Epigenomic Dysregulation in Preeclampsia-Associated Chronic Hypertension

NCT ID: NCT01682304

Last Updated: 2022-10-12

Study Results

Results pending

The study team has not published outcome measurements, participant flow, or safety data for this trial yet. Check back later for updates.

Basic Information

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Recruitment Status

COMPLETED

Total Enrollment

12 participants

Study Classification

OBSERVATIONAL

Study Start Date

2012-05-31

Study Completion Date

2014-03-31

Brief Summary

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Preliminary data from the investigator's lab identified novel patterns of differential DNA methylation in genes regulating cardiovascular and metabolic function in blood from women during the first trimester of pregnancy who were destined to develop preeclampsia (PE) in the third trimester. Further, common patterns of differential DNA methylation were found in the common genes from placental tissue at time of birth in the same women after diagnosis with PE, suggesting that the epigenomic patterns that predict pregnancy-induced hypertension may also underlie the development of chronic hypertension years after.

It is unknown whether aberrant DNA methylation in pregnancy-induced hypertension is the mechanism by which chronic hypertension develops in these women remote from pregnancy nor is it known if hypertension remote from PE is as responsive to therapeutic treatment of hypertension compared to women who develop hypertension without history of PE. The investigators plan to objectively test the central hypothesis and attain the objective of this project

Detailed Description

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Women comprise 51% of the total heart disease deaths in the United States (NC with an estimated economic cost expected to climb to more than $258 billion. Hypertension, a prevalent manifestation of early cardiovascular disease, is a silent condition that contributes to significant adverse health consequences. Preeclampsia (PE), a form of pregnancy-induced hypertension diagnosed in the second half of pregnancy, is now established as a non-modifiable risk factor for future development of hypertension. As PE carries a familial risk for future development of PE in female offspring, the implications of increased risk for PE-associated future development of chronic hypertension further compounds the significance of this unique cardiovascular risk. This raises an important health concern, though little is known about the mechanisms underlying risk of PE-associated future chronic hypertension. As epigenetic patterns of DNA methylation are associated with transfer across generations and are known to be dysregulated in PE, we propose to test the central hypothesis that differential DNA methylation patterns in key cardiovascular genes identified in women with PE serve as a biomarker and predictor for therapeutic responsiveness for the remote diagnosis and prognosis of chronic hypertension, respectively. Therefore, the purpose of this study is to identify distinct epigenetic patterns of DNA methylation associated with preeclampsia (PE) that underlie the future development of hypertension and to determine the implication on responses to moderators and therapeutic interventions in the management of chronic hypertension.Univariate analysis of variance will be used to test associations between DNA methylation in genes and chronic hypertension among women with and without a history of preeclampsia. We will use multiple linear regression to examine differences in treatment responses to high blood pressure based on DNA methylation patterns in candidate cardiovascular genes.

Conditions

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Preeclampsia Hypertension Pregnancy Induced Hypertension

Study Design

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Observational Model Type

CASE_CONTROL

Study Time Perspective

PROSPECTIVE

Study Groups

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History of Preeclampsia

Chronic hypertension with history of preeclampsia Chronic hypertension without history of preeclampsia

No interventions assigned to this group

Eligibility Criteria

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Inclusion Criteria

* Female gender
* history of prior pregnancy
* diagnosis of chronic hypertension
* current treatment of chronic hypertension
* age 30 - 50 years old

Exclusion Criteria

* presence of comorbid conditions that influence cardiovascular health (SLE, congenital cardiac anomalies
Minimum Eligible Age

30 Years

Maximum Eligible Age

65 Years

Eligible Sex

FEMALE

Accepts Healthy Volunteers

No

Sponsors

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Ohio State University

OTHER

Sponsor Role lead

Responsible Party

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Cindy Anderson

PhD, WHNP-BC, FAAN

Responsibility Role PRINCIPAL_INVESTIGATOR

Principal Investigators

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Cindy M Anderson, PhD

Role: PRINCIPAL_INVESTIGATOR

Ohio State University

Locations

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The Ohio State University

Columbus, Ohio, United States

Site Status

Countries

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United States

Other Identifiers

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GFHNRC611

Identifier Type: -

Identifier Source: org_study_id

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