The Pathogenesis of Valvular Thickening in Rheumatic Heart Disease

Recently Magarey (1949, 1951) has shown the part played by repeated fibrin deposition in the pathogenesis of valvular thickening in rheumatic heart disease. He showed that fibrin deposited on the surface of a thickened valve became hyalinized, lost its fibrin-staining qualities, and became covered over by endothelium on which further fibrin might be deposited before the first was organized to fibro-cellular tissue. As many as three layers of fibrin in varying stages of organization were described. By implication (though not explicitly) he suggests that buried hyaline material in valves is usually or always buried fibrin, though he does not specifically discuss the question of how to decide whether buried homogenous acidophil material is altered fibrin or a degenerative change in underlying collagen. He dealt with changes in the chronic stages of the disease and did not con- sider at length the part played by vegetations in acute rheumatic valvulitis or the changes preceding thrombus deposition. It is the purpose of this communication to suggest that all such collections of homogeneous acidophil material found in rheumatic valves are organizing or incompletely organized thrombotic deposits and that there is no compelling histological evidence that they are ever degenerated swollen collagen or a ground substance change. A further conclusion is that the myxomatous swelling associated with fibroblastic proliferation that is seen in acute rheumatic valvulitis is not a precursor of so called fibrinoid degeneration but a result of rapid organization of thrombus. In addition, Magarey's views on the importance of thrombus deposition in the thicken- ing of valves and in the stenosis of valve ostia are confirmed and extended to include the stage of acute valvulitis. During the study particular attention was paid to the lesions preceding thrombus deposition.