Prichard's structures of the fossa ovalis are not histogenetically relatedto cardiac myxoma

Citation
E. Acebo et al., Prichard's structures of the fossa ovalis are not histogenetically relatedto cardiac myxoma, HISTOPATHOL, 39(5), 2001, pp. 529-535
Citations number
21
Categorie Soggetti
Research/Laboratory Medicine & Medical Tecnology","Medical Research Diagnosis & Treatment
Journal title
HISTOPATHOLOGY
ISSN journal
03090167 → ACNP
Volume
39
Issue
5
Year of publication
2001
Pages
529 - 535
Database
ISI
SICI code
0309-0167(200111)39:5<529:PSOTFO>2.0.ZU;2-E
Abstract
Aims: Cardiac myxomas are neoplasms of unknown histogenesis. They are thoug ht to arise from hypothetical subendothelial vasoformative reserve cells or from primitive cells which reside in the fossa ovalis and surrounding endo cardium. In 1951 Prichard described a kind of microscopic endocardial struc ture with a predilection for the interatrial septum. which were suggested t o be related to cardiac myxomas. To confirm the existence of Prichard's str uctures and to clarify their role in the genesis of cardiac myxomas. we exa mined histologically the rossa ovalis and we performed an immunohistochemic al study of the endocardial abnormalities that were found. Methods and results: A prospective histological study of 100 interatrial se pta and an immunohistochemical study of three out of the 12 endocardial abn ormalities that were detected, as well as of four conventional cardiac myxo mas were accomplished. Antibodies were used to vimentin, CD31, CD34, alpha -smooth muscle actin, S100 protein. thrombomodulin, calretinin and c-kit (C D117). a tyrosine kinase growth factor receptor for stem cell factor usuall y expressed by embryonic/fetal endothelium. Structures similar to the ones described by Prichard were found in 12% of septa. most of them in the left side of the fossa ovalis. The hearts with these structures were from patien ts 10 years older than the ones without them (72 +/- 10 versus 62 +/- 16 ye ars, P=0.006). Immunohistochemically the cells comprising Prichard's struct ures were positive for vimentin. CD31, CD34 and thrombomodulin, and negativ e for alpha -smooth muscle actin, S100 protein, calretinin and c-kit. There fore these cells seem to be mature endothelial cells, but not primitive mul tipotential mesenchymal cells. Furthermore, these cells were not found in t he atrial tissue from the bases of any of the conventional cardiac myxomas. Conclusions: Our study suggests that there is no apparent relation between Prichard's structures and cardiac myxomas, and that Prichard's minute endoc ardial deformities are age-related phenomena.