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Sociodemographic Regulation of Cardiovascular Function and Structure

This study has been completed.
Information provided by:
National Heart, Lung, and Blood Institute (NHLBI) Identifier:
First received: May 25, 2000
Last updated: July 28, 2016
Last verified: May 2009
To establish the aspects of ethnicity that are associated with the differential expression of cardiovascular disease processes in African Americans and Caucasian Americans twin children.

Cardiovascular Diseases Heart Diseases Hypertension

Study Type: Observational

Further study details as provided by National Heart, Lung, and Blood Institute (NHLBI):

Study Start Date: September 1996
Study Completion Date: November 2005
Primary Completion Date: November 2005 (Final data collection date for primary outcome measure)
Detailed Description:


Given increasing awareness of the extent to which environments typically faced by ethnic groups differ, environmental influence on these processes may be an important factor that is an aspect of ethnicity. Socioeconomic status (SES) is a useful index of such environments and is associated with cardiovascular disease (CVD). Since behavior is one pathway through which SES influences are thought to be expressed in disease, this study focuses specifically on stress responsivity, which is thought to be linked to the pathophysiology of CVD. Since such disease has its antecedents in childhood, a multiethnic pediatric sample is employed. In addition, the subject sample consists of twins. Investigation of the impact of environments on the expression of CVD can be achieved only with proper control for biological influences.


Subjects completed three laboratory stressors: a video game task, a structured social interview, and the cold pressor. Stress responsivity was assessed, with particular interest being paid to systemic vascular resistance (SVR). Left ventricular mass (LVM) was also assessed. Sophisticated environmentally and genetically informative analyses permitted quantification of environmental impact upon systemic vascular resistance responsivity and left ventricular mass. It was hypothesized that environmental influences (SES) accounted for a greater proportion of the variance in systemic vascular resistance responsivity and left ventricular mass in African Americans than Caucasian Americans. The hypothesis that systemic vascular resistance responsivity was a pathway through which SES exerted its influence on left ventricular mass was also tested.

The study has been extended through November 2005 to continue examination of the investigator's Twin CV Health cohort (519 pairs of twins who will be 14 to 25 years old). The study provides the unique opportunity to better understand the effects of sodium ion (Na+) retention as a mechanism augmenting systemic vascular resistance responsivity (SVR) and changes in vascular function (i.e., endothelium dependent arterial dilation; EDAD), ventricular structure (i.e., left ventricular mass; LVM) and 24-hour ambulatory BP (ABP). The specific aims are to determine: 1) To what extent is environmental stress related to stress induced Na+ retention, SVR responsivity and preclinical markers of essential hypertension risk and are these relationships stronger in African Americans than Caucasian Americans; 2) Whether stress induced Na+ retention is a pathway linking environmental stress with preclinical markers of essential hypertension risk; and 3) Whether behavioral factors (i.e. John Henryism, anger expression, social support, physical activity) moderate effects of environmental stress on stress induced Na+ retention and/or SVR responsivity and in the preclinical markers of essential hypertension risk, particularly in African Americans.


Ages Eligible for Study:   up to 100 Years   (Child, Adult, Senior)
Sexes Eligible for Study:   Male
Accepts Healthy Volunteers:   No
No eligibility criteria
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Please refer to this study by its identifier: NCT00005476

Sponsors and Collaborators
National Heart, Lung, and Blood Institute (NHLBI)
OverallOfficial: Frank Treiber Augusta University
  More Information

Publications: Identifier: NCT00005476     History of Changes
Other Study ID Numbers: 4960
R01HL056622 ( U.S. NIH Grant/Contract )
Study First Received: May 25, 2000
Last Updated: July 28, 2016

Additional relevant MeSH terms:
Cardiovascular Diseases
Heart Diseases processed this record on August 22, 2017