title: Difference in elevation of N-terminal pro-BNP and conventional cardiac markers between patients with ST elevation vs non-ST elevation acute coronary syndrome.
abstract: BACKGROUND
  N-terminal pro-B-type natriuretic peptide (NT-proBNP) is elevated in patients with acute coronary syndrome (ACS), and is a powerful predictor of long-term mortality. Differences in the clinical utility and pathophysiological implication of NT-proBNP and conventional cardiac markers in patients with ST elevation (STE) vs non-STE (NSTE) ACS were investigated in the present study.
  
  
  RESULTS
  Ninety consecutive patients admitted with acute chest pain and a diagnosis of unstable angina or acute myocardial infarction were analyzed. Patients with >or=Killip class II were excluded to focus on the effect of myocardial ischemia on the release of cardiac markers. The markers were measured on admission and analyzed according to the time from onset. Conventional cytosolic marker (creatine kinase-MB) and myofibril marker (troponin T: TnT) were both significantly higher in STE-ACS patients compared with NSTE-ACS patients. Conversely, NT-proBNP was significantly higher in NSTE-ACS patients than STE-ACS especially within 3 h of onset, suggesting a larger ischemic insult despite the smaller extent of myocardial necrosis compared with STE-ACS patients. There was no significant correlation between NT-proBNP level and left ventricular ejection fraction (LVEF) obtained at acute-phase echocardiography in either NSTE-ACS patients (LVEF 57.7+/-11.2%) or STE-ACS patients (LVEF 55.1+/-12.7%). Comparison between NT-proBNP and TnT levels revealed a marked difference of elevations, with significantly augmented elevation of NT-proBNP (p<0.001) in NSTE-ACS patients as compared with prominent elevation of TnT in STE-ACS patients.
  
  
  CONCLUSIONS
  NT-proBNP is an early sensitive marker of myocardial ischemia that rises much higher in the earlier phase as compared with conventional markers of myocardial damage, especially in NSTE-ACS patients.
authors.affiliation: The First Department of Internal Medicine, Nippon Medical School, Tokyo 113-8603, Japan.
authors.forename: Akio
authors.initials: A
authors.lastname: Ogawa
authors.forename: Yoshihiko
authors.initials: Y
authors.lastname: Seino
authors.forename: Teruyo
authors.initials: T
authors.lastname: Yamashita
authors.forename: Ken-ichi
authors.initials: K
authors.lastname: Ogata
authors.forename: Teruo
authors.initials: T
authors.lastname: Takano
mesh_terms: D000368:Aged; D000789:Angina, Unstable / Q000097:blood*; D015415:Biomarkers / Q000097:blood; D003328:Coronary Thrombosis / Q000097:blood / Q000503:physiopathology; D052279:Creatine Kinase, MB Form / Q000097:blood*; D004562:Electrocardiography; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000097:blood*; D017202:Myocardial Ischemia / Q000097:blood* / Q000503:physiopathology; D009206:Myocardium / Q000473:pathology; D020097:Natriuretic Peptide, Brain / Q000097:blood*; D009336:Necrosis / Q000473:pathology; D010446:Peptide Fragments / Q000097:blood*; D013577:Syndrome; D013616:Tachycardia, Sinus / Q000097:blood / Q000503:physiopathology; D020107:Troponin T / Q000097:blood*; D018487:Ventricular Dysfunction, Left / Q000503:physiopathology
chemical_list: D015415:Biomarkers; D010446:Peptide Fragments; D020107:Troponin T; C109794:pro-brain natriuretic peptide (1-76); D020097:Natriuretic Peptide, Brain; D052279:Creatine Kinase, MB Form