title: Metabolic abnormalities characteristic of dysmetabolic syndrome predict the development of transplant coronary artery disease: a prospective study.
abstract: BACKGROUND
  This study examines the hypothesis that metabolic abnormalities of dysmetabolic syndrome are risk factors for transplant coronary artery disease (TxCAD).
  
  
  RESULTS
  Sixty-six patients without overt diabetes, 2 to 4 years after surgery, underwent intracoronary ultrasound (ICUS), measurement of plasma glucose and insulin after oral glucose (75 g), and fasting lipid and lipoproteins. TxCAD incidence by angiography or autopsy was prospectively determined during subsequent follow-up (8 years). Coronary artery intimal thickness (IT) and subsequent outcomes were compared in patients stratified as having "high" versus "low" plasma glucose (>8.9 mmol/L) and insulin (>760 pmol/L) 2 hours after glucose challenge; and "abnormal" versus "normal" fasting lipid and lipoprotein concentrations as defined by the National Cholesterol Education
  
  
  METHODS
  Patients with high glucose or insulin concentrations had greater IT: 0.38+/-0.05 versus 0.22+/-0.02 mm, P</=0.05, and 0.39+/-0.05 versus 0.20+/-0.02 mm, P</=0.01, respectively. Freedom from TxCAD was 56+/-11% versus 81+/-6% (P<0.01) in patients with high versus low glucose and 57+/-10% versus 82+/-7% (P<0.05) in patients with high versus low insulin. Actuarial survival was 60+/-12% versus 92+/-5% (P<0.005) in patients with high versus low glucose and 72+/-9% versus 88+/-6% (P<0.05) in patients with high versus low insulin. Triglycerides and VLDL were higher and HDL was lower in patients with IT >0.3 mm than with IT </=0.3 mm. TxCAD incidence was higher in patients with high plasma TG and VLDL and low HDL.
  
  
  CONCLUSIONS
  These data suggest that insulin resistance plays a role in TXCAD:
authors.affiliation: Division of Cardiovascular Medicine, Department of Cardiothoracic Surgery, Stanford University, Stanford, California, USA.
authors.forename: H
authors.initials: H
authors.lastname: Valantine
authors.forename: P
authors.initials: P
authors.lastname: Rickenbacker
authors.forename: M
authors.initials: M
authors.lastname: Kemna
authors.forename: S
authors.initials: S
authors.lastname: Hunt
authors.forename: Y D
authors.initials: YD
authors.lastname: Chen
authors.forename: G
authors.initials: G
authors.lastname: Reaven
authors.forename: E B
authors.initials: EB
authors.lastname: Stinson
mesh_terms: D000328:Adult; D000368:Aged; D001786:Blood Glucose / Q000032:analysis; D002423:Cause of Death; D015331:Cohort Studies; D003324:Coronary Artery Disease / Q000097:blood / Q000000981:diagnostic imaging / Q000453:epidemiology* / Q000209:etiology; D003430:Cross-Sectional Studies; D018572:Disease-Free Survival; D005951:Glucose Tolerance Test; D016027:Heart Transplantation / Q000401:mortality; D006801:Humans; D007328:Insulin / Q000097:blood; D007333:Insulin Resistance; D015993:Life Tables; D008055:Lipids / Q000097:blood; D008074:Lipoproteins / Q000097:blood; D024821:Metabolic Syndrome / Q000097:blood* / Q000150:complications; D008875:Middle Aged; D011183:Postoperative Complications / Q000000981:diagnostic imaging / Q000453:epidemiology* / Q000209:etiology / Q000378:metabolism; D011446:Prospective Studies; D012307:Risk Factors; D016019:Survival Analysis; D017539:Tunica Intima / Q000000981:diagnostic imaging; D014463:Ultrasonography
chemical_list: D001786:Blood Glucose; D007328:Insulin; D008055:Lipids; D008074:Lipoproteins