title: C-terminal provasopressin (copeptin) is associated with left ventricular dysfunction, remodeling, and clinical heart failure in survivors of myocardial infarction.
abstract: BACKGROUND
  Acute myocardial infarction (AMI) is associated with left ventricular (LV) dysfunction and clinical heart failure. Arginine vasopressin is elevated in heart failure and the C-terminal of provasopressin (Copeptin) is associated with adverse outcome post-AMI. The aim of this study was to describe the association between Copeptin with LV dysfunction, volumes, and remodeling and clinical heart failure post-AMI.
  
  
  RESULTS
  We studied 274 subjects with AMI. Copeptin was measured from plasma at discharge and subjects underwent echocardiography at discharge and follow-up (median 155 days). Subjects were followed for clinical heart failure for a median of 381 days. Remodeling was assessed as the change (Delta) in LV volumes between echo examinations. Copeptin correlated directly with wall motion index score (WMIS) and inversely with LV ejection fraction (LVEF) at discharge (WMIS, r=0.276, P < .001; LVEF, r=-0.188, P=.03) and follow-up (WMIS, r=0.244, P < .001; LVEF, r=-0.270, P < .001) and with ventricular volumes at follow-up (LVEDV, r=0.215, P=.002; LVESV, r=0.299, P < .001). Copeptin was associated with ventricular remodeling; DeltaEDV; r=0.171, P=0.015, DeltaESV; r=0.186, P=.008. Subjects with increasing LVESV had higher levels of Copeptin (median 6.30 vs. 5.75 pmol/L, P=.012). Subjects with clinical heart failure (n=30) during follow-up had higher Copeptin before discharge (median 13.55 vs. 5.80, P < .001). In a Cox proportional hazards model, Copeptin retained association with clinical heart failure. Kaplan-Meier assessment revealed increased risk in subjects with Copeptin >6.31 pmol/L.
  
  
  CONCLUSIONS
  Copeptin is associated with LV dysfunction, volumes, and remodeling and clinical heart failure post-AMI. Measurement of Copeptin may provide prognostic information and the AVP system may be a therapeutic target in post-MI LV dysfunction.
authors.affiliation: Department of Cardiovascular Sciences, University of Leicester, UK. kelly.dominic@talk21.com
authors.forename: Dominic
authors.initials: D
authors.lastname: Kelly
authors.forename: Iain B
authors.initials: IB
authors.lastname: Squire
authors.forename: Sohail Q
authors.initials: SQ
authors.lastname: Khan
authors.forename: Paulene
authors.initials: P
authors.lastname: Quinn
authors.forename: Joachim
authors.initials: J
authors.lastname: Struck
authors.forename: Nils G
authors.initials: NG
authors.lastname: Morgenthaler
authors.forename: Joan E
authors.initials: JE
authors.lastname: Davies
authors.forename: Leong L
authors.initials: LL
authors.lastname: Ng
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D015415:Biomarkers / Q000097:blood; D005260:Female; D005500:Follow-Up Studies; D006020:Glycopeptides / Q000097:blood*; D006333:Heart Failure / Q000097:blood* / Q000401:mortality; D006801:Humans; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000097:blood* / Q000401:mortality; D015996:Survival Rate / Q000639:trends; D014667:Vasopressins / Q000097:blood*; D018487:Ventricular Dysfunction, Left / Q000097:blood* / Q000401:mortality; D020257:Ventricular Remodeling / Q000502:physiology*
chemical_list: D015415:Biomarkers; D006020:Glycopeptides; C048197:copeptins; D014667:Vasopressins