Abstract
Introduction Whether in patients with acute central sub-massive or non-massive pulmonary embolism, mild troponin I increase (> 0.03 μg/L) predicts in-hospital occurrence of hemodynamic instability and death independent to prognostically relevant clinical, laboratory and echocardiographic information is not fully established. Methods and results We evaluated consecutively patients admitted to the Emergency Room for pulmonary embolism; those in stable hemodynamics in whom central pulmonary embolism was confirmed by spiral-computed tomography were recruited. All participants underwent standardized study protocol, including clinical and diagnostic evaluation for assessment of severity of pulmonary embolism; therapy was established accordingly; troponin I was measured, but treatment protocol was not affected by knowledge of troponin I levels. Of 90 patients enrolled in the study, 33 (37%) developed hemodynamic instability during hospitalization (on average, 90 h ± 20 from admission). Troponin I was > 0.03 μg/L in 56% of the study population at admission, and predicted occurrence of hemodynamic instability during hospitalization (adjusted hazard ratio 9.8, 95% confidence interval 1.2–79.2), independent to age, gender, co-morbidity, systolic blood pressure, CK-MB, echocardiographic right ventricular dysfunction and other covariates. Twelve patients died during hospitalization (mean time to event 107 h ± 24 from admission); troponin I > 0.03 μg/L predicted mortality in univariate analysis, but not after accounting for age, sex and clinical variables. Nevertheless, higher troponin as continuous variable correlated with higher likelihood of in-hospital death (adjusted likelihood ratio 2.2/μg/L, 95% confidence interval 1.1–4.3) in multivariate analysis. In a further multivariate model, CK-MB predicted mortality independent of covariates and troponin I. Conclusions In patients with acute central sub-massive or non-massive pulmonary embolism, even mild increase in troponin I > 0.03 μg/L may provide relevant short-term prognostic information independent to clinical, laboratory and echocardiographic data.
Published Version
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