Cardiovascular risk indicators and perceived race/ethnic discrimination in the Dallas Heart Study

The objective of the study was to evaluate the association between race/ethnic (r/e) discrimination and subclinical cardiovascular disease (CVD). Although r/e discrimination is a chronic stressor that might have negative health effects, cardiovascular data related to experiences with discrimination among different r/e groups in the United States remain sparse.

Using data from the Dallas Heart Study, we assessed the association between perceived r/e discrimination and traditional CVD risk factors, C-reactive protein (CRP), aortic plaque area and wall thickness, and coronary calcium (CAC) score among black, white, and Hispanic participants. Prevalent CAC was defined as a CAC score > or =10 Agatston units; CRP elevation was defined as > or =3 mg/L. Participants were asked, "Have you ever been discriminated against due to your race/ethnicity? (responses: yes, no, or don't know)".

Blacks reported r/e discrimination more frequently than whites or Hispanics (P < .0001). Blacks who reported r/e discrimination were more likely to be college graduates, to have a family history of myocardial infarction, and to be more physically active than blacks who did not report r/e discrimination (each P < .05). Hispanics who reported r/e discrimination had a higher prevalence of smoking (P < .01) and were more likely to be born in the United States. In models that adjusted for traditional CVD risk factors and medication use, we generally found no association between reports of r/e discrimination and aortic wall thickness, aortic plaque area, prevalent CAC, or elevated CRP in any of the r/e groups. Among blacks, stratification by gender and education did not change the observed relationship between perceived r/e discrimination and CAC or CRP.

Although perceived r/e discrimination is associated with certain health characteristics that may result in negative health outcomes, in general, we found no association of r/e discrimination with either subclinical atherosclerosis as determined by CAC score, aortic wall thickness and aortic plaque area, or inflammation as assessed by elevated CRP levels.