S144 Canadian Journal of CardiologyVolume 29 2013

Characterization of aortic remodeling following Kawasakidisease: Toward a fully-developed automatic bi-parametricmodel. Medical Physics 2012;30(10):6104-6110.

Neonatal and current biometric dataIUGR (n=18) Normal (n=17) p value

Birth-weight (g) 1 438 ± 614 3 317 ± 510 0.000

Umbilical artery pulsatility index 1.54 ± 0.36 1.23 ± 0.21 0.007

Current Weight (z-score -0.18 ± 1.05 0.48 ± 1.14 0.089

Current Height (z-score) -0.52 ± 0.88 0.43 ± 1.23 0.013

Current BMI (z-score) -0.06 ± 1.08 0.22 ± 1.25 0.746

Current Systolic BP (z-score) 0.38 ± 0.72 -0.27 ± 0.91 0.023

Current Diastolic BP (z-score) 0.08 ± 0.65 -0.26 ± 0.57 0.103

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Featured Research

140IMPACT OF MATERNAL PRE-PREGNANCY DYSLIPIDEMIAEXPOSURE ON ADULT OFFSPRING LIPID LEVELS

M Mendelson, A Lyass, RB D'Agostino, Sr., D Levy

Boston, Massachusetts

OBJECTIVE: To examine the relationship between maternalhypercholesterolemia prior to pregnancy and variations inadult offspring lipid levels.BACKGROUND: Maternal health and in utero exposures areimportant determinants of cardiovascular disease outcomesamong adult offspring. The risk of developing dyslipidemia isnot fully explained by known genetic variants and lifestylefactors. Epigenetic factors, influenced by maternal inheritanceor fetal intrauterine exposure, may explain part of the vari-ability and ‘missing heritability’ of lipid traits.METHODS: Analysis of prospectively collected clinical and labo-ratory data from the three generations of Framingham HeartStudy (FHS) participants. The study sample included adultoffspring in the second and third generation cohorts of the FHSwith maternal examinations prior to the participants’ birth. Theprimary outcome was offspring total cholesterol (TC) andsecondary outcomes included LDL and HDL, measured at thefirst assessment in the FHS, with all outcomes examined ascontinuous and dichotomous variables. Dyslipidemia wasdefined as TC �5.17mmol/L, LDL �3.36mmol/L, or HDL<1.03mmol/L in men and<1.29mmol/L in women. Exposuremeasures includedmaternal lipids (TC, LDL, andHDL) prior topregnancy with the effect of maternal lipids w30 years afterpregnancy used as a comparison group. Analysis includedsummary statistics, and multiple linear and logistic regressionmodels adjusting for age, gender, and additional covariates.RESULTS: There were 493 FHS participants with maternal ex-aminations prior to pregnancy. The average maternal age at

assessment was 31 (SD 6) years, BMI 22.9 (3.2) kg/m2, and theaverage offspring age at assessment was 22 (5) years, BMI 24.2(4.8) kg/m2. In fully adjusted models, the odds ratio for offspringdyslipidemia was increased to 3.2 (95% CI 1.6-3.2, p¼0.0008)from 1.9 (1.0-3.5, p¼0.044) for abnormal TC, increased to 4.7(2.0-11, p¼0.0004) from 1.6 (0.8-3.5, p¼0.21) for abnormalLDL, and decreased to 2.5 (1.3-5.0, p¼0.008) from 6.7 (2.5-18,p¼0.0002) for abnormal HDL, with exposure to maternal pre-pregnancy as compared to post-pregnancy dyslipidemia.CONCLUSION: The odds of adult offspring dyslipidemia withabnormal TC and LDL arew1.5 and 3x greater, respectively, ifthe mother had dyslipidemia prior to pregnancy as compared todyslipidemia post-pregnancy. Further research examining theinfluence of maternal dyslipidemia exposure on offspringepigenetic elements, especially modifiable factors, in relation tolipid and CVD outcomes, is needed. Interventions to reducedyslipidemia among women prior to pregnancy may influencemaladaptive epigenetic changes and modify the vicious trans-generational cycle of dyslipidemia and CVD-morbidity.

141MATERNAL HYPOTHYROIDISM MAY BE ASSOCIATED WITHCONGENITAL HEART DISEASE IN OFFSPRING

M Grattan, D Thomas, L Hornberger, R Hamilton, W Midodzi,S Vohra

Edmonton, Alberta

OBJECTIVES: This study tested whether mothers with maternalhypothyroidism had increased odds of congenital heart disease(CHD) in their offspring.BACKGROUND: Maternal hypothyroidism increases the risk offetal demise, prematurity and pre-eclampsia, and can negativelyimpact on neurodevelopment. Prior studies have postulateda relationship between maternal thyroid function and CHDbut this relationship has not been directly investigated.METHODS AND RESULTS: A retrospective maternal-child dyadssurvey was conducted in the Echocardiography Laboratory atthe Hospital for Sick Children, Toronto, Canada over a 17month period to obtain a history of maternal thyroid status.Pediatric echocardiograms were evaluated prospectively forCHD by a blinded pediatric cardiologist. Logistic analysis wasperformed to examine the association between CHD andmaternal hypothyroidism.

Of the 998 maternal-child dyads with complete data, 10%(99/998) of the mothers reported a history of prenatal hy-pothyroidism. The overall incidence of CHD in the studysample was 63.1% (630/998). Mothers with a history ofhypothyroidism were significantly more likely to have offspringwith CHD (72.4%) compared to mothers without a history ofhypothyroidism (61.1%). After adjustment in the multivariatemodel for maternal age (>35 years), risk of fetal aneuploidy,maternal diabetes and family history of CHD, the odds ratio(95% confidence interval) for CHD in offspring associated withreported maternal hypothyroidism was 1.68 (1.02-2.78).CONCLUSION: This study suggests that maternal hypothy-roidism is a risk factor for the development of CHD. Further