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Aims: Despite growing interest in biomarkers application for risk evaluation in acute pulmonary embolism(APE), no decision-making levels have been defined. Methods and results: We developed a biomarker-based risk stratification in 100 consecutive, normotensive on admission, APE patients(35 males, 65 females, 62± 18 years). On admission serum NT-proBNP and cardiac troponin T(cTnT) levels were assessed and echocardiography was performed. All-cause 40-day mortality was 15% and APE mortality was 8% . In univariable analysis, cTnT >0.07 μ g/L predicted all-cause mortality, hazard ratio(HR)9.2(95% CI: 3.3-26.1, P< 0.0001), and APE mortality, HR 18.1(95% CI: 3.6-90.2, P=0.0004); similarly, NT-proBNP >7600 ng/L predicted all-cause and APE mortalities[HR 6.7(95% CI: 2.4-19.0, P=0.0003) and 7.3(95% CI: 1.7-30.6, P=0.007)]. NT-proBNP< 600 ng/L indicated uncomplicated outcome. Multivariable analysis revealed that cTnT >0.07 μ g/L was the most significant independent predictor, whereas NT-proBNP and systemic systolic blood pressure measured on admission and echocardiographic parameters were non-significant. APE mortality in patients with NT-proBNP ≥ 600 ng/L and cTnT ≥ 0.07 μ g/L reached 33% . NT-proBNP< 600 ng/L indicated group without deaths. APE mortality for patients with NT-proBNP ≥ 600 ng/L and cTnT< 0.07 μ g/L was 3.7% . Incorporation of echocardiographic data did not improve group selection. Conclusion: Simultaneous measurement of serum cTnT and NT-proBNP allows for precise APE prognosis. Normotensive patients on admission with cTnT ≥ 0.07 μ g/L and NT-proBNP ≥ 600 ng/L are at high risk of APE mortality, whereas NT-proBNP< 600 ng/L indicates excellent prognosis.
Aims: Despite growing interest in biomarkers application for risk evaluation in acute pulmonary embolism (APE), no decision-making levels have been defined. Methods and results: We developed a biomarker-based risk stratification in 100 consecutive, normotensive on admission, APE patients (35 males, 65 females, 62 ± 18 years). On admission serum NT-proBNP and cardiac troponin T (cTnT) levels were assessed and echocardiography was performed. All-cause 40-day mortality was 15% and APE mortality was 8% The hazard ratio (HR) 9.2 (95% CI: 3.3-26.1, P <0.0001), and APE mortality, HR 18.1 (95% CI: 3.6 -90.2, P = 0.0004); similarly, NT-proBNP> 7600 ng / Lpredicted all-cause and APE mortalities [HR 6.7 30.6, P = 0.007)]. NT-proBNP <600 ng / L indicates uncomplicated outcome. Multivariable analysis revealed that cTnT> 0.07 μg / L was the most significant independent predictor, whereas NT-proBNP and systemic systolic blood pressure measured on admission and echocardiographic parameters were non-significant. APE mortality in patients with NT-proBNP ≥ 600 ng / L and cTnT ≥ 0.07 μg / L reached 33%. NT-proBNP <600 ng / L group without deaths. APE mortality for patients with NT-proBNP ≥ 600 ng / L and cTnT <0.07 μg / L was 3.7%. Incorporation of echocardiographic data did not improve group selection. Conclusion: Simultaneous measurement of serum cTnT and NT-proBNP allows for precise APE prognosis. Normotensive patients on admission with cTnT ≥ 0.07 μg / L and NT-proBNP ≥ 600 ng / L are at high risk of APE mortality, and NT-proBNP <600 ng / L indicates excellent prognosis.