title: Prognostic value of admission glycosylated hemoglobin and glucose in nondiabetic patients with ST-segment-elevation myocardial infarction treated with percutaneous coronary intervention.
abstract: BACKGROUND
  In nondiabetic patients with ST-segment-elevation myocardial infarction, acute hyperglycemia is associated with adverse outcome. Whether this association is due merely to hyperglycemia as an acute stress response or whether longer-term glycometabolic derangements are also involved is uncertain. It was our aim to determine the association between both acute and chronic hyperglycemia (hemoglobin A(₁c) [HbA(₁c)]) and outcome in nondiabetic patients with ST-segment-elevation myocardial infarction.
  
  
  RESULTS
  This observational study included consecutive patients (n=4176) without known diabetes mellitus admitted with ST-segment-elevation myocardial infarction. All patients were treated with primary percutaneous intervention. Both glucose and HbA(1c) were measured on admission. Main outcome measure was total long-term mortality; secondary outcome measures were 1-year mortality and enzymatic infarct size. One-year mortality was 4.7%, and mortality after total follow-up (3.3 ± 1.5 years) was 10%. Both elevated HbA(1c) levels (P<0.001) and elevated admission glucose (P<0.001) were associated with 1-year and long-term mortality. After exclusion of early mortality (within 30 days), HbA(₁c) remained associated with long-term mortality (P<0.001), whereas glucose lost significance (P=0.09). Elevated glucose, but not elevated HbA(₁c), was associated with larger infarct size. After multivariate analysis, HbA(₁c) (hazard ratio, 1.2 per interquartile range; P<0.01), but not glucose, was independently associated with long-term mortality.
  
  
  CONCLUSIONS
  In nondiabetic patients with ST-segment-elevation myocardial infarction, both elevated admission glucose and HbA(₁c) levels were associated with adverse outcome. Both of these parameters reflect different patient populations, and their association with outcome is probably due to different mechanisms. Measurement of both parameters enables identification of these high-risk groups for aggressive secondary risk prevention.
authors.affiliation: Department of Cardiology, Isala Klinieken, Groot Wezenland 20, 8011 JW Zwolle, The Netherlands.
authors.forename: Jorik R
authors.initials: JR
authors.lastname: Timmer
authors.forename: Miriam
authors.initials: M
authors.lastname: Hoekstra
authors.forename: Maarten W N
authors.initials: MW
authors.lastname: Nijsten
authors.forename: Iwan C C
authors.initials: IC
authors.lastname: van der Horst
authors.forename: Jan Paul
authors.initials: JP
authors.lastname: Ottervanger
authors.forename: Robbert J
authors.initials: RJ
authors.lastname: Slingerland
authors.forename: Jan-Henk E
authors.initials: JH
authors.lastname: Dambrink
authors.forename: Henk J G
authors.initials: HJ
authors.lastname: Bilo
authors.forename: Felix
authors.initials: F
authors.lastname: Zijlstra
authors.forename: Arnoud W J
authors.initials: AW
authors.lastname: van 't Hof
mesh_terms: D000328:Adult; D015906:Angioplasty, Balloon, Coronary; D000925:Anticoagulants / Q000627:therapeutic use; D015415:Biomarkers; D001786:Blood Glucose / Q000032:analysis*; D003131:Combined Modality Therapy; D003924:Diabetes Mellitus, Type 2 / Q000097:blood / Q000175:diagnosis; D004562:Electrocardiography; D005260:Female; D005500:Follow-Up Studies; D044882:Glucose Metabolism Disorders / Q000097:blood* / Q000150:complications; D006442:Glycated Hemoglobin / Q000032:analysis*; D006801:Humans; D006943:Hyperglycemia / Q000097:blood*; D053208:Kaplan-Meier Estimate; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000097:blood* / Q000188:drug therapy / Q000401:mortality / Q000473:pathology / Q000628:therapy; D009426:Netherlands / Q000453:epidemiology; D010343:Patient Admission; D011379:Prognosis; D016016:Proportional Hazards Models
chemical_list: D000925:Anticoagulants; D015415:Biomarkers; D001786:Blood Glucose; D006442:Glycated Hemoglobin