Rotura del septum interventricular post infarto agudo al miocardio: una complicación potencialmente letal Revisión de la literatura a propósito de un caso clínico / Ventricular septal rupture after acute myocardial infarction: a potentially lethal complication Case report and literature review

Rupture of the ventricular septum with the appearance of an interventricular communication is an infrequent and life-threatening mechanical complication after acute myocardial infarction. The advent of coronary reperfusion therapies has reduced the incidence of this complication, but mortality remains high. The clinical presentation varies from mild compromise with exertional dyspnea to severe compromise with cardiogenic shock. In this pathology, early diagnosis is fundamental and surgical repair is the treatment of choice. In this article we report an interesting clinical case about a 77-year-old woman who was belatedly referred to our hospital and diagnosed with postinfarction rupture of the ventricular septum with an unfortunately fatal evolution. Relevance of this case lies in its atypical clinical presentation which led to a delay in diagnosis and a missed opportunity for early reperfusion therapy. An updated literature review about rupture of the ventricular septum complicating acute myocardial infarction was carried out.

Bases Fisiopatológicas Del Espectro De Neuromielitis Óptica: ¿Qué Sabemos? / Pathophysiological Basis Of Neuromyelitis Optica Spectrum Disorders: What do we know?

Resumen El espectro de Neuromielitis óptica (NMOSD por su sigla en inglés) corresponde a un conjunto de manifestaciones clínicas derivadas de un proceso inflamatorio y desmielinizante del sistema nervioso central, que causa lesiones primariamente en la médula espinal y nervios ópticos, pero también en otras regiones como tronco encefálico, diencéfalo o áreas cerebrales específicas. La mayoría de los pacientes con NMOSD son seropositivos para autoanticuerpos contra AQP4, el principal canal de agua de los astrocitos, sin embargo, existe un porcentaje no despreciable de pacientes, cercano al 25%, quienes son seronegativos para estos anticuerpos y en quienes la presencia de anticuerpos dirigidos contra mielina (anti-MOG) podrían tener un rol patogénico, el cual a la fecha no ha sido bien dilucidado. La evidencia científica actual, ha permitido reconocer que AQP4-IgG es patogénico en NMOSD, probablemente por un mecanismo que involucra citotoxicidad celular dependiente de la activación del complemento, generando infiltración leucocitaria, liberación de citokinas y disrupción de la barrera hemato-encefálica, lo cual lleva a muerte de oligodendrocitos, pérdida de mielina y muerte neuronal. Este artículo presenta una revisión basada en la evidencia, la cual enfatiza los principales aspectos de la patogénesis de NMOSD.

Neuromyelitis Optica Spectrum Disorders (NMOSD) is a set of clinical manifestations derived from an inflammatory and demyelinating process of the central nervous system that causes lesions primarily in spinal cord and optic nerves but also in other regions such as brainstem, diencephalon or specific brain areas. Most patients with NMOSD are seropositive for autoantibodies against AQP4, the major water channel of astrocytes, however there is a non-negligible percentage of patients, close to 25%, who are seronegative for these antibodies and in whom the presence of antibodies directed against myelin (anti-MOG) could have a pathogenic role that to date has not been well elucidated. Current scientific evidence has allowed recognize that AQP4-IgG is pathogenic in NMOSD, probably by a mechanism involving complement dependent cellular cytotoxicity, causing leucocyte infiltration, cytokine release and blood-brain barrier disruption, which leads to oligodendrocyte death, myelin loss and neuron death. This article presents an evidence-based review, which emphasizes the main aspects in NMOSD pathogenesis.