Browsing by Author "Valdes, Gloria"

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    Association of Remote Hypertension in Pregnancy With Coronary Artery Disease A Case-Control Study
    (LIPPINCOTT WILLIAMS & WILKINS, 2009) Valdes, Gloria; Quezada, Felipe; Marchant, Eugenio; von Schultzendorff, Astrid; Moran, Sergio; Padilla, Oslando; Martinez, Alejandro
    Because hypertensive pregnancies have been associated with increased cardiovascular disease, we aimed to identify whether angiographically characterized coronary artery disease differed in women with previous normotensive pregnancies or hypertensive pregnancies (HPs). The study group included 217 parous women, aged 60.9 +/- 9.2 (SD) years, who required coronary angiography between January 2006 and December 2007, 36.8 +/- 9.9 and 28.8 +/- 10.5 years after their first and last pregnancy, respectively; 146 had normotensive pregnancies and 71 had >= 1 HP, according to a questionnaire including reproductive history and cardiovascular risks. Body mass index, smoking, and frequency of diabetes were similar in both groups. Chronic hypertension (93% versus 78%; P=0.007), hyperlipidemia (82% versus 69%; P=0.049), and premature familial cardiovascular disease (42% versus 20%; P=0.001) prevailed in HPs. Participants with HPs were younger (58.9 +/- 8.3 versus 61.9 +/- 9.6 years; P=0.025) than participants with normotensive pregnancies. Although 49% of all participants had hemodynamically significant coronary artery disease (>= 70% stenosis), no differences were observed between groups in the number of stenotic arteries; however, their number increased by 28% and 22% over a 10-year period in HPs and normotensive pregnancies, respectively (P=0.034). Multivariate analysis showed that HPs had a nonsignificant risk of having coronary artery disease (odds ratio: 1.21; 95% CI: 0.64 to 2.28), and being a current smoker (odds ratio: 4.13; 95% CI: 1.85 to 9.25), a diabetic (odds ratio: 2.29; 95% CI: 1.85 to 9.25), or having a family history of premature cardiovascular disease (odds ratio: 2.34; 95% CI: 1.17 to 2.39) significantly increased the risk of coronary artery disease. This study demonstrates that women with HPs have earlier coronary disease, probably related to intermediate cardiovascular risks that have a gestational expression. (Hypertension. 2009; 53: 733-738.)
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    Bradykinin Exerts Independent Effects on Trophoblast Invasion and Blood Pressure in Pregnant Guinea Pigs
    (2020) Valdes, Gloria; Acuna, Stephanie; Schneider, Daniela; Ortiz, Rita; Padilla, Oslando
    Introduction: The pleiotropic kininogen-kallikrein-kinin system is upregulated in pregnancy and localizes in the uteroplacental unit. To identify the systemic and local participation of the bradykinin type 2 receptor (B2R), this was antagonized by Bradyzide (BDZ) during 2 periods: from days 20 to 34 and from days 20 to 60 in pregnant guinea pigs. Methods: Pregnant guinea pigs received subcutaneous infusions of saline or BDZ from gestational day 20 until sacrifice on day 34 (Short B2R Antagonism [SH-B2RA]) or on day 60 (Prolonged B2R Antagonism [PR-B2RA]). In SH-BDZA, systolic blood pressure was determined on day 34, while in PR-BDZA it was measured preconceptionally, at days 40 and 60. On gestational day 60, plasma creatinine, uricemia, proteinuria, fetal, placental and maternal kidney weight, and the extent of trophoblast invasion were evaluated. Results: The SH-B2RA increased systolic blood pressure on day 34 and reduced trophoblast myometrial invasion, spiral artery remodeling, and placental sufficiency. The PR-B2RA suppressed the normal blood pressure fall observed on days 40 and 60; vascular transformation, placental efficiency, urinary protein, serum creatinine, and uric acid did not differ between the groups. The proportion of all studied mothers with lost fetuses was greater under BDZ infusion than in controls. Conclusion: The increased systolic blood pressure and transient reduction in trophoblast invasion and fetal/placental weight in the SH-B2R blockade and the isolated impact on blood pressure in the PR-B2R blockade indicate that bradykinin independently modulates systemic hemodynamics and the uteroplacental unit through cognate vascular and local B2R receptors.
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    Endothelial dysfunction - A link among preeclampsia, recurrent pregnancy loss, and future cardiovascular events?
    (LIPPINCOTT WILLIAMS & WILKINS, 2007) Germain, Alfredo M.; Romanik, Mary Carmen; Guerra, Irene; Solari, Sandra; Soledad Reyes, Maria; Johnson, Richard J.; Price, Karen; Karumanchi, S. Ananth; Valdes, Gloria
    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.
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    Expression of kallikrein, bradykinin B2 receptor, and endothelial nitric oxide synthase in placenta in normal gestation, preeclampsia, and placenta accreta
    (2006) Corthorn, Jenny; Germain, Alfredo A.; Chacon, Cecilia; Rey, Sergio; Soto, Gloria X.; Figueroa, Carlos D.; Mueller-Esterl, Werner; Duarte, Ignacio; Valdes, Gloria
    In an effort to define the varied expression of three vasoactive markers in the clinical models of normal placenta/normal invasion (n = 11), preeclampsia/restricted trophoblast invasion (n = 15), and placenta accreta/exaggerated invasion (n = 6), we performed semiquantitative immunohistochemistry for kallikrein, bradykinin 132 receptor, and endothelial nitric oxide synthase (eNOS). In the floating villi, the syncytiotrophoblast expressed more kallikrein in placenta accreta (p < 0.05), than in normal and preeclamptic placentas, while the bradykinin B2 receptor and eNOS were similarly expressed in all groups; in the fetal endothelium, the bradykinin B2 receptor was enhanced in placenta accreta (p < 0.005), but kallikrein and eNOS were similarly expressed in the other two groups. in the extravillous trophoblast, both kallikrein and eNOS expression were higher in placenta accreta (p < 0.001), while the bradykinin B2 receptor signal was only enhanced in preeclampsia (p < 0.05). The presence and localization of kallikrein, the bradykinin B2 receptor, and eNOS in the fetomaternal interface in the three study conditions supports a local role for interrelated vasodilatory/antiaggregating systems. This first report of the variations observed in kallikrein and eNOS in a condition of exaggerated trophoblast invasion supports the participation of vasodilatation in trophoblast migration.