You are here

  • Home
  • Archive
  • Volume 78, Issue 9
  • Exploring the role of blood pressure in the black-white disparity in cardiovascular disease mortality: a causal mediation analysis

Article Text

Article menu
Download PDFPDF
Original research
Exploring the role of blood pressure in the black-white disparity in cardiovascular disease mortality: a causal mediation analysis
  1. Fan Zhao1,
  2. Risha Gidwani2,3,
  3. May C Wang4,
  4. Liwei Chen1,
  5. Roch A Nianogo1,5
  1. 1 Department of Epidemiology, Fielding School of Public Health, University of California Los Angeles (UCLA), Los Angeles, California, USA
  2. 2 RAND, Santa Monica, California, USA
  3. 3 Department of Health Policy and Management, Fielding School of Public Health, University of California, Los Angeles (UCLA), Los Angeles, California, USA
  4. 4 Department of Community Health Science, Fielding School of Public Health, University of California, Los Angeles (UCLA), Los Angeles, California, USA
  5. 5 5California Center for Population Research (CCPR), Los Angeles, California, USA
  1. Correspondence to Dr Fan Zhao, Epidemiology, University of California Los Angeles, Los Angeles, CA 90095-1772, USA; zhaofan1996{at}g.ucla.edu

Abstract

Background Cardiovascular diseases (CVDs) are the leading cause of death in the USA, and high blood pressure is a major risk factor for CVD. Despite the overall declining rates of CVD mortality in the USA in recent years, marked disparities between racial and ethnic groups persist, with black adults having a higher mortality rate than white adults. We investigated the extent to which blood pressure mediated the black-white disparity in CVD mortality.

Methods Data came from the Multi-Ethnic Study of Atherosclerosis, a diverse longitudinal cohort. We included 1325 black and 2256 white community-based adults aged 45–80 years free of clinical CVD at baseline and followed for 14 years. We used causal mediation analysis to estimate the effect of race on CVD mortality that was mediated through blood pressure.

Results Black participants had a higher hazard of dying from CVD compared with white participants (adjusted hazard ratio (HR): 1.28 (95% CI 0.88, 1.88)), though estimates were imprecise. Systolic blood pressure mediated 27% (HR: 1.02, 95% CI 1.00, 1.06) and diastolic blood pressure mediated 55% (HR: 1.07, 95% CI 1.01, 1.10) of the racial disparities in CVD mortality between white and black participants. Mediation effects were present in men but not in women.

Conclusions We found that black-white differences in blood pressure partially explain the observed black-white disparity in CVD mortality, particularly among men. Our findings suggest that public health interventions targeting high blood pressure prevention and management could be important strategies for reducing racial disparities in CVD mortality.

  • BLOOD PRESSURE
  • EPIDEMIOLOGY
  • CARDIOVASCULAR DISEASES

Data availability statement

Data are available upon reasonable request. Data from the Multi-Ethnic Study of Atherosclerosis (MESA) are publicly available upon request (https://www.mesa-nhlbi.org). The analysis codes for implementing the mediation analysis are available upon reasonable request.

https://doi.org/10.1136/jech-2024-222037

Statistics from Altmetric.com

    Request Permissions

    If you wish to reuse any or all of this article please use the link below which will take you to the Copyright Clearance Center’s RightsLink service. You will be able to get a quick price and instant permission to reuse the content in many different ways.

    Data availability statement

    Data are available upon reasonable request. Data from the Multi-Ethnic Study of Atherosclerosis (MESA) are publicly available upon request (https://www.mesa-nhlbi.org). The analysis codes for implementing the mediation analysis are available upon reasonable request.

    View Full Text

    Footnotes

    • Contributors FZ contributed to the problem definition, conducted the data analysis and wrote the first draft. FZ is also responsible for the overall content as the guarantor. FZ accepts full responsibility for the work and/or the conduct of the study, had access to the data, and controlled the decision to publish. RAN obtained funding for this study; led the problem definition; conceptualised, implemented and supervised the analysis; contributed to the interpretation of the results; and reviewed and revised the manuscript. MCW, RG and LC contributed to the interpretation of the results and critically reviewed and revised the manuscript. All authors read and approved the final manuscript.

    • Funding This work was supported by grant (1K01MD014163-01A1) from the National Institute on Minority Health and Health Disparities (NIMHD), National Institutes of Health, Bethesda, Maryland.

    • Disclaimer The funder had no role in study design, data collection and analysis, decision to publish or preparation of the manuscript.

    • Competing interests None declared.

    • Provenance and peer review Not commissioned; externally peer reviewed.

    • Supplemental material This content has been supplied by the author(s). It has not been vetted by BMJ Publishing Group Limited (BMJ) and may not have been peer-reviewed. Any opinions or recommendations discussed are solely those of the author(s) and are not endorsed by BMJ. BMJ disclaims all liability and responsibility arising from any reliance placed on the content. Where the content includes any translated material, BMJ does not warrant the accuracy and reliability of the translations (including but not limited to local regulations, clinical guidelines, terminology, drug names and drug dosages), and is not responsible for any error and/or omissions arising from translation and adaptation or otherwise.