Cardiovascular disease (CVD), including heart disease, heart attack, high blood pressure,
and stroke, is most commonly caused by atherosclerosis, or a hardening of the arteries.
Traditional risk factors for CVD include age, high blood pressure, high cholesterol,
diabetes, and smoking. Although these established risk factors can be helpful in determining
people at risk for developing CVD, the addition of novel gene markers for subclinical, or
suspected, atherosclerosis (SA) may enhance CVD risk prediction and understanding of disease
mechanisms. This study will compare specific genes of white blood cells in people with
significant SA versus people without SA to improve identification of those at risk for
developing CVD and to better understand the biological basis of SA.
CVD is the leading cause of death worldwide and accounts for almost 40% of deaths each year
in the United States. In a person with CVD, oxygenated blood is not adequately distributed
throughout the body because of impaired function in the heart and blood vessels. This
restricted blood flow can eventually lead to organ damage, heart attack, and stroke. Risk
prediction for CVD, which is largely associated with SA, relies on the use of certain
traditional risk factors. The widely used Framingham risk score (FRS) has provided excellent
risk discrimination and reliable estimates of 10-year risk for CVD, but it does not account
for the genetics behind SA. Although numerous studies have investigated novel genetic
biomarkers to attempt to add predictive value to the FRS, no single biomarker to date has
been able to improve risk prediction in a meaningful way. A multi-marker approach that
identifies several novel markers unrelated to traditional risk factors may be more effective
in improving the identification of those at risk for CVD. This study will first construct a
multi-marker approach that is based on patterns of gene expression in peripheral blood
leukocytes (PBLs) and that can serve to identify people with substantial SA. The study will
then use this approach to determine whether gene expression patterns of PBLs in people with
SA are distinct from those in people without SA.
This study will use previously collected data and specimens, including blood samples and SA
imaging, from participants in the Multi-Ethnic Study of Atherosclerosis (MESA) trial and
from healthy female participants from Northwestern University. Blood samples will be used
for analysis of patterns of gene expression in PBLs. There will be no new study visits for
The study completion date listed in this record was obtained from the "Completed Date"
entered in the Query View Report System (QVR).
- Female participant from the MESA study who has a low Framingham risk score and has
either SA or no evidence of SA
- Healthy female below the age of 40 from Northwestern University.