4.3 Article

C-Reactive Protein and Incident Hypertension in Black and White Americans in the REasons for Geographic And Racial Differences in Stroke (REGARDS) Cohort Study

期刊

AMERICAN JOURNAL OF HYPERTENSION
卷 34, 期 7, 页码 698-706

出版社

OXFORD UNIV PRESS
DOI: 10.1093/ajh/hpaa215

关键词

blood pressure; C-reactive protein; hypertension; inflammation; preventive medicine; racial disparities

资金

  1. National Institute of Neurological Disorders and Stroke (NINDS), National Institutes of Health, Department of Health and Human Service [U01 NS041588]
  2. National Institute on Aging (NIA), National Institutes of Health, Department of Health and Human Service [U01 NS041588]

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Inflammation, quantified by higher CRP levels, may partially explain the higher incidence of hypertension among Black US adults.
BACKGROUND More inflammation is associated with greater risk incident hypertension, and Black United States (US) adults have excess burden of hypertension. We investigated whether increased inflammation as quantified by higher C-reactive protein (CRP) explains the excess incidence in hypertension experienced by Black US adults. METHODS We included 6,548 Black and White REasons for Geographic and Racial Differences in Stroke (REGARDS) participants without hypertension at baseline (2003-2007) who attended a second visit (2013-2016). Sexstratified risk ratios (RRs) for incident hypertension at the second exam in Black compared to White individuals were estimated using Poisson regression adjusted for groups of factors known to partially explain the Black-White differences in incident hypertension. We calculated the percent mediation by CRP of the racial difference in hypertension. RESULTS Baseline CRP was higher in Black participants. The Black-White RR for incident hypertension in the minimally adjusted model was 1.33 (95% confidence interval 1.22, 1.44) for males and 1.15 (1.04, 1.27) for females. CRP mediated 6.6% (95% confidence interval 2.7, 11.3%) of this association in females and 19.7% (9.8, 33.2%) in males. In females, CRP no longer mediated the Black-White RR in a model including waist circumference and body mass index, while in males the Black-White difference was fully attenuated in models including income, education and dietary patterns. CONCLUSIONS Elevated CRP attenuated a portion of the unadjusted excess risk of hypertension in Black adults, but this excess risk was attenuated when controlling for measures of obesity in females and diet and socioeconomic factors in males. Inflammation related to these risk factors might explain part of the Black-White disparity in hypertension.

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