The development of cardiac myxomas and papillary endocardial lesions from mural thrombus

A morphologic study of 466 cardiac mural thrombi, 66 examples of nonbacterial thrombotic endocarditis, 25 myxomas, and 12 papillary endocardial lesions was performed. It appeared that three different sequences of organization of endocardial thrombi are possible. (1) Ordinary mural thrombi are converted into a flat, fibrous scar by fibroblast proliferation and collagen and elastic fiber deposition. (2) Papillary endocardial lesions develop from nonbacterial thrombotic endocarditis as additional thrombus material is acquired in some foci and lost in others. No ingrowth of granulation tissue occurs at the base of these lesions. The thrombus material of the papillae is gradually replaced by fibrous tissue, and the lesion eventually is identical to a large Lambl's excrescence. (3) Myxomas enlarge in part as do the papillary endocardial lesions. In addition, their size increases as a result of influx into the myxoma of fluid from the basal granulation tissue. Although myxomas cannot be differentiated from ordinary mural thrombi on the basis of the cellular and ground substance components, their mode of development results in a distinctive appearance. The mature lesion is composed of three zones: a basal layer of small vascular channels, undifferentiated mesenchymal cells, and ground substance; a middle, acellular zone of ground substance; and a cortical layer of mesenchymal cells. The peculiar arrangement of endothelial cells and undifferentiated mesenchymal cells, the examples of apparent atrial wall invasion, and the cases of embolic “metastases” provide no conclusive evidence of neoplasia, since these features may also be seen with ordinary mural thrombi.