title: Elevated D-dimer concentration identifies patients with incomplete recanalization of pulmonary artery thromboemboli despite 6 months anticoagulation after the first episode of acute pulmonary embolism.
abstract: BACKGROUND
  Despite long-term anticoagulation in some patients after acute pulmonary embolism (APE) pulmonary thrombi are not completely resolved. We hypothesized that elevated D-dimer concentration reflecting increased endogenous fibrinolysis may indicate incomplete pulmonary thrombi resolution after the first episode of PE.
  
  
  METHODS
  55 patients aged 54.7+/-18.6 years were anticoagulated for 6 months with acenocumarol (74.5% patients) or low molecular weight heparin (25.5% patients) when control spiral computed tomography (sCT), lung perfusion scintigraphy and D-dimer assessment were performed.
  
  
  RESULTS
  Incomplete recanalization of pulmonary circulation was found in 39 (70.9%) patients - thrombi at sCT and/or > or =1 wedge-shaped perfusion defect at scintigraphy. Age, sex, rate of unprovoked APE, malignancies, thrombolysis in the acute phase and type of long-term anticoagulation were similar in patients without and with complete recanalization. D-dimer at follow-up but not on admission was higher in patients with then without incomplete recanalization (median 340 (80-2280) vs 160 (60-390) ng/mL, p=0.02). All 11 (20%) patients with D-dimer level >500 ng/mL at follow-up did not resolve thromboemboli completely. ROC analysis showed that D-dimer at follow-up identified patients with incomplete recanalization (AUC 0.709, 95% CI (0.560-0.831), p=0.007). Multivariable analysis confirmed that D-dimer >350 ng/mL at follow-up and right ventricle dysfunction at the diagnosis were independent predictors of incomplete recanalization (OR 18.58 (95% CI 1.97-175.19) and 7.03 (95% CI 1.43-34.6), respectively, p=0.0006).
  
  
  CONCLUSIONS
  Elevated D-dimer after 6 months anticoagulation and right ventricular dysfunction at the diagnosis predict incomplete recanalization of pulmonary circulation after first episode of APE.
authors.affiliation: Department of Internal Medicine and Cardiology, Medical University of Warsaw, Poland.
authors.forename: Anna
authors.initials: A
authors.lastname: Kaczyńska
authors.forename: Maciej
authors.initials: M
authors.lastname: Kostrubiec
authors.forename: Ryszard
authors.initials: R
authors.lastname: Pacho
authors.forename: Jolanta
authors.initials: J
authors.lastname: Kunikowska
authors.forename: Piotr
authors.initials: P
authors.lastname: Pruszczyk
mesh_terms: D000074:Acenocoumarol / Q000627:therapeutic use; D000328:Adult; D000368:Aged; D000925:Anticoagulants / Q000627:therapeutic use*; D019540:Area Under Curve; D015415:Biomarkers / Q000097:blood; D005260:Female; D005338:Fibrin Fibrinogen Degradation Products / Q000378:metabolism*; D005500:Follow-Up Studies; D006495:Heparin, Low-Molecular-Weight / Q000627:therapeutic use; D006801:Humans; D008297:Male; D008875:Middle Aged; D011651:Pulmonary Artery / Q000601:surgery*; D011655:Pulmonary Embolism / Q000000981:diagnostic imaging / Q000188:drug therapy* / Q000601:surgery*; D036542:Tomography, Spiral Computed
chemical_list: D000925:Anticoagulants; D015415:Biomarkers; D005338:Fibrin Fibrinogen Degradation Products; D006495:Heparin, Low-Molecular-Weight; C036309:fibrin fragment D; D000074:Acenocoumarol