- Email: [email protected]
[301-POS]
Abstracts / Pregnancy Hypertension: An International Journal of Women’s Cardiovascular Health 5 (2015) 53–156
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P300 mg/24 h, or P2+ protein dipstick, or random protein-creatinine ratio P30 mg protein/mmol. Results: As of June 30, 1018 participants (791 Canadian, 113 Australian, 61 Argentinean, 11 Jamaican and 42 UK participants) have been randomized. Conclusions: Results will establish if high dose folic acid supplementation is an effective preventative strategy in women at high risk of developing PE. Disclosures: S. Wen: None. L. Gaudet: None. J. Champagne: None. R. Rennicks White: None. N. Rybak: None. M. Walker: None. doi:10.1016/j.preghy.2014.10.307
[302-POS] Cardiovascular disease in a pregnant woman’s partner as a risk factor for preeclampsia Claire E. Parker, Dorota A. Doherty, Barry N.J Walters (The University of Western Australia, Subiaco, Australia) Disclosures: N.R. Hart: None. doi:10.1016/j.preghy.2014.10.306
[301-POS] Effect of folic acid supplementation in pregnancy on preeclampsia – Folic Acid Clinical Trial (FACT) Shi Wu Wen, Laura Gaudet, Josee Champagne, Ruth Rennicks White, Natalie Rybak, Mark Walker (Ottawa Hospital Research Institute, Ottawa, ON, Canada) Objectives: FACT is an international, multi-center, doubleblind, placebo-controlled, Phase III trial of 3656 women, sponsored by the Ottawa Hospital Research Institute (OHRI) and funded by the Canadian Institutes of Health Research (CIHR). Observational studies suggest that folic acid supplementation during pregnancy reduces the risk of preeclampsia (PE). No randomized controlled trial has been conducted to demonstrate the effect of folic acid supplementation on PE. FACT aims to determine efficacy of a PE prevention strategy using high dose folic acid supplementation from early pregnancy until delivery in women at high risk of developing PE. Methods: Pregnant women between 80/7 and 166/7 weeks gestation, aged P18 years, taking 61.1 mg of folic acid supplementation with at least 1 of the following risk factors for PE: pre-existing hypertension, pre-pregnancy diabetes, twin pregnancy, history of PE, BMI P35 kg/m2. Primary Outcome: PE, defined as Pd90 mmHg on 2 occasions P4 h apart and proteinuria developed in pregnancy P200/7 weeks gestation, or HELLP, hemolysis, serum LDH P600 U/L, serum AST P70 U/L, platelets <100 109/L. Or, superimposed PE, defined as history of pre-existing hypertension with new proteinuria. Proteinuria is defined as: urinary protein
Objectives: Assessing risk of developing a hypertensive disorder of pregnancy (HDP) in nulliparous women is imprecise. Previous evidence suggests that self-reported family history of cardiovascular disease and risk (in particular risk in the woman’s father) may improve identification of preeclampsia (Parker, ISOM 2012). The aim of this study was to evaluate maternal report of paternal family history of cardiovascular disease (CVD) or risk (CVR) as a risk factor for HDP including preeclampsia. Methods: Women were recruited prospectively and reported on cardiovascular health in themselves, their partners and first degree relatives (n = 997). HDP diagnoses were assigned using SOMANZ (2008) criteria. Results: Preeclampsia was diagnosed in 12.6% of women, gestational hypertension in 6.2%. CVD/CVR was reported by 22.3% of mothers (1.7% CVD alone) and 9.3% of partners (1.7% CVD alone). Median age of the women was 27 years (range 16–45), median age of the partners was 30 years (range 26–34). All partners with CVD were under 45 years old (median 32, range 24–39). The median age of men with risk alone was 33 years (range 29–38). Partners’ CVD increased risk of preeclampsia (5.6% vs. 1.7%; OR = 5.07, 95% CI 1.72–14.94, p = .003) adjusted for maternal age, BMI, smoking and maternal CVD/CVR. No increase in risk of gestational hypertension was evident. Partners’ CVR did not appear to increase risk of HDP. Conclusions: History of CVD in the woman’s partner may indicate elevated risk of preeclampsia however, the low frequency of CVD in partners at this young age impacts on the sample size and should be examined in future research. Disclosures: C.E. Parker: None. D.A. Doherty: None. B.N. Walters: None. doi:10.1016/j.preghy.2014.10.308
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P300 mg/24 h, or P2+ protein dipstick, or random protein-creatinine ratio P30 mg protein/mmol. Results: As of June 30, 1018 participants (791 Canadian, 113 Australian, 61 Argentinean, 11 Jamaican and 42 UK participants) have been randomized. Conclusions: Results will establish if high dose folic acid supplementation is an effective preventative strategy in women at high risk of developing PE. Disclosures: S. Wen: None. L. Gaudet: None. J. Champagne: None. R. Rennicks White: None. N. Rybak: None. M. Walker: None. doi:10.1016/j.preghy.2014.10.307
[302-POS] Cardiovascular disease in a pregnant woman’s partner as a risk factor for preeclampsia Claire E. Parker, Dorota A. Doherty, Barry N.J Walters (The University of Western Australia, Subiaco, Australia) Disclosures: N.R. Hart: None. doi:10.1016/j.preghy.2014.10.306
[301-POS] Effect of folic acid supplementation in pregnancy on preeclampsia – Folic Acid Clinical Trial (FACT) Shi Wu Wen, Laura Gaudet, Josee Champagne, Ruth Rennicks White, Natalie Rybak, Mark Walker (Ottawa Hospital Research Institute, Ottawa, ON, Canada) Objectives: FACT is an international, multi-center, doubleblind, placebo-controlled, Phase III trial of 3656 women, sponsored by the Ottawa Hospital Research Institute (OHRI) and funded by the Canadian Institutes of Health Research (CIHR). Observational studies suggest that folic acid supplementation during pregnancy reduces the risk of preeclampsia (PE). No randomized controlled trial has been conducted to demonstrate the effect of folic acid supplementation on PE. FACT aims to determine efficacy of a PE prevention strategy using high dose folic acid supplementation from early pregnancy until delivery in women at high risk of developing PE. Methods: Pregnant women between 80/7 and 166/7 weeks gestation, aged P18 years, taking 61.1 mg of folic acid supplementation with at least 1 of the following risk factors for PE: pre-existing hypertension, pre-pregnancy diabetes, twin pregnancy, history of PE, BMI P35 kg/m2. Primary Outcome: PE, defined as Pd90 mmHg on 2 occasions P4 h apart and proteinuria developed in pregnancy P200/7 weeks gestation, or HELLP, hemolysis, serum LDH P600 U/L, serum AST P70 U/L, platelets <100 109/L. Or, superimposed PE, defined as history of pre-existing hypertension with new proteinuria. Proteinuria is defined as: urinary protein
Objectives: Assessing risk of developing a hypertensive disorder of pregnancy (HDP) in nulliparous women is imprecise. Previous evidence suggests that self-reported family history of cardiovascular disease and risk (in particular risk in the woman’s father) may improve identification of preeclampsia (Parker, ISOM 2012). The aim of this study was to evaluate maternal report of paternal family history of cardiovascular disease (CVD) or risk (CVR) as a risk factor for HDP including preeclampsia. Methods: Women were recruited prospectively and reported on cardiovascular health in themselves, their partners and first degree relatives (n = 997). HDP diagnoses were assigned using SOMANZ (2008) criteria. Results: Preeclampsia was diagnosed in 12.6% of women, gestational hypertension in 6.2%. CVD/CVR was reported by 22.3% of mothers (1.7% CVD alone) and 9.3% of partners (1.7% CVD alone). Median age of the women was 27 years (range 16–45), median age of the partners was 30 years (range 26–34). All partners with CVD were under 45 years old (median 32, range 24–39). The median age of men with risk alone was 33 years (range 29–38). Partners’ CVD increased risk of preeclampsia (5.6% vs. 1.7%; OR = 5.07, 95% CI 1.72–14.94, p = .003) adjusted for maternal age, BMI, smoking and maternal CVD/CVR. No increase in risk of gestational hypertension was evident. Partners’ CVR did not appear to increase risk of HDP. Conclusions: History of CVD in the woman’s partner may indicate elevated risk of preeclampsia however, the low frequency of CVD in partners at this young age impacts on the sample size and should be examined in future research. Disclosures: C.E. Parker: None. D.A. Doherty: None. B.N. Walters: None. doi:10.1016/j.preghy.2014.10.308