Defecto septal atrial. Estudio morfopatológico, embriológico / Atrial septal defect. A morphopathological and embryological study

To contribute to a better understanding of the morphopathology of atrial septal defects (ASD), we describe and classify topographically a series of hearts obtained from necropsies. We performed an anatomo-embryological correlation to gain insight on the pathogenesis of this type of congenital heart disease. Seventy-one hearts with ASD and twenty-three normal hearts with patent foramen ovale from the collection at the Instituto Nacional de Cardiologia lgnacio Chavez were studied morphologically; segmental sequential analysis was used. The topography of the interatrial septum was determined on the basis of the structures related to it in order to classify the ASD. The FS area was projected on the right septal surface using pins. To stablish the anatomo-embryological correlation, the ASD's anatomy was compared with the embryological processes that take place in atrial septation. The most frequent ASD was the OO type (FS) with 64.78%, followed by common atrium, true FS, FP, superior and inferior sinus venosus, types each one with 2.81% and one coronary sinus venosus type (1.40%). The FS area was projected below the superior vena cava. The morphologically and topographically knowledge of atrial septal defect is useful to interpret the imaging studies of this cardiopathy and is basic for the surgeon and the interventionist cardiologist. Abnormal apoptosis and retarded developmental growth are proposed as pathogenic mechanisms.

Cell cycle regulators during human atrial development

OBJECTIVES: The molecular mechanisms that regulate cardiomyocyte cell cycle and terminal differentiation in humans remain largely unknown. To determine which cyclins, cyclin dependent kinases (CDKs) and cyclin kinase inhibitors (CKIs) are important for cardiomyocyte proliferation, we have examined protein levels of cyclins, CDKs and CKIs during normal atrial development in humans. METHODS: Atrial tissues were obtained in the fetus from inevitable abortion and in the adult during surgery. Cyclin and CDK proteins were determined by Western blot analysis. CDK activities were determined by phosphorylation amount using specific substrate. RESULTS: Most cyclins and CDKs were high during the fetal period and their levels decreased at different rates during the adult period. While the protein levels of cyclin D1, cyclin D3, CDK4, CDK6 and CDK2 were still detectable in adult atria, the protein levels of cyclin E, cyclin A, cyclin B, cdc2 and PCNA were not detectable. Interestingly, p27KIP1 protein increased markedly in the adult period, while p21CIP1 protein in atria was detectable only in the fetal period. While the activities of CDK6, CDK2 and cdc2 decreased markedly, the activity of CDK4 did not change from the fetal period to the adult period. CONCLUSION: These findings indicate that marked reduction of protein levels and activities of cyclins and CDKs, and marked induction of p27KIP1 in atria, are associated with the withdrawal of cardiac cell cycle in adult humans.