BACKGROUND: Increased γ-glutamyl transferase (GGT) level is associated with increased oxidative stress, all-cause mortality, the development of cardiovascular disease, and metabolic syndrome. However, its role in acute pulmonary embolism (PE) is unknown. In this study, we aimed to investigate the relationship between GGT and early mortality in patients with acute PE. METHODS: A total of 127 consecutive patients with confirmed PE were evaluated. The optimal cutoff value of GGT to predict early mortality was measured as more than 55 IU/L with 94.4% sensitivity and 66.1% specificity. Patients with acute PE were categorized prospectively as having no increased (group I) or increased (group II) GGT based on a cutoff value. RESULTS: Of these 127 patients, 18 patients (14.2%) died during follow-up. Among these 18 patients, 1 (1.4%) patient was in group I, and 17 (30.9%) patients were in group II (P < .001). γ-Glutamyl transferase level on admission, presence of shock, heart rate, oxygen saturation, right ventricular dilatation/hypokinesia, main pulmonary artery involvement, troponin I, alanine aminotransferase, alkaline phosphatase, and creatinine levels were found to have prognostic significance in univariate analysis. In the multivariate Cox proportional hazards model, GGT level on admission (hazard ratio [HR], 1.015; P = .017), presence of shock (HR, 15.124; P = .005), age (HR, 1.107; P = .010), and heart rate (HR, 1.101; P = .032) remained associated with an increased risk of acute PE-related early mortality after the adjustment of other potential confounders. CONCLUSIONS: We have shown that a high GGT level is associated with worse hemodynamic parameters, and it seems that GGT helps risk stratification in patients with acute PE.
BACKGROUND: Increased γ-glutamyl transferase (GGT) level is associated with increased oxidative stress, all-cause mortality, the development of cardiovascular disease, and metabolic syndrome. However, its role in acute pulmonary embolism (PE) is unknown. In this study, we aimed to investigate the relationship between GGT and early mortality in patients with acute PE. METHODS: A total of 127 consecutive patients with confirmed PE were evaluated. The optimal cutoff value of GGT to predict early mortality was measured as more than 55 IU/L with 94.4% sensitivity and 66.1% specificity. Patients with acute PE were categorized prospectively as having no increased (group I) or increased (group II) GGT based on a cutoff value. RESULTS: Of these 127 patients, 18 patients (14.2%) died during follow-up. Among these 18 patients, 1 (1.4%) patient was in group I, and 17 (30.9%) patients were in group II (P < .001). γ-Glutamyl transferase level on admission, presence of shock, heart rate, oxygen saturation, right ventricular dilatation/hypokinesia, main pulmonary artery involvement, troponin I, alanine aminotransferase, alkaline phosphatase, and creatinine levels were found to have prognostic significance in univariate analysis. In the multivariate Cox proportional hazards model, GGT level on admission (hazard ratio [HR], 1.015; P = .017), presence of shock (HR, 15.124; P = .005), age (HR, 1.107; P = .010), and heart rate (HR, 1.101; P = .032) remained associated with an increased risk of acute PE-related early mortality after the adjustment of other potential confounders. CONCLUSIONS: We have shown that a high GGT level is associated with worse hemodynamic parameters, and it seems that GGT helps risk stratification in patients with acute PE.