title: Insulin resistance, lipoproteins, body fat and hemostasis in nonobese men with angina and a normal or abnormal coronary angiogram.
abstract: OBJECTIVE
  The aim of this study was to compare metabolic risk factors in men with anginal chest pain and a normal or abnormal coronary angiogram with those in healthy men.
  
  
  BACKGROUND
  Risk factors for coronary heart disease, including lipoprotein abnormalities, hypertension and adiposity, may be metabolically interlinked, with insulin resistance and hyperinsulinemia being pivotal to these disturbances.
  
  
  METHODS
  Glucose and insulin metabolism, lipids and lipoproteins, hemostasis, blood pressure and body fat distribution were measured in 77 nonobese middle-aged men who had anginal chest pain (39 with an abnormal coronary angiogram and 38 with no detectable angiographic abnormality) and were compared with those of 40 healthy men of similar age and body mass index.
  
  
  RESULTS
  Patients with chest pain had higher insulin responses to an intravenous glucose challenge, lower insulin sensitivity, lower high density lipoprotein (HDL) and subfraction 2 cholesterol, lower apolipoprotein AI, higher triglycerides, greater android fat and higher systolic blood pressure at rest compared with levels in healthy control subjects (p < 0.05). Those with an abnormal coronary angiogram had lower tissue plasminogen activator levels, higher plasminogen activator inhibitor 1 levels and more android fat than did those with a normal angiogram (p < 0.05). Insulin sensitivity correlated positively with HDL (p < 0.05) and subfraction 2 (p < 0.001) cholesterol and negatively with triglycerides (p < 0.01), android fat proportion (p < 0.01) and systolic blood pressure (p < 0.05), whereas insulin response showed converse correlations.
  
  
  CONCLUSIONS
  These findings provide new evidence of the central role of insulin resistance and hyperinsulinemia in the development of risk factors associated with coronary heart disease.
authors.affiliation: Wynn Institute for Metabolic Research, London, England, United Kingdom.
authors.forename: C J
authors.initials: CJ
authors.lastname: Ley
authors.forename: J
authors.initials: J
authors.lastname: Swan
authors.forename: I F
authors.initials: IF
authors.lastname: Godsland
authors.forename: C
authors.initials: C
authors.lastname: Walton
authors.forename: D
authors.initials: D
authors.lastname: Crook
authors.forename: J C
authors.initials: JC
authors.lastname: Stevenson
mesh_terms: D000328:Adult; D000787:Angina Pectoris / Q000097:blood / Q000175:diagnosis / Q000453:epidemiology*; D001823:Body Composition / Q000502:physiology*; D017023:Coronary Angiography; D005951:Glucose Tolerance Test; D006487:Hemostasis / Q000502:physiology*; D006801:Humans; D006946:Hyperinsulinism / Q000453:epidemiology / Q000503:physiopathology; D007333:Insulin Resistance / Q000502:physiology*; D008055:Lipids / Q000097:blood*; D008074:Lipoproteins / Q000097:blood*; D008297:Male; D008875:Middle Aged; D012307:Risk Factors
chemical_list: D008055:Lipids; D008074:Lipoproteins