title: Comparison of 8 biomarkers for prediction of right ventricular hypokinesis 6 months after submassive pulmonary embolism.
abstract: BACKGROUND
  Elevated blood concentrations of troponin proteins or brain natriuretic peptide (BNP) worsen the prognosis of patients with pulmonary embolism (PE). Novel biomarkers that reflect mechanisms of right ventricle (RV) damage from PE may provide additional prognostic value. We compare the prognostic use of BNP, troponin I, D-dimer, monocyte chemoattractant protein-1, matrix metalloproteinase, myeloperoxidase, C-reactive protein, and caspase 3 as biomarkers of RV damage and adverse outcomes in submassive PE.
  
  
  METHODS
  This article used a prospective cohort study of normotensive (systolic blood pressure always >100 mm Hg) patients with computed tomographic angiography-diagnosed PE. All patients underwent echocardiography and phlebotomy at diagnosis, and survivors had another echocardiography 6 months later. We tested each biomarker for prognostic significance, requiring a lower limit 95% CI >0.50 for the area under the receiver operating characteristic curve (AUROC) with a reference standard positive of RV hypokinesis on either echocardiogram. Biomarkers with prognostic significance were dichotomized at the concentration that yielded highest likelihood ratio positive and mortality rates compared (Fisher exact test).
  
  
  RESULTS
  We enrolled 152 patients with complete data. Thirty-seven (24%, 95% CI 18%-32%) had RV hypokinesis. Only BNP and troponin had significant AUROC values as follows: 0.71 (95% CI 0.60-0.81) and 0.71 (95% CI 0.62-0.82), respectively. Overall mortality was 13/153 (8.5%); mortality rate for BNP >100 versus < or =100 pg/mL was 23% versus 3% (P = .003), respectively. Mortality rate for troponin I >0.1 versus < or =0.1 ng/mL was 13% versus 6% (P = .205), respectively.
  
  
  CONCLUSIONS
  Of 8 mechanistically plausible biomarkers, only BNP and troponin I had significant prognostic use with BNP having an advantage for predicting mortality.
authors.affiliation: Department of Emergency Medicine, Carolinas Medical Center, Charlotte, NC 28323-2861, USA. jkline@carolina.rr.com
authors.forename: Jeffrey A
authors.initials: JA
authors.lastname: Kline
authors.forename: Raghid
authors.initials: R
authors.lastname: Zeitouni
authors.forename: Michael R
authors.initials: MR
authors.lastname: Marchick
authors.forename: Jackeline
authors.initials: J
authors.lastname: Hernandez-Nino
authors.forename: Geoffrey A
authors.initials: GA
authors.lastname: Rose
mesh_terms: D015415:Biomarkers / Q000097:blood*; D002097:C-Reactive Protein / Q000032:analysis; D053148:Caspase 3 / Q000097:blood; D018932:Chemokine CCL2 / Q000097:blood; D005338:Fibrin Fibrinogen Degradation Products / Q000032:analysis; D006801:Humans; D020782:Matrix Metalloproteinases / Q000097:blood; D008875:Middle Aged; D020097:Natriuretic Peptide, Brain / Q000097:blood*; D009195:Peroxidase / Q000032:analysis; D011379:Prognosis; D011446:Prospective Studies; D011655:Pulmonary Embolism / Q000097:blood* / Q000150:complications; D012372:ROC Curve; D019210:Troponin I / Q000097:blood*; D014463:Ultrasonography; D018497:Ventricular Dysfunction, Right / Q000097:blood* / Q000000981:diagnostic imaging / Q000209:etiology
chemical_list: D015415:Biomarkers; C111835:CCL2 protein, human; D018932:Chemokine CCL2; D005338:Fibrin Fibrinogen Degradation Products; D019210:Troponin I; C036309:fibrin fragment D; D020097:Natriuretic Peptide, Brain; D002097:C-Reactive Protein; D009195:Peroxidase; D053148:Caspase 3; D020782:Matrix Metalloproteinases