title: Preeclampsia and future cardiovascular disease: potential role of altered angiogenesis and insulin resistance.
abstract: Altered angiogenesis and insulin resistance are associated with preeclampsia and cardiovascular disease (CVD), and women with preeclampsia appear to be at increased risk of future CVD. We hypothesized that these factors are detectable in asymptomatic postpartum women with a history of preeclampsia and may represent pathophysiological mechanisms bridging preeclampsia and future CVD. We measured fasting insulin, glucose, vascular endothelial growth factor, and its circulating inhibitor, soluble fms-like tyrosine kinase (sFlt-1) in 29 normotensive women with a history of preeclampsia and 32 women with prior normotensive pregnancies at 18.0 +/- 9.7 months postpartum. The homeostasis model of insulin resistance (HOMA(IR)) [(insulin [microunits per milliliter] x glucose [millimoles per liter])/22.5] was calculated. Compared with women with normal pregnancies, women with prior preeclampsia had significantly increased levels of sFlt-1 (41.6 +/- 6.7 vs. 30.4 +/- 10.2; P < 0.01) and median HOMA(IR) (2.8 vs. 1.9; P = 0.04). Membership in the upper quartile of either sFlt-1 or HOMA(IR) was associated with prior preeclampsia (odds ratio 5.7; 95% confidence interval 1.7, 20.0; P < 0.01), and all five women in the upper quartiles of both sFlt-1 and HOMA(IR) had a history of preeclampsia. Women with a history of preeclampsia demonstrate altered expression of angiogenesis-related proteins and increased HOMA(IR) more than 1 yr postpartum. These factors may contribute to their risk of future CVD.
authors.affiliation: Renal Unit, Massachusetts General Hospital, Boston, Massachusetts 02114, USA.
authors.forename: Myles
authors.initials: M
authors.lastname: Wolf
authors.forename: Carl A
authors.initials: CA
authors.lastname: Hubel
authors.forename: Chun
authors.initials: C
authors.lastname: Lam
authors.forename: Marybeth
authors.initials: M
authors.lastname: Sampson
authors.forename: Jeffrey L
authors.initials: JL
authors.lastname: Ecker
authors.forename: Roberta B
authors.initials: RB
authors.lastname: Ness
authors.forename: Augustine
authors.initials: A
authors.lastname: Rajakumar
authors.forename: Ashi
authors.initials: A
authors.lastname: Daftary
authors.forename: Alia S M
authors.initials: AS
authors.lastname: Shakir
authors.forename: Ellen W
authors.initials: EW
authors.lastname: Seely
authors.forename: James M
authors.initials: JM
authors.lastname: Roberts
authors.forename: Vikas P
authors.initials: VP
authors.lastname: Sukhatme
authors.forename: S Ananth
authors.initials: SA
authors.lastname: Karumanchi
authors.forename: Ravi
authors.initials: R
authors.lastname: Thadhani
mesh_terms: D000328:Adult; D001786:Blood Glucose / Q000032:analysis; D002318:Cardiovascular Diseases / Q000209:etiology*; D016022:Case-Control Studies; D005215:Fasting / Q000097:blood; D005260:Female; D006801:Humans; D007328:Insulin / Q000097:blood; D007333:Insulin Resistance; D009389:Neovascularization, Pathologic / Q000150:complications* / Q000209:etiology*; D011225:Pre-Eclampsia / Q000097:blood / Q000150:complications* / Q000503:physiopathology*; D011247:Pregnancy; D012995:Solubility; D042461:Vascular Endothelial Growth Factor A / Q000097:blood; D040281:Vascular Endothelial Growth Factor Receptor-1 / Q000097:blood / Q000737:chemistry
chemical_list: D001786:Blood Glucose; D007328:Insulin; D042461:Vascular Endothelial Growth Factor A; D040281:Vascular Endothelial Growth Factor Receptor-1