Cinética de la enolasa neuroespecífica: una herramienta adicional para el pronóstico neurológico después de una parada cardiaca / Neuron-specific enolase kinetics: an additional tool for neurological prognostication after cardiac arrest

INTRODUCCIÓN Y OBJETIVOS: Analizar la cinética de la enolasa neuroespecífica (EN) como biomarcador de pronóstico neurológico de los pacientes que sobreviven a una parada cardiaca tratados con control de temperatura. MÉTODOS: Análisis retrospectivo de pacientes ingresados tras sufrir una parada cardiaca dentro o fuera del hospital entre septiembre de 2006 y mayo de 2018 en un centro terciario y enfriados a 32-34°C durante 24 h. Las muestras de EN se tomaron al ingreso hospitalario y a las 24, 48 y 72 h del retorno a circulación espontánea (RCE). El estado neurológico se evaluó a los 3 meses mediante la escala Cerebral Performance Category (CPC) y se categorizó como favorable (CPC 1-2) o desfavorable (CPC 3-5). RESULTADOS: De los 451 pacientes, 320 cumplían los criterios de inclusión (el 80,3% varones; media de edad, 61+/-14,1 años). De estos, 174 (54,4%) sobrevivieron con una evolución neurológica favorable. Los pacientes con estado neurológico desfavorable tenían valores de EN más altos al ingreso hospitalario y a las 24, 48 y 72 h del RCE. A las 48 y las 72 h, los valores de EN predijeron un estado neurológico desfavorable, con áreas bajo la curva de 0,85 (IC95%, 0,81-0,90) y 0,88 (IC95%, 0,83-0,93). Además, el área bajo la curva de los valores delta de EN entre las 72 h y el ingreso hospitalario fue de 0,90 (IC95%, 0,85-0,95), y en el análisis multivariante resultó predictor independiente (p <0,001). CONCLUSIONES: En pacientes que sobrevivieron a una parada cardiaca tratados con control de la temperatura, se ha demostrado que los valores delta de EN entre las 72 h del RCE y el ingreso hospitalario son un potente predictor de resultado neurológico desfavorable

INTRODUCTION AND OBJECTIVES: To analyze neuron-specific enolase (NSE) kinetics as a prognostic biomarker of neurological outcome in cardiac arrest survivors treated with targeted temperature management. METHODS: We performed a retrospective analysis of patients resuscitated from in- or out-of-hospital cardiac arrest admitted from September 2006 to May 2018 in a single tertiary care center and cooled to 32°C to 34°C for 24 hours. Blood samples for measurement of NSE values were drawn at hospital admission and at 24, 48, and 72hours after return of spontaneous circulation (ROSC). Neurological outcome was evaluated by means of the Cerebral Performance Category (CPC) score at 3 months and was characterized as good (CPC 1-2) or poor (CPC 3-5). RESULTS: Of 451 patients, 320 fulfilled the inclusion criteria and were analyzed (80.3% male, mean age 61+/-14.1 years). Among these, 174 patients (54.4%) survived with good neurological status. Poor outcome patients had higher median NSE values at hospital admission and at 24, 48 and 72 hours after ROSC. At 48 and 72 hours after ROSC, NSE predicted poor neurological outcome with areas under the receiver-operating characteristic curves of 0.85 (95%CI, 0.81-0.90) and 0.88 (95%CI, 0.83-0.93), respectively. In addition, delta NSE values between 72hours after ROSC and hospital admission predicted poor neurological outcome with an area under the receiver-operating characteristic curve of 0.90 (95%CI, 0.85-0.95) and was an independent predictor of unfavorable outcome on multivariate analysis (P <.001). CONCLUSIONS: In cardiac arrest survivors treated with targeted temperature management, delta NSE values between 72 hours after ROSC and hospital admission strongly predicted poor neurological outcome

Neuron-specific enolase kinetics: an additional tool for neurological prognostication after cardiac arrest.

INTRODUCTION AND OBJECTIVES: To analyze neuron-specific enolase (NSE) kinetics as a prognostic biomarker of neurological outcome in cardiac arrest survivors treated with targeted temperature management. METHODS: We performed a retrospective analysis of patients resuscitated from in- or out-of-hospital cardiac arrest admitted from September 2006 to May 2018 in a single tertiary care center and cooled to 32°C to 34°C for 24 hours. Blood samples for measurement of NSE values were drawn at hospital admission and at 24, 48, and 72hours after return of spontaneous circulation (ROSC). Neurological outcome was evaluated by means of the Cerebral Performance Category (CPC) score at 3 months and was characterized as good (CPC 1-2) or poor (CPC 3-5). RESULTS: Of 451 patients, 320 fulfilled the inclusion criteria and were analyzed (80.3% male, mean age 61±14.1 years). Among these, 174 patients (54.4%) survived with good neurological status. Poor outcome patients had higher median NSE values at hospital admission and at 24, 48 and 72 hours after ROSC. At 48 and 72 hours after ROSC, NSE predicted poor neurological outcome with areas under the receiver-operating characteristic curves of 0.85 (95%CI, 0.81-0.90) and 0.88 (95%CI, 0.83-0.93), respectively. In addition, delta NSE values between 72hours after ROSC and hospital admission predicted poor neurological outcome with an area under the receiver-operating characteristic curve of 0.90 (95%CI, 0.85-0.95) and was an independent predictor of unfavorable outcome on multivariate analysis (P <.001). CONCLUSIONS: In cardiac arrest survivors treated with targeted temperature management, delta NSE values between 72 hours after ROSC and hospital admission strongly predicted poor neurological outcome.

Aortic wall erosion after percutaneous closure of atrial septal defect.

A 26-year-old woman presented with acute hemolysis 1 month after percutaneous closure of an atrial septal defect. Three-dimensional transesophageal echocardiography was used to establish the diagnosis of a fistula from the aorta, toward the device and both atria. The patient required urgent surgical correction. Transcatheter closure of atrial septal defects has proven to be a highly successful alternative to surgery in the appropriate patient. Cardiac perforation and device erosion of the aortic wall are infrequent but potentially lethal complications of percutaneous occluder device insertion. Supportive features of device erosion include a wrong preimplantation assessment of the rims, the device extends across the atrial septum, and the device encroaches on the surrounding structures. In this case, the presumed mechanism of aortic fistula was aortic erosion by the left atrial disk of the occluder device.