Valoración del Euroscore y SAPS III como predictor de mortalidad hospitalaria en el postoperatorio de cirugía cardiaca / Assessment of Euroscore and SAPS III as hospital mortality predicted in cardiac surgery

Objetivos. Realizar una validación externa del Euroscore I, Euroscore II y SAPS III. Pacientes y método. Estudio de cohorte retrospectivo durante 3 años de todos los pacientes adultos intervenidos de cirugía cardiaca. Se revisó la historia clínica siguiendo al paciente hasta el alta hospitalaria (vivo, muerto). Se calcularon las mortalidades predichas por el Euroscore I (EI), II (EII) y SAPS III. La validación de los modelos se determinó mediante la discriminación mediante el área bajo la curva ROC y la calibración mediante el test de Hosmer-Lemeshow. Resultados. Ochocientos sesenta y seis pacientes incluidos, el 62,5% varones, con una edad mediana de 69 años. El 6,1% falleció durante su ingreso hospitalario. Mortalidad predicha: EI 7,94%, EII 3,54, SAPS III 12,1%. Área bajo la curva (IC 95%): EI 0,862 (0,812-0,912); EII 0,861 (0,806-0,915); SAPS III 0,692 (0,601-0,784). Prueba de Hosmer-Lemeshow: EI 14,0046 (p=0,08164); EII 33,67 (p=0,00004660); SAPS III 11,57 (p=0,171). Conclusiones. el EII presentó una discriminación adecuada, aunque la calibración no fue apropiada con cifras de mortalidad predicha menores a la real. El EI mostró la mejor discriminación con una calibración adecuada y una tendencia a sobreestimar la mortalidad. El SAPS III ha mostrado mala discriminación con una calibración adecuada y una tendencia a aumentar exageradamente la predicción de la mortalidad. No hemos observado ninguna mejoría en el rendimiento predictivo del EII sobre el I y rechazamos la utilización del SAPS III en este tipo de enfermos (AU)

Objectives. To perform an external validation of Euroscore I, Euroscore II and SAPS III. Patients and method. Retrospective cohort study over three years on all adult patients who underwent cardiac surgery. We reviewed the clinical data, following the patient until outcome or discharge from hospital (dead, alive). We computed the predicted mortality by Euroscore I (EI), II (EII) and SAPS III. The model validation was assessed by discrimination: area under curve ROC; and calibration (Hosmer-Lemeshow test). Results. 866 patients were included. 62.5% of them male, with a median age of 69 years, 6.1% died during hospitalization. Predicted mortality: E I 7.94%, E II 3.54, SAPS III 12.1%. Area under curve (95% IC): E I 0.862 (0.812-0.912); E II 0.861 (0.806-0.915); SAPS III 0.692 (0.601-0.784). Hosmer-Lemeshow test: E I 14.0046 (P=.08164); E II 33.67 (P=.00004660); SAPS III 11.57 (P=.171). Conclusions. EII had good discrimination, but the calibration was not good with predicted mortality lower than the real mortality. E I showed the best discrimination with good calibration and a tendency to overestimate the mortality. SAPS III showed poor discrimination with good calibration and a tendency to greatly overestimate the predicted mortality. We saw no improvement in the predictive performance of EII over I and we reject the use of SAPS III in this kind of patient (AU)

Assessment of Euroscore and SAPS III as hospital mortality predicted in cardiac surgery. / Valoración del Euroscore y SAPS III como predictor de mortalidad hospitalaria en el postoperatorio de cirugía cardiaca.

OBJECTIVES: To perform an external validation of Euroscore I, Euroscore II and SAPS III. PATIENTS AND METHOD: Retrospective cohort study over three years on all adult patients who underwent cardiac surgery. We reviewed the clinical data, following the patient until outcome or discharge from hospital (dead, alive). We computed the predicted mortality by Euroscore I (EI), II (EII) and SAPS III. The model validation was assessed by discrimination: area under curve ROC; and calibration (Hosmer-Lemeshow test). RESULTS: 866 patients were included. 62.5% of them male, with a median age of 69 years, 6.1% died during hospitalization. Predicted mortality: E I 7.94%, E II 3.54, SAPS III 12.1%. Area under curve (95% IC): E I 0.862 (0.812-0.912); E II 0.861 (0.806-0.915); SAPS III 0.692 (0.601-0.784). Hosmer-Lemeshow test: E I 14.0046 (P=.08164); E II 33.67 (P=.00004660); SAPS III 11.57 (P=.171). CONCLUSIONS: EII had good discrimination, but the calibration was not good with predicted mortality lower than the real mortality. E I showed the best discrimination with good calibration and a tendency to overestimate the mortality. SAPS III showed poor discrimination with good calibration and a tendency to greatly overestimate the predicted mortality. We saw no improvement in the predictive performance of EII over I and we reject the use of SAPS III in this kind of patient.

Coronary reactive hyperaemia after nitric oxide inhibition in the anaesthetized goat.

In the dog it has been shown that, while the inhibition of the endothelial release of nitric oxide reduces the duration, the total hyperaemic flow and the peak flow of the acetylcholine and myogenic coronary vasodilator responses, in the reactive hyperaemia the peak is not affected. The difference has been attributed to the different time required by the coronary blood flow to reach its maximum: long enough when acetylcholine is given or myogenic vasodilatation is elicited, this time is very short in the reactive hyperaemia. Thus it has been argued that only when the time to the peak of a hyperaemic response is sufficiently long, the increased shear stress acting on the coronary endothelium at the beginning of the hyperaemia can enhance the maximum value of the vasodilatation. Such an effect is impaired by NO-inhibition. Since in the goat the time to the peak of the coronary reactive hyperaemia is much longer than in the dog (10-14 s vs 3-4 s), the present study aimed at investigating whether the same effect caused by the NO-inhibition on the maximum flow of the acetylcholine and myogenic hyperaemic responses in the dog, can also be obtained in the goat for the peak flow of the coronary reactive hyperaemia. Experiments performed in anaesthetised goats showed that NO-inhibition reduces the duration of the reactive hyperaemia without affecting the maximum hyperaemic flow. It is suggested that in the reactive hyperaemia the large predominance of metabolic factors prevents the shear stress from playing a role in enhancing the peak flow.