RESUMO
OBJECTIVE: To explore the variations of brain natriuretic peptide (BNP) secretion after left atrial appendage occlusion. BACKGROUND: Left atrial appendage occlusion has been increasingly performed in the last few years, however little is known about the physiological consequences of left atrial appendage occlusion. Left atrial appendage regulates partially intravascular volume via release of brain natriuretic peptide. Brain natriuretic peptide levels have been related to increased risk of stroke in atrial fibrillation patients. METHODS: Venous blood samples were obtained in consecutive patients undergoing left atrial appendage occlusion before, 24 hr after device implantation and at the first visit after discharge (45-60 days) for BNP measurement. RESULTS: Left atrial appendage occlusion was performed in 34 patients with non-valvular atrial fibrillation and contraindication to long-term oral anticoagulation or at high-risk of bleeding. There were no differences in BNP levels between baseline and 24 hr after device implantation. However left atrial appendage closure resulted in a significant decrease in BNP levels at the first follow-up visit (45-60 days) compared to baseline measurements (759.90 pg ml(-1) vs. 636.90 pg ml(-1) , P = 0.013). CONCLUSIONS: Left atrial appendage occlusion modifies BNP levels. These levels decrease after left atrial appendage occlusion. The clinical consequences of these findings need to be evaluated in further studies. © 2015 Wiley Periodicals, Inc.
Assuntos
Apêndice Atrial/cirurgia , Fibrilação Atrial/cirurgia , Cateterismo Cardíaco/métodos , Procedimentos Cirúrgicos Cardíacos/instrumentação , Peptídeo Natriurético Encefálico/sangue , Dispositivo para Oclusão Septal , Acidente Vascular Cerebral/prevenção & controle , Idoso , Apêndice Atrial/diagnóstico por imagem , Fibrilação Atrial/sangue , Fibrilação Atrial/complicações , Ecocardiografia Transesofagiana , Feminino , Seguimentos , Humanos , Incidência , Masculino , Estudos Prospectivos , Fatores de Risco , Espanha/epidemiologia , Acidente Vascular Cerebral/epidemiologia , Acidente Vascular Cerebral/etiologia , Taxa de Sobrevida/tendênciasRESUMO
Wernicke encephalopathy is caused by thiamine deficiency in the central nervous system, and is defined by the triad of confusional symptoms, ocular alterations and ataxia. Some other factors may also predispose alcoholic patients to this deficiency. We report two patients with hyperglicaemia and ketoacidosis due to diabetes mellitus decompensation and chronic alcoholism who developed Wernicke encephalopathy before their hospital admission. The outcome was successful after intravenous thiamine administration and insulinotherapy. The presence of Wernicke encephalopathy in alcoholics with diabetic ketoacidosis, suggests that metabolic decompensation is essential in the onset of the disease.