title: A derangement of the maternal lipid profile is associated with an elevated risk of congenital heart disease in the offspring.
abstract: OBJECTIVE
  Maternal hyperglycaemia and hyperhomocysteinaemia are risk factors for congenital heart disease (CHD). These metabolic derangements and deranged lipid levels are associated with adult cardiovascular disease. We examined whether maternal lipid levels are associated with the risk of CHD offspring.
  
  
  RESULTS
  From 2003 onwards, a case-control study was conducted. Participants were mothers of children with (n = 261) and without (n = 325) CHD. At around 16 months after the index-pregnancy, maternal lipid levels were determined. Maternal characteristics and lipid levels were compared by Student's t-test. In a multivariable logistic regression model, risk estimates were calculated for associations between CHD and lipid levels. Adjustments were made for maternal age, diabetes, ethnicity, body mass index (BMI), parity, periconception folic acid use and total homocysteine levels. Outcome measures are presented in (geometric) means (p5-p95) and odds ratios (ORs) with 95% confidence intervals (CIs). Case mothers showed higher cholesterol (4.9 vs. 4.7 mmol l(-1), P < 0.05), low-density lipoprotein (LDL)-cholesterol (3.2 vs. 3.0 mmol l(-1), P < 0.05), apolipoprotein B (84.0 vs. 80.0 mg dl(-1), P < 0.01) and homocysteine (10.8 vs. 10.2 μmol l(-1), P < 0.05) than controls. LDL-cholesterol above 3.3 mmol l(-1) (OR 1.6 (95%CI, 1.1-2.3)) and apolipoprotein B above 85.0 mg dl(-1) were associated with an almost twofold increased CHD risk (OR 1.8 (95%CI, 1.2-2.6)). This was supported by elevated CHD risks per unit standard deviation increase in cholesterol (OR 1.2 (95% CI 1.03-1.5)), LDL-cholesterol (OR 1.3 (95%CI, 1.1-1.6) and apolipoprotein B (OR 1.3 (95% CI 1.1-1.6)). Apolipoprotein B was most strongly associated with CHD risk.
  
  
  CONCLUSIONS
  A mildly deranged maternal lipid profile is associated with an increased risk of CHD offspring.
authors.affiliation: Obstetrics and Gynaecology, Division of Obstetrics and Prenatal Medicine, Erasmus MC, University Medical Centre, Dr. Molewaterplein 40, 3015 GD Rotterdam, The Netherlands. h.smedts@erasmusmc.nl
authors.forename: H P M
authors.initials: HP
authors.lastname: Smedts
authors.forename: E M
authors.initials: EM
authors.lastname: van Uitert
authors.forename: O
authors.initials: O
authors.lastname: Valkenburg
authors.forename: J S E
authors.initials: JS
authors.lastname: Laven
authors.forename: M J C
authors.initials: MJ
authors.lastname: Eijkemans
authors.forename: J
authors.initials: J
authors.lastname: Lindemans
authors.forename: E A P
authors.initials: EA
authors.lastname: Steegers
authors.forename: R P M
authors.initials: RP
authors.lastname: Steegers-Theunissen
mesh_terms: D000328:Adult; D001055:Apolipoproteins B / Q000097:blood; D015992:Body Mass Index; D016022:Case-Control Studies; D002648:Child; D008078:Cholesterol, LDL / Q000097:blood; D005260:Female; D005492:Folic Acid / Q000097:blood; D006330:Heart Defects, Congenital / Q000209:etiology / Q000503:physiopathology*; D006710:Homocysteine / Q000097:blood; D006801:Humans; D006943:Hyperglycemia / Q000097:blood / Q000150:complications / Q000503:physiopathology; D020138:Hyperhomocysteinemia / Q000097:blood / Q000150:complications / Q000503:physiopathology; D016015:Logistic Models; D015999:Multivariate Analysis; D016017:Odds Ratio; D011247:Pregnancy; D011249:Pregnancy Complications, Cardiovascular / Q000209:etiology / Q000503:physiopathology*; D012307:Risk Factors; D055815:Young Adult
chemical_list: D001055:Apolipoproteins B; D008078:Cholesterol, LDL; D006710:Homocysteine; D005492:Folic Acid