title: The influence of natural menopause on postprandial lipemia in heterozygotes for familial hypercholesterolemia.
abstract: BACKGROUND
  Heterozygous familial hypercholesterolemia (hFH) is a genetic disease that leads to premature atherosclerosis. Natural menopause leads to an adverse lipid profile and an enhanced risk of coronary heart disease (CHD). Raised plasma triglyceride (TG) levels also contribute to the risk of vascular events. The aim of this study was to evaluate the postprandial TG levels (after a standardized fatty meal) in premenopausal and postmenopausal women with hFH.
  
  
  METHODS
  Thirty-three Greek women with hFH were divided into the premenopausal group--n = 16, mean age 34(SD = 7), mean total cholesterol = 330(30) mg/dl--and the postmenopausal group--n = 17, mean age 62(5), mean total cholesterol = 346(63) mg/dl. Plasma TG concentrations were measured before and 2, 4, 6, and 8 hours after a standardized fat load. A value of >219 mg/dl (2.5 mmol/L) was taken as an abnormal response to the fat load, according to our previous studies.
  
  
  RESULTS
  Postmenopausal women had higher TG levels at 2 (p = 0.001), 4 (p = 0.003), 6 (p = 0.003), and 8 hours (p = 0.005) after the fatty meal compared to premenopausal women. Forty-one percent of postmenopausal hFH women had abnormal TG response (hFH-A) after a fatty meal, and such women had higher fasting TG levels than postmenopausal hFH women with a normal response to the fatty meal (hFH-N) (p = 0.0014).
  
  
  CONCLUSIONS
  Women with hFH tend to have an abnormal TG response to a fatty meal after the menopause. Fasting TG levels may be able to predict the abnormal response to a fatty meal.
authors.affiliation: 1st Cardiology Department, Onassis Cardiac Surgery Center, Athens, Greece. Genkolovou@mail.gr
authors.forename: Genovefa D
authors.initials: GD
authors.lastname: Kolovou
authors.forename: Katherine K
authors.initials: KK
authors.lastname: Anagnostopoulou
authors.forename: Nektarios D
authors.initials: ND
authors.lastname: Pilatis
authors.forename: Mirto
authors.initials: M
authors.lastname: Giannopoulou
authors.forename: Ioannis S
authors.initials: IS
authors.lastname: Hoursalas
authors.forename: Antonis N
authors.initials: AN
authors.lastname: Pavlidis
authors.forename: Evdokia
authors.initials: E
authors.lastname: Adamopoulou
authors.forename: Alexandra I
authors.initials: AI
authors.lastname: Valaora
authors.forename: Dimitri P
authors.initials: DP
authors.lastname: Mikhailidis
authors.forename: Dennis V
authors.initials: DV
authors.lastname: Cokkinos
mesh_terms: D000328:Adult; D000368:Aged; D000704:Analysis of Variance; D001054:Apolipoproteins A / Q000097:blood; D001057:Apolipoproteins E / Q000097:blood; D008076:Cholesterol, HDL / Q000097:blood; D008078:Cholesterol, LDL / Q000097:blood; D003324:Coronary Artery Disease / Q000209:etiology / Q000517:prevention & control; D004041:Dietary Fats / Q000008:administration & dosage*; D005260:Female; D006115:Greece; D006579:Heterozygote; D006801:Humans; D006938:Hyperlipoproteinemia Type II / Q000097:blood / Q000235:genetics / Q000503:physiopathology*; D008055:Lipids / Q000097:blood*; D008593:Menopause; D008875:Middle Aged; D019518:Postprandial Period; D012307:Risk Factors; D013997:Time Factors; D014280:Triglycerides / Q000097:blood
chemical_list: D001054:Apolipoproteins A; D001057:Apolipoproteins E; D008076:Cholesterol, HDL; D008078:Cholesterol, LDL; D004041:Dietary Fats; D008055:Lipids; D014280:Triglycerides