title: Altered hemostatic balance and endothelial activation in pregnant women with familial hypercholesterolemia.
abstract: BACKGROUND
  Patients with familial hypercholesterolemia (FH) are prone to premature cardiovascular disease. During pregnancy plasma lipids reach higher absolute values in FH than in healthy women. Pregnancy is associated with activation of coagulation and possibly also of vascular endothelium, which might further increase the risk of cardiovascular disease in FH. However, whether hemostatic and endothelial activation markers are increased in pregnant FH women compared with non-FH pregnancies, is unknown.
  
  
  METHODS
  Activation markers of hemostasis and endothelium were analyzed in blood samples collected prospectively from 22 heterozygous FH women during pregnancy and compared with those of a reference group of 149 healthy, pregnant women.
  
  
  RESULTS
  A procoagulant pattern was detected in both groups, but was more evident among FH women at least partly due to their enhanced thrombin generation, and because tissue factor pathway inhibitor type 1 increased in the reference group only. Furthermore, plasminogen activator inhibitor type 2 antigen increased more in FH than in the reference group. Whereas C-reactive protein, intercellular adhesion marker-1 and E-selectin did not change appreciably, vascular endothelial cell adhesion molecule 1 rose markedly in FH.
  
  
  CONCLUSIONS
  Increased lipid levels as well as a net procoagulant activity and an enhanced endothelial activation possibly confer additional risks of cardiovascular disease among pregnant FH women.
authors.affiliation: Department of Nutrition, Institute of Basic Medical Sciences, University of Oslo, Oslo, Norway.
authors.forename: Agot L
authors.initials: AL
authors.lastname: Amundsen
authors.forename: Janette
authors.initials: J
authors.lastname: Khoury
authors.forename: Per M
authors.initials: PM
authors.lastname: Sandset
authors.forename: Ingebjørg
authors.initials: I
authors.lastname: Seljeflot
authors.forename: Leiv
authors.initials: L
authors.lastname: Ose
authors.forename: Serena
authors.initials: S
authors.lastname: Tonstad
authors.forename: Tore
authors.initials: T
authors.lastname: Henriksen
authors.forename: Kjetil
authors.initials: K
authors.lastname: Retterstøl
authors.forename: Per O
authors.initials: PO
authors.lastname: Iversen
mesh_terms: D000328:Adult; D001779:Blood Coagulation Factors / Q000032:analysis / Q000037:antagonists & inhibitors; D002318:Cardiovascular Diseases / Q000209:etiology*; D016022:Case-Control Studies; D004730:Endothelium, Vascular / Q000378:metabolism*; D005260:Female; D006801:Humans; D006938:Hyperlipoproteinemia Type II / Q000378:metabolism*; D008055:Lipids / Q000097:blood*; D008075:Lipoproteins, HDL / Q000097:blood; D008077:Lipoproteins, LDL / Q000097:blood; D011247:Pregnancy; D011249:Pregnancy Complications, Cardiovascular / Q000378:metabolism*; D012307:Risk Factors; D014280:Triglycerides / Q000097:blood
chemical_list: D001779:Blood Coagulation Factors; D008055:Lipids; D008075:Lipoproteins, HDL; D008077:Lipoproteins, LDL; D014280:Triglycerides