Abstract
IntroductionThe aim of prospective study was to evaluate the ability of echocardiography and cardiac biomarkers to predict in-hospital mortality and the risk of brain infarction during a 12-month follow-up period (FUP) with anticoagulation in pulmonary embolism (PE) patients. MethodsEighty-eight consecutive acute PE patients (39 men, mean age 63 years) were enrolled; 78 underwent baseline echocardiography and brain magnetic resonance imaging (MRI). After a 12-month FUP, 58 underwent brain MRI. In-hospital mortality and the rates of new ischemic brain lesions (IBL) on MRI with clinical ischemic stroke (IS) events were predicted based on echocardiography (patent foramen ovale presence with right-to-left shunt – PFO/RLS; right/left ventricle diameter ratio – RV/LD; tricuspid annulus plane systolic excursion – TAPSE; tricuspid annulus systolic velocity – ST; pulmonary artery systolic pressure – PASP) and biomarkers results (amino-terminal fragment of brain natriuretic peptide – NT-proBNP and cardiac troponin T – cTnT). ResultsOur series involved 88 patients, of whom 11 (12.5%) presented high-risk PE, 24 (27.3%) intermediate-high risk PE, 19 (21.6%) intermediate-low risk PE and 34 (38.6%) patients had low risk PE.Nine patients (10.2%) died during hospitalization including high-risk PE [6/9 (66.6%)] and intermediate-high-risk PE [3/24 (12.5%)]. cTnT [odds ratio (OR) 4.3; 95% confidence interval 0.59–31.3, P=0.014], NT-proBNP (OR 14.2 [1.5–133.4], P=0.02), RV/LD ≥0.79 (OR 36.6 [4.2–316.4], P=0.001), TAPSE (OR 0.55 [0.34–0.92, P=0.022) and PASP ≥51.5mmHg (OR 33.3 [3.8–292.6], P=0.022) were predictors of in-hospital mortality.Seventeen patients (19.3%) experienced IS (n=8) or new IBL (n=9). On multivariate analysis, PFO/RLS (OR 27.1 [3.0–245.3], P=0.003) and ST ≤14.5cm/s (OR 34.1 [CI 3.4–344.0], P=0.003) were independent predictors of IS and IBL risk. ConclusionsHigh blood troponin T, NT-proBNP, RV dilatation/systolic dysfunction and pulmonary hypertension predicted in-hospital mortality. PFO/RLS presence and ST were predictors of clinically apparent/silent brain infarction.
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