title: Correlation between ST-T-segment changes with markers of hemostasis in patients with acute coronary syndromes.
abstract: BACKGROUND
  Disturbance of the hemostatic and the inflammatory system plays an important role in the pathophysiology of acute coronary syndromes (ACS). Their markers have been shown to predict further coronary events in patients with ACS. The prognostic value of the admission electrocardiogram (ECG), which is commonly used to evaluate ischemia, was studied previously. We investigated the correlation between serum markers of the hemostatic/inflammatory system and ECG changes in ACS.
  
  
  METHODS
  A standard 12-lead ECG was obtained from 85 patients with ACS on admission (0d). Markers of the hemostatic and inflammatory system were measured on admission and after 2 days (2d).
  
  
  RESULTS
  Patients with ST-T-changes had higher fibrinogen and thrombin-antithrombin III complex (TAT) levels than patients without ECG alterations at both times (fibrinogen: 0d: 492 +/- 38 vs. 357 +/- 36 mg/dl, p < 0.01; 2d: 633 +/- 55 vs. 440 +/- 50 mg/dl, p < 0.02; TAT: 0d: 7.2 +/- 1.3 vs. 3.6 +/- 0.7 microg/l, p < 0.05; 2d: 5.3 +/- 0.9 vs. 3.2 +/- 0.5 microg/l, p < 0.05). Tissue-type plasminogen activator (TPA) was elevated in patients with ECG changes initially (10.1 +/- 0.6 vs. 7.2 +/- 0.7 ng/ml, p < 0.02). D-dimers, the acute-phase proteins C-reactive protein, serum amyloid A and the soluble adhesion molecules showed no significance.
  
  
  CONCLUSIONS
  The data reveal a correlation between electrocardiographic changes and hemostasis in patients with ACS. The association of myocardial damage and a disturbed hemostatic system might stratify patients who are at high risk of suffering further coronary events.
authors.affiliation: Medizinische Klinik, Abteilung III, Eberhard-Karls-Universität, Tübingen, Germany. rehlers@rics.bwh.harvard.edu
authors.forename: Raila
authors.initials: R
authors.lastname: Ehlers
authors.forename: Eva
authors.initials: E
authors.lastname: Büttcher
authors.forename: Holger K
authors.initials: HK
authors.lastname: Eltzschig
authors.forename: Silke
authors.initials: S
authors.lastname: Kazmaier
authors.forename: Sebastian
authors.initials: S
authors.lastname: Szabo
authors.forename: Uwe
authors.initials: U
authors.lastname: Helber
authors.forename: Hans Martin
authors.initials: HM
authors.lastname: Hoffmeister
mesh_terms: D000208:Acute Disease; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D001053:Apolipoproteins / Q000097:blood; D015415:Biomarkers / Q000097:blood; D002097:C-Reactive Protein / Q000378:metabolism; D003327:Coronary Disease / Q000097:blood* / Q000175:diagnosis / Q000453:epidemiology; D003331:Coronary Vessels / Q000473:pathology; D004562:Electrocardiography; D005260:Female; D005340:Fibrinogen / Q000378:metabolism; D005500:Follow-Up Studies; D005858:Germany / Q000453:epidemiology; D006487:Hemostasis / Q000502:physiology*; D006801:Humans; D018799:Intercellular Adhesion Molecule-1 / Q000097:blood; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000097:blood / Q000401:mortality; D010343:Patient Admission; D011237:Predictive Value of Tests; D012307:Risk Factors; D000685:Serum Amyloid A Protein; D013223:Statistics as Topic; D016019:Survival Analysis; D013577:Syndrome; D010959:Tissue Plasminogen Activator / Q000097:blood; D019010:Vascular Cell Adhesion Molecule-1 / Q000097:blood
chemical_list: D001053:Apolipoproteins; D015415:Biomarkers; D000685:Serum Amyloid A Protein; D019010:Vascular Cell Adhesion Molecule-1; D018799:Intercellular Adhesion Molecule-1; D005340:Fibrinogen; D002097:C-Reactive Protein; D010959:Tissue Plasminogen Activator