Background
Cardiovascular disease (CVD) remains the leading cause of death among adults and affects over 70 million people in the United States[
1]. Despite marked declines in overall prevalence of CVD, racial and ethnic disparities in CVD prevalence exist[
1‐
3]. Increasing evidence suggests that psychosocial factors may play a role in the development of CVD [
4], although this is still debated[
5]. Psychosocial factors including stress, depression, anger, anxiety, and lack of social support have been linked to CVD[
4,
6].
Racial discrimination is gaining attention as an independent factor for CVD. Conceptually defined as a source of acute and lifelong chronic stress [
7‐
10], discrimination may contribute to CVD, indirectly by negatively impacting mental health [
11,
12], inducing unhealthy behavior [
13], or more directly [
14], by inducing inflammation and platelet aggregation, which is an underlying pathophysiologic mechanism of atherosclerosis[
15]. Internalizing unfair treatment rather than talking to others about the experience may further reinforce such stress[
9,
16,
17]. The relationship between racial discrimination and hypertension has been the focus of prior investigations, for which the results have been equivocal[
18‐
20]. However, investigations of racial discrimination and subclinical CVD are limited[
21,
22].
Recent advances in computed tomography (CT) scanning have allowed for the measurement of coronary artery calcification (CAC), which may assist in detecting subclinical CVD by assessing the extent of atherosclerosis[
23]. CAC is a noninvasive measure of subclinical atherosclerotic plaque calcification of the coronary arteries [
23] and has been shown to independently predict coronary heart disease [
6,
24] and coronary events in all racial/ethnic groups[
25,
26]. The presence of CAC has also demonstrated variable ability to detect clinically apparent coronary artery disease[
27].
A study of 181 African-American women revealed that higher levels of CAC were associated with chronic exposure to discrimination[
28]. Investigators reported that for every unit increase in experiencing discrimination, there was a 2.8 fold increase in the odds of having coronary calcification. However, the study sample was limited to middle-aged women, and the measure of discrimination was not specific to racial discrimination. Available literature indicates that this study provided one of the few previous examinations of discrimination as an independent factor for CAC. Our study examined the relationship between self-reported racial discrimination, reaction to unfair treatment and CAC in a population of 571 asymptomatic adults. We hypothesized that discrimination would be associated with higher prevalence of coronary calcification and that individuals who internalized experiences of unfair treatment (i.e., passive response) would also have a higher prevalence of CAC compared to those who talked to others about such experiences (i.e, active response). To our knowledge, this represents the first study to examine these associations in a population of male and female individuals of multiple racial/ethnic groups.
Results
Table
1 depicts the characteristics of the study population. One hundred eighty-six participants (32.6%) had CAC present with scores ranging from 0 to 5098 Agatston (mean = 33, standard deviation = 385). Participants with CAC were older, male, white, had higher BMI, smoked, were diabetic, were hypertensive, had hyperlipidemia, and had a first degree relative with heart disease (p < 0.05 for all variables) compared to participants without calcification. The prevalence of CAC was similar in different education level groups, those reporting high or low depressive symptomatology, and those actively or passively responding to unfair treatment. Among those reporting any discrimination, 46.8% were African American, 36.1% were Hispanic, and 17.1% were white. Discrimination was reported by 35.5% of participants with coronary calcification and by 38.6% of participants without calcification (p = 0.50).
Results of the simple logistic regression model are shown in Table
2. Age and BMI were significantly associated with CAC. Men were 2.5 times more likely to have CAC present compared to females, while African Americans and Hispanics were 45% and 63%, respectively, less likely to have calcification compared to whites. Those who smoked, had diabetes, had hypertension, and had hyperlipidemia were more likely to have CAC present. Those with a 1
st degree relative with heart disease were approximately 1.5 times more likely to have CAC present. Education, depressive symptomatology, response to unfair treatment, and discrimination were not associated with CAC presence in these unadjusted models.
Race/ethnicity did not modify the relationship between discrimination and CAC. However, response to unfair treatment was found to significantly modify this relationship (p < 0.001). Hence, the simple logistic regression model assessing the relationship between discrimination and CAC and the multiple logistic regression results were stratified by active and passive response to unfair treatment. The sensitivity analysis found depression symptomatology to decrease the fit of the model; hence, it was not included in the final adjusted model.
The simple logistic regression models for discrimination and CAC stratified by response to unfair treatment are presented in Table
3. Among those who passively responded, participants who had experienced discrimination were 25% more likely to have CAC present, although this was not statistically significant. Table
4 provides results for the adjusted logistic regression model. Among those who actively responded to unfair treatment, only increasing age, being male, and being Hispanic were significantly associated with the presence of CAC. Among those who passively responded to unfair treatment, increasing age, being male, being African American, and having a positive smoking status were significantly associated with CAC. Interestingly, the odds of having CAC present were approximately 3 times higher for those who experienced discrimination and passively responded to unfair treatment.
Discussion
This study of asymptomatic U.S. adults of different racial/ethnic identity is the first to our knowledge to support the association between experiencing racial discrimination and an increased risk of coronary artery calcification, a marker for atherosclerosis. Our results contradict two other studies that have investigated the influence of racial discrimination or unfair treatment and subclinical atherosclerosis[
28,
36]. Both previous studies were restricted to women and both found that "everyday" discrimination was associated with subclinical coronary artery disease, measured by coronary calcium [
28] and intima-media thickness,[
36] although one reported the association only among African American females and the relationship was not statistically significant[
36]. However, when both studies restricted this association to racial discrimination, the association was no longer apparent. The authors concluded that it is not the attribution of discrimination but the experience of chronic discrimination that influences CAC. Neither study assessed how response to unfair treatment modified the association between self-reported discrimination and sub-clinical atherosclerosis. Our findings parallel studies that have found discrimination to be associated with hypertension among those who passively respond, or internalize their response, to unfair treatment[
9,
16,
17]. Hence, it appears that coping mechanisms, such as speaking out in response to racist events, mitigates the impact of racial discrimination on CAC. These results remained significant after adjusting for smoking status and BMI and suggest future interventional studies are needed that empower individuals and communities to address and respond to everyday inequalities.
Several potential mechanisms linking psychosocial stressors such as self-reported discrimination to the development of coronary artery calcified plaque have been proposed[
10]. Inflammatory induction is a pathophysiologic process that may be mediated by psychosocial stressors. Emerging evidence indicates that CVD development may involve the release of cytokines such as interleukin-6 and tumor necrosis factor α in an inflammatory response to epithelial damage stimulated by acute stressors[
37]. Other possible mechanisms involve adverse health behaviors such as smoking, alcohol consumption, or poor diet in response to stress, which may contribute to risk,[
38] although our results found several of these factors (i.e., smoking, and BMI) did not account for all of the adverse effect from racial discrimination.
The strengths of this study include the use of a validated instrument to measure discrimination and response to unfair treatment, the inclusion of multiracial/ethnic asymptomatic adults, and the use of the MSCT scan to detect coronary calcification. However, our results are subject to a number of limitations. We attempted to measure cumulative discrimination by determining whether participants ever experienced racial discrimination, although it is possible that recall may not be complete. In addition, we did not measure discrimination attributable to other characteristics, such as gender. The cross-sectional nature of the study precludes any statements about causal associations.
Previous research has confirmed that the experience of discrimination or unfair treatment may act as a stressor and that the appraisal of stress may also be important to measure[
18,
20]. Future investigations should include measures of discrimination attributed to multiple characteristics, whether psychosocial factors are intermediate factors in this association, and the moderating effects of coping resources. Potential variation by gender, race, and level of educational attainment should also be incorporated. Finally, the measure of discrimination investigated should reflect a lifecourse perspective and account for cumulative experiences of unfair treatment that may influence the disease process since atherosclerosis develops over an extended period. Moreover, factors that may impact how self-reported and perceived racism is reported should be examined. Variations on how one interprets discrimination, whether due to social status, geographic variation, or personal history, may affect how discrimination is measured[
39]. For example, one study was able to extract thoughts or reports of past racist events among its participants only when they went into in-depth discussions[
40]. Also, types of racist experiences in society have changed over time from more overt events to more subtle ones [
41], such as suppression in social status and its impact on home ownership or higher educational opportunities.
Conclusions
The persistence of racial disparities of CVD warrants investigations regarding the contribution of subjective experiences of discrimination and unfair treatment. Stress-related health literature has the potential to provide future direction. Focused efforts to elucidate whether racial and ethnic minorities differ in response to stressful situations, or types of stressful situations, may provide valuable insight for prevention and amelioration of CVD burden. Finally, because of the temporal lag between subclinical atherosclerosis and clinical coronary heart disease, the use of CAC as an endpoint should be emphasized in future epidemiologic studies of racial disparities in CVD.
Acknowledgements
The authors are grateful for the assistance of Ana L. Chiapa, Mayra Rodriguez, Lorna Brooks and the Primary Care Research Institute staff of the University of North Texas Health Science Center. We also want to thank the clinicians of the North Texas Primary Care Research Network who helped recruit study participants. The project described was supported by Grant Number P20MD001633 from the National Center On Minority Health And Health Disparities and the NIH Loan Repayment Program. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Center On Minority Health and Health Disparities or the National Institutes of Health.
Competing interests
The authors declare that they have no competing interests.
Authors' contributions
RC conceived of the study, design and analyzed the data, and was the primary writer of the manuscript. KMC and KGF assisted in methodology of the study, assisted in data analyses, edited the manuscript. JC oversaw all labs analyses and methodology and edited the manuscript. AE oversaw daily study recruitment and execution of the project and edited the manuscript. CC, JV, RY, and DS all recruited study participants and were involved in manuscript development and editing. All authors read and approved the final manuscript.