title: Endothelial dysfunction: a link among preeclampsia, recurrent pregnancy loss, and future cardiovascular events?
abstract: We tested the hypothesis that endothelial dysfunction could cause placentation-related defects, persist after the complicated pregnancy, and probably cause cardiovascular disease later in life. Brachial arterial reactivity and factors related to endothelial dysfunction, such as circulating cholesterol, uric acid, nitrites, l-arginine, asymmetrical dimethylarginine, vascular endothelial growth factor, and soluble vascular endothelial growth factor receptor-1, in women with previous healthy pregnancies (n=22), patients with severe preeclampsia (n=25), or patients with recurrent pregnancy loss (n=29), at day 10 of the luteal phase of an ovulatory cycle an average of 11 to 27 months after pregnancy were evaluated. Both groups with placentation defects had a significant decrease in endothelium-dependent dilatation, a higher rate of endothelial dysfunction, lower serum nitrites, and higher cholesterol as compared with control subjects; subjects with previous preeclampsia additionally had higher normal blood pressures and a greater parental prevalence of cardiovascular disease. Patients with recurrent pregnancy loss also demonstrated a significantly lower endothelium-independent vasodilatation. A trend to an inverse correlation was found between serum cholesterol serum and endothelial-mediated vasodilatation in the whole study population. Uric acid, l-arginine, asymmetrical dimethylarginine, vascular endothelial growth factor, and soluble vascular endothelial growth factor receptor-1 were similar in all of the groups. We postulate that endothelial dysfunction may represent a link between preeclampsia and increased cardiovascular disease latter in life and propose that women with unexplained recurrent miscarriages are also at increased cardiovascular risk. The identification and correction of endothelial dysfunction detected during the reproductive stage on obstetric outcome and on cardiovascular diseases needs to be elucidated.
authors.affiliation: Departmentos de Obstetricia/Ginecología, Escuela de Medicina Pontificia Universidad Católica, Santiago, Chile.
authors.forename: Alfredo M
authors.initials: AM
authors.lastname: Germain
authors.forename: Mary Carmen
authors.initials: MC
authors.lastname: Romanik
authors.forename: Irene
authors.initials: I
authors.lastname: Guerra
authors.forename: Sandra
authors.initials: S
authors.lastname: Solari
authors.forename: María Soledad
authors.initials: MS
authors.lastname: Reyes
authors.forename: Richard J
authors.initials: RJ
authors.lastname: Johnson
authors.forename: Karen
authors.initials: K
authors.lastname: Price
authors.forename: S Ananth
authors.initials: SA
authors.lastname: Karumanchi
authors.forename: Gloria
authors.initials: G
authors.lastname: Valdés
mesh_terms: D000026:Abortion, Habitual / Q000097:blood / Q000503:physiopathology*; D000328:Adult; D001794:Blood Pressure; D002318:Cardiovascular Diseases / Q000209:etiology*; D002784:Cholesterol / Q000097:blood; D003971:Diastole; D004730:Endothelium, Vascular / Q000503:physiopathology*; D005260:Female; D006801:Humans; D008499:Medical Records; D010922:Placenta Diseases / Q000209:etiology; D011225:Pre-Eclampsia / Q000097:blood / Q000503:physiopathology*; D011247:Pregnancy; D012307:Risk Factors; D012720:Severity of Illness Index; D013997:Time Factors; D014664:Vasodilation
chemical_list: D002784:Cholesterol