title: Prichard's structures of the fossa ovalis are not histogenetically related to cardiac myxoma.
abstract: OBJECTIVE
  Cardiac myxomas are neoplasms of unknown histogenesis. They are thought to arise from hypothetical subendothelial vasoformative reserve cells or from primitive cells which reside in the fossa ovalis and surrounding endocardium. In 1951 Prichard described a kind of microscopic endocardial structure with a predilection for the interatrial septum, which were suggested to be related to cardiac myxomas. To confirm the existence of Prichard's structures and to clarify their role in the genesis of cardiac myxomas, we examined histologically the fossa ovalis and we performed an immunohistochemical study of the endocardial abnormalities that were found.
  
  
  RESULTS
  A prospective histological study of 100 interatrial septa and an immunohistochemical study of three out of the 12 endocardial abnormalities that were detected, as well as of four conventional cardiac myxomas were accomplished. Antibodies were used to vimentin, CD31, CD34, alpha-smooth muscle actin, S100 protein, thrombomodulin, calretinin and c-kit (CD117), a tyrosine kinase growth factor receptor for stem cell factor usually 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 patients 10 years older than the ones without them (72 +/- 10 versus 62 +/- 16 years, P=0.006). Immunohistochemically the cells comprising Prichard's structures were positive for vimentin, CD31, CD34 and thrombomodulin, and negative for alpha-smooth muscle actin, S100 protein, calretinin and c-kit. Therefore these cells seem to be mature endothelial cells, but not primitive multipotential mesenchymal cells. Furthermore, these cells were not found in the 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 endocardial deformities are age-related phenomena.
authors.affiliation: Department of Anatomical Pathology, Marqués de Valdecilla University Hospital, Medical Faculty, University of Cantabria, Santander, Spain.
authors.forename: E
authors.initials: E
authors.lastname: Acebo
authors.forename: J F
authors.initials: JF
authors.lastname: Val-Bernal
authors.forename: J J
authors.initials: JJ
authors.lastname: Gómez-Román
mesh_terms: D000199:Actins / Q000032:analysis; D000328:Adult; D018952:Antigens, CD34 / Q000032:analysis; D064032:Calbindin 2; D004699:Endocardium / Q000737:chemistry / Q000473:pathology; D006338:Heart Neoplasms / Q000378:metabolism / Q000473:pathology*; D006346:Heart Septum / Q000737:chemistry / Q000473:pathology*; D006801:Humans; D007150:Immunohistochemistry; D009130:Muscle, Smooth / Q000737:chemistry; D009214:Myoma / Q000378:metabolism / Q000473:pathology*; D019408:Platelet Endothelial Cell Adhesion Molecule-1 / Q000032:analysis; D064030:S100 Calcium Binding Protein G / Q000032:analysis; D009418:S100 Proteins / Q000032:analysis; D018180:Thrombomodulin / Q000032:analysis; D014746:Vimentin / Q000032:analysis
chemical_list: D000199:Actins; D018952:Antigens, CD34; C576764:CALB2 protein, human; D064032:Calbindin 2; D019408:Platelet Endothelial Cell Adhesion Molecule-1; D064030:S100 Calcium Binding Protein G; D009418:S100 Proteins; D018180:Thrombomodulin; D014746:Vimentin