Edmund F. Funai, M.D.
Associate Professor, Yale University School of Medicine ResearchMajor research interest: the pathophysiology of preeclampsia, especially with regard to nitric oxide availability and metabolism. I am also interested in potential long-term health consequences of this disease, especially as in relation to future cardiovascular morbidity. Other research interests: Molecular mechanism(s) of human parturition, both term and preterm; Biometric predictors of preterm birth: specifically how the length of the cervix may predict preterm birth, and the clinical challenge of how to manage a short cervix. “Preeclampsia: Causes and Consequences” Preeclampsia is a multi-system disorder of pregnancy. It is manifested by new-onset hypertension and proteinuria, and causes derangements of the cardiovascular, renal, and central nervous systems. It affects over 200,000 pregnancies each year in the U.S., occurring in 3-7% of all deliveries. Preeclampsia is also the leading cause of indicated (iatrogenic) preterm birth. The etiology of preeclampsia is still unclear, and the only means of treatment is delivery of the placenta and fetus. While preeclampsia is the second leading cause of acute maternal mortality in the world, little is known about the long-term implications of this disease. Our previous research has shown that following preeclampsia, women have more than a two-fold increase in their long-term risk of death when compared to women who never had preeclampsia. We have also shown that the principal contributor to this excess mortality is cardiovascular disease.  Is preeclampsia a direct cause of cardiovascular-related mortality? It is not clear if preeclampsia, which is well-known to be associated with endothelial cell activation, promotes or hastens atherosclerosis following delivery. While preeclampsia may trigger a cascade of events that result in early mortality, it is also possible that the converse might be true. Women at risk for cardiovascular disease might also be at risk for preeclampsia; this pregnancy complication would thus be a harbinger, a "risk marker", rather than a cause, of future morbidity and mortality. The NHLBI Working Group on Research on Hypertension During Pregnancy recently emphasized the importance of addressing these questions of potential cause and effect. We posit that preeclampsia and cardiovascular disease share a common genetic predilection. We also hypothesize that assessment of maternal vascular response will reveal that some women have prolonged endothelial cell activation following preeclampsia, which may be the result of an intermediate phenotype in the potential clinical spectrum between preeclampsia and cardiovascular disease. Recent PublicationsStraszewski S.L, Abrahams V.M. , Funai EF, Mor G. XIAP Confers Human Trophoblast Cell Resistance to Fas-Mediated Apoptosis. Mol Hum Reprod. 2004 Jan;10(1):33-41 Levey KA, MacKenzie AP, Stephenson C, Bercik R, Kuczynski E, Funai EF. Increased rates of chorioamnionitis with extra-amniotic saline infusion method of labor induction. Obstet Gynecol. 2004 Apr;103(4):724-8. Roque H, Paidas M, Kuczynski E, Funai EF, Lockwood CJ. Inherited thrombophilias are not associated with first trimester pregnancy loss. Thromb Haemost. 2004 Feb;91(2):290-5. Mackenzie, A, Stephenson C, Funai EF, Lee MJ, Timor-Tritsch I. 3-Dimensional ultrasound to differentiate “TRAP” sequence from omphalopagus conjoined twins. (In press: Am J Obstet Gynecol) Funai EF, Friedlander Y, Paltiel OB, Tiram E, Xue X, Hoffman D, Harlap S. Long-term mortality after preeclampsia. (In press: Epidemiology) Funai EF, Paltiel OB, Malaspina D, Friedlander Y Hoffman D, Harlap S. Obstetric risk factors for preeclampsia have similar effects among nulliparous and parous women. (In press: Ped Peri Epi) Stephenson C, Roque H, Funai EF, Lee MJ. Afibrinogenemia in pregnancy; report of two cases. (In press: Am J Hematol) |
