Plasma glial fibrillary acidic protein levels are associated with 90-day mortality in patients with cardiogenic shock

Background Glial fibrillary acidic protein (GFAP) has emerged as a potential biomarker for central nervous system injuries in various conditions. Cardiogenic shock (CS) causes systemic hypoperfusion often leading to mental disturbances, but it is not known if GFAP can be used to assess potential cerebral damage and prognosis in CS. Purpose To determine the prognostic value of GFAP as a biomarker in CS. Methods Baseline levels of plasma GFAP were measured from patients that were enrolled in the prospective, multicentre CardShock study conducted between 2010 and 2012. The primary outcome was 90-day all-cause mortality. Survival analyses were performed using the Kaplan-Meier method. The predictive power of the modified CardShock risk score (CSS) for 90-day mortality was assessed using the area under the curve (AUC) of the receiver operating characteristics (ROC) curve. Results Plasma samples from 117 patients were included in this study. Mean age was 67 (±12) years and 88 (75%) were men. Acute coronary syndrome (ACS) was the main aetiology of CS (85%). Confusion was detected in 79 (70%) patients at presentation. Twenty-eight (25%) patients had been resuscitated before inclusion. 90-day all-cause mortality of the overall cohort was 45%. Median plasma GFAP level at baseline was 460 ng/L (interquartile range (IQR) 272–697) for the study cohort. The cutoff value (465 ng/L) for GFAP at baseline was determined using the highest Youden index of the ROC analysis. Using the established cutoff value, we found that higher GFAP levels were associated with increased mortality (Figure 1). GFAP was moderately correlated with lactate at baseline with Spearman correlation coefficient (rs) 0.504 (p < 0.001). GFAP levels were higher in patients with confusion at presentation [median 473 ng/L, (IQR 317–778) vs. 342 ng/L, (IQR 194–636), p = 0.009] and in patients that had been resuscitated from cardiac arrest before inclusion [525 ng/L (IQR 376–909) vs. 395 ng/L (IQR 230–668), p = 0.024]. Adding GFAP level above 465 ng/L as a variable to the CSS slightly improved the model’s predictive power on 90-day all-cause mortality [AUC 0.81, (95% CI 0.73–0.89) vs. AUC 0.79, (95% CI 0.73–0.86)]. Conclusion Higher levels of GFAP at baseline are associated with 90-day all-cause mortality and demonstrate potential as a biomarker for risk stratification in patients experiencing cardiogenic shock.