as emboli, 

 to distant parts. If the micro-organisms are likewise trans- 

 ported, metastatic abscesses in various organs are produced. 



Chronic endocarditis results in various distortions of the af- 

 fected leaflets of the valves, and, in consequence, serious dis- 

 turbances in the circulation. The vegetations become fibrous 

 and have a broad base. As in all chronic inflammations, there 

 is a tendency toward the overproduction of connective tissue. 

 The proliferating endothelial and connective-tissue cells and 

 infiltrating leukocytes become organized into fibrous tissue. 

 The valves are thickened, rigid, and eventually retracted and 

 distorted. The opposed inflamed leaflets of the valve may 

 become agglutinated or firmly adherent to the adjacent heart- 

 wall and cause still further deformity. The chordae tendinese 



