title: Hyperglycemia is associated with enhanced thrombin formation, platelet activation, and fibrin clot resistance to lysis in patients with acute coronary syndrome.
abstract: OBJECTIVE
  Acute hyperglycemia on admission for acute coronary syndrome worsens the prognosis in patients with and without known diabetes. Postulated mechanisms of this observation include prothrombotic effects. The aim of this study was to evaluate the effect of elevated glucose levels on blood clotting in acute coronary syndrome patients.
  
  
  METHODS
  We studied 60 acute coronary syndrome patients within the first 12 h after pain onset, including 20 subjects with type 2 diabetes, 20 subjects with no diagnosed diabetes but with glucose levels >7.0 mmol/l, and 20 subjects with glucose levels <7.0 mmol/l. We determined generation of thrombin-antithrombin complexes (TATs) and soluble CD40 ligand (sCD40L), a platelet activation marker, at the site of microvascular injury, together with ex vivo plasma fibrin clot permeability and lysis time.
  
  
  RESULTS
  The acute coronary syndrome patients with no prior diabetes but elevated glucose levels had increased maximum rates of formation and total production of TATs (by 42.9%, P < 0.0001, and by 25%, P < 0.0001, respectively) as well as sCD40L release (by 16.2%, P = 0.0011, and by 16.3%, P < 0.0001, respectively) compared with those with normoglycemia, whereas diabetic patients had the highest values of TATs and sCD40L variables (P < 0.0001 for all comparisons). Patients with hyperglycemia, with no previously diagnosed diabetes, had longer clot lysis time (by approximately 18%, P < 0.0001) similar to that in diabetic subjects, but not lower clot permeability compared with that in normoglycemic subjects.
  
  
  CONCLUSIONS
  Hyperglycemia in acute coronary syndrome is associated with enhanced local thrombin generation and platelet activation, as well as unfavorably altered clot features in patients with and without a previous history of diabetes.
authors.affiliation: Institute of Cardiology, Jagiellonian University School of Medicine, Cracow, Poland. mmundas@cyf-kr.edu.pl
authors.forename: Anetta
authors.initials: A
authors.lastname: Undas
authors.forename: Ilona
authors.initials: I
authors.lastname: Wiek
authors.forename: Ewa
authors.initials: E
authors.lastname: Stêpien
authors.forename: Krzysztof
authors.initials: K
authors.lastname: Zmudka
authors.forename: Wieslawa
authors.initials: W
authors.lastname: Tracz
mesh_terms: D054058:Acute Coronary Syndrome / Q000097:blood* / Q000150:complications; D000208:Acute Disease; D000368:Aged; D001777:Blood Coagulation; D003924:Diabetes Mellitus, Type 2 / Q000097:blood / Q000150:complications* / Q000188:drug therapy; D003925:Diabetic Angiopathies / Q000097:blood; D005260:Female; D005337:Fibrin / Q000378:metabolism*; D005342:Fibrinolysis / Q000502:physiology*; D006801:Humans; D006943:Hyperglycemia / Q000097:blood* / Q000453:epidemiology; D007004:Hypoglycemic Agents / Q000627:therapeutic use; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000097:blood; D015539:Platelet Activation; D011379:Prognosis; D013917:Thrombin / Q000378:metabolism*
chemical_list: D007004:Hypoglycemic Agents; D005337:Fibrin; D013917:Thrombin