ABSTRACT
Resumen El número de personas en tratamiento con fármacos anticoagulantes o antiplaquetarios está en crecimiento constante debido al aumento de la supervivencia de los pacientes con fibrilación auricular, válvulas cardiacas mecánicas o que han sufrido un evento isquémico o trombótico agudo. Cuando estos pacientes necesitan un procedimiento radiológico intervencionista que acarrea riesgo de sangrado, es necesario analizar el riesgo trombótico del paciente al interrumpir la medicación frente al riesgo hemorrágico del procedimiento para tomar la decisión más adecuada en cada caso. Por tanto, es una decisión individualizada y supone un desafío para los/as radiólogos/as que realicen estas técnicas. Nuestro objetivo en esta revisión es mostrar las recomendaciones actuales sobre el manejo perioperatorio de la medicación anticoagulante y antiplaquetaria, adaptada al intervencionismo radiológico.
Abstract The number of people treated with anticoagulant or antiplatelet agents is constantly growing due to the increased survival of patients with atrial fibrillation, mechanical cardiac valves or who have suffered an acute thrombotic or ischemic event. When these patients need an interventional radiological procedure that carries a risk of bleeding, it is necessary to analyze the thrombotic risk of the patient when interrupting the medication against the hemorrhagic risk of the procedure, to make the most appropriate decision in each case. Therefore, it is an individualized decision, and it is a challenge for radiologists who perform these techniques. Our goal in this review is to update the current recommendations on the perioperative management of anticoagulant and antiplatelet agents, adapted to the radiological interventionism.
ABSTRACT
Most cells of the developing mammalian brain derive from the ventricular (VZ) and the subventricular (SVZ) zones. The VZ is formed by the multipotent radial glia/neural stem cells (NSCs) while the SVZ harbors the rapidly proliferative neural precursor cells (NPCs). Evidence from human and animal models indicates that the common history of hydrocephalus and brain maldevelopment starts early in embryonic life with disruption of the VZ and SVZ. We propose that a "cell junction pathology" involving adherent and gap junctions is a final common outcome of a wide range of gene mutations resulting in proteins abnormally expressed by the VZ cells undergoing disruption. Disruption of the VZ during fetal development implies the loss of NSCs whereas VZ disruption during the perinatal period implies the loss of ependyma. The process of disruption occurs in specific regions of the ventricular system and at specific stages of brain development. This explains why only certain brain structures have an abnormal development, which in turn results in a specific neurological impairment of the newborn. Disruption of the VZ of the Sylvian aqueduct (SA) leads to aqueductal stenosis and hydrocephalus, while disruption of the VZ of telencephalon impairs neurogenesis. We are currently investigating whether grafting of NSCs/neurospheres from normal rats into the CSF of hydrocephalic mutants helps to diminish/repair the outcomes of VZ disruption.