The Pathogenesis of Valvular Thickening in Rheumatic Heart Disease

Abstract

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 consider 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 thickening 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.Pathogenesis of Valve Thickening. The commonly accepted view of the pathogenesis of the thickening of valve cusps is that it is due to an acute valvulitis often, but not necessarily, with inflammatory cell infiltration, cedema, degeneration of collagen, marked fibroblastic proliferation, and subsequent cicatrization. Koniger (1903) emphasized the presence of marked swelling of subendothelial connective tissues which had undergone a "homogenizing hyaline necrosis" (called by Klinge, (1933) "fibrinoid degeneration"). Coombs (1911, 1924) stressed the part played by submiliary nodules which he identified with those described by Aschoff and Tawara (1906).In addition to the above-mentioned writers, Gross and Friedberg (1936), Wilson (1940), and Murphy (1952, hold similar views. Gross and Friedberg (1936a) also emphasize the part played by the incorporation of chordae tendineae into the valve cusps and mutual fusion of the chorde and of cusps at the commissures, which is also mentioned by Rokitansky (1852), Rindfleisch (1872), Wilson (1940), andBrock (1952). Coombs denies that this happens in the case of the mitral valve, but allows that it occurs in the aortic valve. Magarey's ...

Cardiovascular Diseases (Medical)

“…An important new insight into the mechanism of rheumatic valvular def0rmity is reported by Tweedy (115) who showed that the valvular thickening and chorda fusion result from a transformation of deposited fibrin rather than from fibroplasia with "fibrinoid degeneration," a term which he feels should be discarded. A similar mechanism is perhaps the basis of fibroelastosis' of the endocardium (116), the pulmonary vascular lesion of recurrent pulmonary embolism (117), certain types of myocardial lesions (118), and perhaps even certain aspects of atherosclerosis (119).…”

Mitral valve reconstruction by posterior cusp advancement using a pericardial graft. Long-term follow-up in nine patients.

“…The presence of blood vessels in the zone between the graft and the overlying fibrous tissue layer, also reported by Sauvage et al (1966), suggests that an active process of granulation tissue replacement is responsible for the gradual conversion of the graft into fibrous tissue, and that this process is, in turn, responsible for the increase in thickness of the graft. This may be augmented by the organization of surface fibrin deposits as described by Tweedy (1956) in rheumatic heart disease.…”

Studies on thromboplastic and fibrinolytic activities of valvular tissue in rheumatic valvular disease

“…He suggested that thrombus organization, in the course of several years, might lead to the development of MS. Tweedy [10] also noted a high incidence of thrombus deposits in the acute stage of RVD and reported that these deposits could be found in any age group and in any of the cusps. These findings suggest that thrombotic deposits play an important role in the development of RVD.…”