title: Lipoprotein phenotype and adhesion molecules correlate with diurnal triglyceride profiles in patients with coronary artery disease.
abstract: OBJECTIVE
  To assess the relationships between different diurnal triglyceride (TG) profiles (p) and the atherogenicity of the lipoprotein phenotype and adhesion molecule concentrations in patients with coronary artery disease (CAD).
  
  
  RESULTS
  Repeated measurements of fasting TG and TGp were made in 29 CAD patients; fasting cholesterol levels (total-C, VLDL, LDL, HDL and small dense LDL) and soluble cell adhesion molecules (sCAM) (ICAM-1 and E-selectin) were measured once. Three different TGps were defined: fasting (137.0 +/- 60.7 mg/dL) and all other TG levels <200 mg/dL (LL; n=7); a fasting TG level <200 mg/dL (147.0 +/- 49.9 mg/dL) and maximum TG levels >200 mg/dL (LH; n=13); and both fasting (225.1+/-76.2 mg/dL) and maximum TG levels >200 mg/dL (HH; n=9). We then analysed the associations between the TGp types and the lipoprotein phenotype and CAMs. LL had significantly lower values than LH (p<0.05 for all parameters except sE-selectin) and HH (p<0.05 for all parameters) of VLDL (11.2 +/- 5.8, 18.8 +/- 9.4, 28.1 +/- 8.8 mg/dL), LDL-5 (11.6 +/- 3.3, 16.4 +/- 4.5, 22.1 +/-7.9 mg/dl) and LDL-6 (12.0 +/- 3.2, 17.0 +/- 5.7, 25.7 +/- 9.6 mg/dL), sICAM-1 (209.4 +/- 30.3, 267.5 +/- 60.6, 273.4 +/- 59.1 ng/dL) and sE-selectin (25.1 +/- 17.6, 35.5 +/- 11.5, 48.5 +/- 20.2 ng/dL).
  
  
  CONCLUSIONS
  Although the differences in fasting TG levels between the LL and LH groups were not significantly different, LH had a more atherogenic lipoprotein phenotype and higher concentrations of adhesion molecules. TGp measurements seem to be suitable for identifying CAD patients with an unfavourable diurnal TG and atherosclerosis-prone lipoprotein metabolism.
authors.affiliation: Freiburg University Hospital, Center for Internal Medicine, Department of Rehabilitative and Preventive Sports Medicine, Freiburg, Germany. schmidt@msm1.ukl.uni-freiburg.de
authors.forename: A
authors.initials: A
authors.lastname: Schmidt-Trucksäss
authors.forename: M W
authors.initials: MW
authors.lastname: Baumstark
authors.forename: C
authors.initials: C
authors.lastname: Daub
authors.forename: S
authors.initials: S
authors.lastname: Espenschied
authors.forename: D
authors.initials: D
authors.lastname: Grathwohl
authors.forename: A
authors.initials: A
authors.lastname: Berg
mesh_terms: D000368:Aged; D001786:Blood Glucose / Q000378:metabolism; D015815:Cell Adhesion Molecules / Q000097:blood*; D002784:Cholesterol / Q000097:blood; D002940:Circadian Rhythm / Q000502:physiology*; D003324:Coronary Artery Disease / Q000097:blood* / Q000209:etiology; D019040:E-Selectin / Q000097:blood; D005260:Female; D006801:Humans; D006949:Hyperlipidemias / Q000097:blood* / Q000150:complications; D018799:Intercellular Adhesion Molecule-1 / Q000097:blood; D008075:Lipoproteins, HDL / Q000097:blood; D008077:Lipoproteins, LDL / Q000097:blood; D008297:Male; D008875:Middle Aged; D010641:Phenotype; D012307:Risk Factors; D014280:Triglycerides / Q000097:blood*
chemical_list: D001786:Blood Glucose; D015815:Cell Adhesion Molecules; D019040:E-Selectin; D008075:Lipoproteins, HDL; D008077:Lipoproteins, LDL; D014280:Triglycerides; D018799:Intercellular Adhesion Molecule-1; D002784:Cholesterol