title: Endothelin is not elevated in acute pulmonary embolism.
abstract: BACKGROUND
  In acute pulmonary embolism (APE) the increase of pulmonary vascular resistance depends on the thromboli load and potentially on the pulmonary bed contraction caused by neurohormonal reaction. Plasma levels of endothelin were reported to be elevated in pulmonary arterial hypertension. However, there are only a few studies assessing endothelin in patients with APE.
  
  
  METHODS
  Therefore in our study we evaluated endothelin concentration in 55 patients (29M, 26F, age 57+/-19 yrs) with confirmed APE for potential value in risk stratification. Patients were compared with 24 healthy volunteers at similar age. On admission blood samples were collected for plasma endothelin concentration. The quantitative assessment of right ventricular (RV) function was performed by echocardiography.
  
  
  RESULTS
  Endothelin concentrations were similar in APE patients and in control group (1.41(0.22-9.68)pg/mL vs. 1.62(0.27-8.92)pg/mL; p = NS). There was no differences in endothelin levels between APE patients with and without RV dysfunction (1.46(0.38-4.54)pg/mL vs. 1.41(0.22-9.68)pg/mL; p = NS). Endothelin concentration did not differ between patients with serious adverse events and APE group with event-free clinical course (3.19(0.38-4.27)pg/mL vs. 1.38(0.22-9.68)pg/mL; p = NS). There was no significant correlation between endothelin levels and blood saturation, time from the first symptoms, heart rate, blood pressure, tricuspid valve regurgitation pressure gradient and other echocardiographic parameters.
  
  
  CONCLUSIONS
  We concluded that plasma endothelin concentrations assessed on admission are not elevated in patients with APE and it does not play as important role in acute phase of increase of pressure in pulmonary arteries as in chronic pulmonary hypertension.
authors.affiliation: Department of Internal Medicine & Cardiology, The Medical University of Warsaw, Warsaw, Poland. maciej.kostrubiec@wum.edu.pl
authors.forename: Maciej
authors.initials: M
authors.lastname: Kostrubiec
authors.forename: Justyna
authors.initials: J
authors.lastname: Pedowska-Włoszek
authors.forename: Michał
authors.initials: M
authors.lastname: Ciurzyński
authors.forename: Piotr
authors.initials: P
authors.lastname: Bienias
authors.forename: Szymon
authors.initials: S
authors.lastname: Pacho
authors.forename: Marzena
authors.initials: M
authors.lastname: Piaskowska
authors.forename: Piotr
authors.initials: P
authors.lastname: Pruszczyk
mesh_terms: D000208:Acute Disease; D000328:Adult; D000368:Aged; D016022:Case-Control Studies; D004452:Echocardiography / Q000009:adverse effects; D016232:Endothelins / Q000097:blood*; D005260:Female; D006801:Humans; D006976:Hypertension, Pulmonary / Q000097:blood* / Q000000981:diagnostic imaging / Q000503:physiopathology; D008297:Male; D008875:Middle Aged; D011651:Pulmonary Artery / Q000000981:diagnostic imaging / Q000503:physiopathology*; D011655:Pulmonary Embolism / Q000000981:diagnostic imaging* / Q000503:physiopathology; D018497:Ventricular Dysfunction, Right / Q000000981:diagnostic imaging / Q000209:etiology / Q000503:physiopathology*
chemical_list: D016232:Endothelins