title: Thirty day prognosis of patients with acute pulmonary oedema complicating acute coronary syndromes.
abstract: OBJECTIVE
  To investigate the characteristics of the acute coronary syndromes underlying acute pulmonary oedema and their 30 day prognosis.
  
  
  METHODS
  185 consecutive patients with acute coronary syndromes and acute pulmonary oedema admitted to a tertiary care centre.
  
  
  METHODS
  Clinical, ECG, echocardiographic, enzymatic, and angiographic features were prospectively investigated.
  
  
  RESULTS
  Non-ST segment elevation myocardial infarction (NSTEMI) was the most frequent cause of acute pulmonary oedema (61%) followed by unstable angina (UA; 21%) and ST segment elevation myocardial infarction (STEMI; 18%). In each group, mean age was > or = 70 years, but NSTEMI patients were the oldest and > or = 65% of patients had chronic hypertension. Moreover, patients with NSTEMI and UA were older and had a higher incidence of diabetes, previous myocardial infarction, and moderate to severe mitral regurgitation but a similarly reduced ejection fraction (NSTEMI, 41%; UA, 39%; and STEMI, 39%) and increased incidence of diastolic dysfunction and rate of multivessel disease (94%, 87%, and 86%, respectively). However, patients with STEMI had a higher creatine kinase MB peak concentration (158 v 76 microg/l in the NSTEMI group, p < 0.001) and 30 day mortality (26% v 9% in the NSTEMI group and 8% in the UA group, p < 0.024). Multivariate analysis identified ejection fraction < 40% and a peak creatine kinase MB concentration > 100 microg/l as the main prognostic markers (p < 0.03).
  
  
  CONCLUSIONS
  Acute pulmonary oedema is mostly a complication of elderly hypertensive patients with NSTEMI or UA (82%) and with multivessel disease often associated with mitral regurgitation. On the other hand, the larger infarct size and higher mortality in patients with STEMI with a similarly reduced ejection fraction suggest a more extensive acute systolic loss.
authors.affiliation: Unitat Coronària, Servei de Cardiologia, Hospital General Universitari d'Hebron, Universitat Autònoma de Barcelona, P Vall d'Hebron 119-129, 08035 Barcelona, Spain. 5751jfb@comb.es
authors.forename: J
authors.initials: J
authors.lastname: Figueras
authors.forename: C
authors.initials: C
authors.lastname: Peña
authors.forename: J
authors.initials: J
authors.lastname: Soler-Soler
mesh_terms: D000208:Acute Disease; D000367:Age Factors; D000368:Aged; D000789:Angina, Unstable / Q000150:complications* / Q000401:mortality / Q000503:physiopathology; D017023:Coronary Angiography / Q000379:methods; D003402:Creatine Kinase / Q000097:blood; D052279:Creatine Kinase, MB Form; D004452:Echocardiography / Q000379:methods; D004562:Electrocardiography / Q000379:methods; D005260:Female; D006801:Humans; D007527:Isoenzymes / Q000097:blood; D008297:Male; D009203:Myocardial Infarction / Q000150:complications* / Q000401:mortality / Q000503:physiopathology; D011379:Prognosis; D011446:Prospective Studies; D011654:Pulmonary Edema / Q000209:etiology* / Q000401:mortality / Q000503:physiopathology; D012008:Recurrence
chemical_list: D007527:Isoenzymes; D003402:Creatine Kinase; D052279:Creatine Kinase, MB Form