title: Is abnormal postprandial lipemia a familial risk factor for coronary artery disease in individuals with normal fasting concentrations of triglycerides and cholesterol?
abstract: OBJECTIVE
  To assess the postprandial response to a fat load in patients with coronary artery disease (CAD) and age-matched controls.
  
  
  METHODS
  Postprandial lipemia was assessed in patients with CAD confirmed by angiography (study group, n = 44) and in patients without coronary lesions (control group, n = 20). Family members of patients with CAD were also included (spouses group, n = 22; progeny group, n = 33). Fasting triglyceride and cholesterol concentrations in the control and study groups were less than 2.3 and 6.47 mmol/l, respectively. After initial blood sampling, the patients consumed 30% cream (200 ml/m2 body area). Repeat measurements of triglycerides, total cholesterol and high-density lipoprotein were made after 2, 4, 6, and 8 h.
  
  
  RESULTS
  Changes were most marked in triglyceride concentrations. Peak values were observed after 4 h in the spouses, progeny, and control groups, and after 6 h in the study group. To compensate for the large age span (8-40 years) of the progeny, two subgroups were formed, taking 25 years as the cut-off value. Triglycerides continued to increase until the 4th hour in both subgroups, but the subgroups differed as to the absolute concentration of triglycerides. During the first 6 h of the test, the concentrations were significantly greater in the subgroup of older progeny than in their fathers with CAD.
  
  
  CONCLUSIONS
  These findings indicate that triglycerides are metabolized at a slower rate and remain longer in the circulation of patients with CAD, as compared with patients without CAD. A significantly greater level of postprandial lipemia has been observed in adult progeny of patients with CAD, suggesting a genetic disorder of triglyceride metabolism in these individuals.
authors.affiliation: Department of Cardiology, Pomeranian Academy of Medicine, Szczecin, Poland.
authors.forename: K
authors.initials: K
authors.lastname: Przybycień
authors.forename: Z
authors.initials: Z
authors.lastname: Kornacewicz-Jach
authors.forename: B
authors.initials: B
authors.lastname: Torbus-Lisiecka
authors.forename: M
authors.initials: M
authors.lastname: Naruszewicz
mesh_terms: D000328:Adult; D015415:Biomarkers / Q000097:blood; D002784:Cholesterol / Q000097:blood*; D008076:Cholesterol, HDL / Q000097:blood; D003327:Coronary Disease / Q000097:blood / Q000209:etiology / Q000235:genetics*; D018450:Disease Progression; D005215:Fasting / Q000097:blood*; D020022:Genetic Predisposition to Disease / Q000235:genetics*; D006801:Humans; D006949:Hyperlipidemias / Q000097:blood* / Q000150:complications / Q000235:genetics; D008875:Middle Aged; D019518:Postprandial Period / Q000502:physiology*; D012307:Risk Factors; D014280:Triglycerides / Q000097:blood*
chemical_list: D015415:Biomarkers; D008076:Cholesterol, HDL; D014280:Triglycerides; D002784:Cholesterol