772: Prenatal vascular endothelial growth factor therapy prevents hypertension in the adult offspring in a murine model of preeclampsia induced by overexpression of sFlt-1

772 Prenatal vascular endothelial growth factor therapy prevents hypertension in the adult offspring in a murine model of preeclampsia induced by overexpression of sFlt-1 Julio Mateus, Gennifer Hurst, Esther Tamayo, Gary DV Hankins, Monica Longo, George Saade The University of Texas Medical Branch, Obstetrics & Gynecology, Galveston, TX, The University of Texas Medical Branch, Department of Obstetrics and Gynecology, Galveston, TX OBJECTIVE: Offspring born to pregnant mice with a preeclampsia-like condition induced by overexpression of sFlt-1 develop hypertension later in life. Our objective was to determine the role of maternal vascular endothelial growth factor therapy in preventing this fetal programming of blood pressure (BP) in this animal model of preeclampsia STUDY DESIGN: At day 8 of gestation, CD-1 pregnant mice were randomly allocated to subcutaneous insertion of osmotic minipump to deliver over 10 days either VEGF-121 at a rate of 400 mcg/kg/day (n 8-10) or phosphate buffered-saline solution (PBS) as a solventcontrol (n 4-6). At day 9 of gestation, mice in the VEGF-121 group were injected through the tail vein with Adv-sFlt-1 (109 PFU) or mFc (109 PFU, used as control of the virus), and mice in the PBS group were injected with Adv-sFlt-1 (109 PFU). BP was evaluated in the unrestrained conscious pups at 3 and 6 months of age using catheters inserted through the left carotid artery and tunneled to a subcutaneous telemetric transmitter. BP was recorded continuously for 7 days. One-way ANOVA and post-hoc Tukey test were used for statistical analysis (significance: p 0.05). RESULTS: At 3 months of age, male offspring from the VEGF-sFlt-1 group had significantly lower mean BP than their PBS-sFlt-1 counterpart (Figure). BP was not significantly different between VEGFsFlt-1 and VEGF-mFc mice. A similar pattern was observed in the 6 month-old male offspring. BP remained normal and not significantly different between the 3 groups in female offspring at both 3 and 6 months of age. CONCLUSION: Adult hypertension in males has an origin in utero, and maternal treatment with VEGF-121 prevents the fetal programming of hypertension in this animal model of preeclampsia. 773 HELLP syndrome(s) and severe preeclampsia differentiation according to maternal outcomes: class 1 HELLP syndrome trumps all others Justin Brewer, James Martin, Ashley Canizaro, Pamela Blake, Marie Darby, Rachael Morris, Michelle Owens, Babbette LaMarca, Imran Sunesara University of Mississippi Medical Center, Maternal Fetal Medicine, Jackson, MS, University of Mississippi Medical Center, Obstetrics and Gynecology, Jackson, MS, University of Mississippi Medical Center, Department of OBGYN, Jackson, MS, University of Mississippi Medical Center, Department of Biostatistics, Jackson, MS OBJECTIVE: We explored the prevalence of major maternal morbidity (MMM) for patients with severe preeclampsia (SPRE) and each defined group of HELLP syndrome. STUDY DESIGN: Retrospective cohort study 2000-2007 of patients categorized either as class 1 HELLP syndrome (HELLP1, platelets 70,LDH 600), class 2 (HELLP2, platelets 50,000-100,000150,000), or partial (HELLP4) with only 2 of 3 diagnostic parameters present. All SPRE patients (no HELLP) 2005-2007 were also evaluated. Total MMM for each group was determined. MMM included cardiopulmonary [cardiogenic or noncardiogenic pulmonary edema, pleural or pericardial effusion, pulmonary embolus, indicated intubation, myocardial infarction or arrest], hematologic/coagulation [DIC, transfused blood products], central nervous system/visual [stroke, cerebral edema, hypertensive encephalopathy, vision loss], hepatic [subcapsular hematoma or rupture] or renal complications [acute tubular necrosis or renal failure]. All HELLP1 and HELLP2 patients received corticosteroids, magnesium sulfate and treatment to reduce severe systolic hypertension. Comparison among groups was done using chi-square or fisher exact test at 95% CI. RESULTS: 420 patients had a form of HELLP syndrome 2000-2007; 688 patients had SPRE 2005-2007. The prevalence of MMM for each patient group was determined: HELLP1 41.5%; HELLP2 10.3%; HELLP3 20.0%; HELLP4 21.0%; and SPRE 17.7%. MMM in HELLP1 was significantly increased over all other groups (P 0.001). Combining MMM for HELLP1 HELLP2 produced a prevalence of 22.1% MMM, insignificantly different from all others including lesser HELLP and SPRE (p 0.19), thereby obscuring the significantly elevated MMM of HELLP1 patients. CONCLUSION: Only patients with HELLP1 have significantly increased MMM compared to other HELLP groups or SPRE. Failing to separately evaluate patients with HELLP1 in studies of HELLP syndrome could lead to mistaken conclusions about the effectiveness of a treatment to reduce MMM; any analysis of HELLP treatment should address how well it functions to reduce patient development of HELLP1 and thus minimize MMM. www.AJOG.org Academic Issues, Antepartum Fetal Assessment, Genetics, Hypertension, Medical-Surgical-Disease Poster Session V