Highly sensitive troponin T assay in normotensive patients with acute pulmonary embolism.

AIMS: To assess the role of cardiac troponin T (cTnT) levels on admission using a new, highly sensitive assay (hsTnT) in the risk assessment of normotensive patients with acute pulmonary embolism (PE). METHODS AND RESULTS: We prospectively studied 156 consecutive normotensive patients with confirmed PE. The prognostic value of hsTnT at baseline was compared with the conventional cTnT troponin assay and with N-terminal pro-brain natriuretic peptide concentrations. Long-term follow-up was available for 153 patients (98.1%). Highly sensitive troponin T values ranged from 0.001 to 357.2 pg/mL [median 27.2 (25th-75th percentile 9.4-69.4) pg/mL]. Overall, 100 patients (64%) had hsTnT > or =14 pg/mL. Baseline hsTnT was higher in patients with an adverse 30-day outcome (> or =1: death, need for catecholamines, endotracheal intubation, or cardiopulmonary resuscitation) compared with an uncomplicated course [71.7 (35.5-117.9) vs. 26.4 (9.2-68.2) pg/mL; P = 0.027]. The cut-off value of 14 pg/mL showed an excellent prognostic sensitivity and negative predictive value (both 100%). In comparison, as many as 50% of the patients with an adverse early outcome would have been misclassified as low risk by cTnT (cut-off 0.03 ng/mL). Logistic regression indicated a two-fold increase in the risk of an adverse outcome for each increase of hsTnT by 1SD of the natural logarithm (P = 0.037). Patients with elevated hsTnT levels had a reduced probability of long-term survival (P = 0.029 by log-rank); by Cox's regression analysis, hsTnT was the only laboratory biomarker predicting an elevated risk of death over the long term. CONCLUSION: Highly sensitive troponin T assays may be capable of improving risk stratification of non-high-risk PE.

A simple score for rapid risk assessment of non-high-risk pulmonary embolism.

OBJECTIVE: We tested whether bedside testing for H-FABP is, alone or integrated in combination models, useful for rapid risk stratification of non-high-risk PE. METHODS: We prospectively studied 136 normotensive patients with confirmed PE. H-FABP was determined using a qualitative bedside-test showing a positive result for plasma concentration >7 ng/ml. RESULTS: Overall, 11 patients (8.1 %) had an adverse 30-day outcome. Of 58 patients (42.6 %) with a positive H-FABP bedside-test, 9 (15.5 %) had an unfavourable course compared to 2 of 78 patients (2.6 %) with a negative test result (p = 0.009). Logistic regression analysis indicated a sevenfold increased risk for an adverse outcome (95 % CI, 1.45-33.67; p = 0.016) for patients with a positive H-FABP bedside-test. Additive prognostic information were obtained by a novel score including the H-FABP bedside-test (1.5 points), tachycardia (2 points), and syncope (1.5 points) (OR 11.57 [2.38-56.24]; p = 0.002 for ≥3 points). Increasing points were associated with a continuous exponential increase in the rate of an adverse 30-day outcome (0 % for patients with 0 points and 44.4 % for ≥5 points). Notably, this simple score provided similar prognostic value as the combination of the H-FABP bedside-test with echocardiographic signs of right ventricular dysfunction (OR 12.73 [2.51-64.43]; p = 0.002). CONCLUSIONS: Bedside testing for H-FABP appears a useful tool for immediate risk stratification of non-high-risk patients with acute PE, who may be at increased risk of an adverse outcome, in particular if integrated in a novel score without the need of echocardiographic examination.