[Clinicopathologic features of cardiac myxoma--a report of 47 cases]

Myxoma is the most common neoplasm of the heart, and has various morphologic structures, but its biological behaviors and histogenesis are still controversial. This study was to summarize the clinical, histomorphologic, and immunophenotypic features of cardiac myxoma.

The clinical data and HE sections of 47 cases of cardiac myxoma were reviewed. Special staining and immunohistochemical staining for 10 kinds of antibodies were carried on some cases to observe the morphologic features.

Of the 47 patients with cardiac myxoma, 32 were women, the youngest was 3 years old. The volume of tumors ranged from 0.7 cm x 0.7 cm x 0.4 cm to 12 cm x 8 cm x 7 cm. Of the 47 tumors, 42 were pedunculated, the rest had broad fundus without pedicel; 43 located in the left atrium, 3 in the right atrium, and 1 in the left ventricle where near to the apex of heart. Tumor cells were stellate, spindle, round, or irregular, and arranged as masses or stripes, with abundant mucus around them. Tumor cells surrounded arterioles in 4 cases. Pseudo-capsule was formed by hyperplastic fibrous tissue in 4 cases. The mesenchyma presented angiomatous fashion in 2 cases. Sheets of old hemorrhage, hemosiderin and iron salt deposition, and fibrosis were observed in 7 cases. One case had foci adenoid structure, 1 lipoid metaplasia and ossification, 1 was rich of cells. Vimentin and CD34 were found in lining cells and parenchymal cells in 12 cases. Cytokine kinase (CK) and epithelial membrane antigen (EMA) were positive in the region of adenoid differentiation. Proliferating cell nuclear antigen (PCNA) and Ki67 were positive in the cell-rich tumor. None of the 21 patients had tumor recurred after follow-up.

Cardiac myxoma has various secondary morphologic changes, including adenoid metaplasia, old hemorrhage, fibrosis, ossification, and lipoid metaplasia. Whether the cell-rich tumors tend to be malignant needs further study. Cardiac myxoma may come from multipotential mesenchymal cells.