TY - JOUR
T1 - Preeclampsia and future cardiovascular disease
T2 - Potential role of altered angiogenesis and insulin resistance
AU - Wolf, Myles
AU - Hubel, Carl A.
AU - Lam, Chun
AU - Sampson, Marybeth
AU - Ecker, Jeffrey L.
AU - Ness, Roberta B.
AU - Rajakumar, Augustine
AU - Daftary, Ashi
AU - Shakir, Alia S.M.
AU - Seely, Ellen W.
AU - Roberts, James M.
AU - Sukhatme, Vikas P.
AU - Karumanchi, S. Ananth
AU - Thadhani, Ravi
PY - 2004/12
Y1 - 2004/12
N2 - 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 (HOMAIR) [(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 HOMAIR (2.8 vs. 1.9; P = 0.04). Membership in the upper quartile of either sFlt-1 or HOMAIR 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 HOMAIR had a history of preeclampsia. Women with a history of preeclampsia demonstrate altered expression of angiogenesis-related proteins and increased HOMAIR more than 1 yr postpartum. These factors may contribute to their risk of future CVD.
AB - 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 (HOMAIR) [(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 HOMAIR (2.8 vs. 1.9; P = 0.04). Membership in the upper quartile of either sFlt-1 or HOMAIR 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 HOMAIR had a history of preeclampsia. Women with a history of preeclampsia demonstrate altered expression of angiogenesis-related proteins and increased HOMAIR more than 1 yr postpartum. These factors may contribute to their risk of future CVD.
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U2 - 10.1210/jc.2004-0548
DO - 10.1210/jc.2004-0548
M3 - Article
C2 - 15579783
AN - SCOPUS:10344233164
SN - 0021-972X
VL - 89
SP - 6239
EP - 6243
JO - Journal of clinical endocrinology and metabolism
JF - Journal of clinical endocrinology and metabolism
IS - 12
ER -
