Abstract 056: Inflammatory Cytokines And Incident Hypertension In The REasons For Geographic And Racial Differences In Stroke (REGARDS) Study

Abstract

Background: Higher C-reactive protein (CRP) is a risk factor for incident hypertension, but this non-specific inflammatory biomarker does not provide insight into specific immune pathways of hypertension. Here, we studied the role of selected cytokines in risk of incident hypertension to better elucidate these pathways. Objective: To determine the risk for incident hypertension disease among adults by level of IL-1β, IL-6, TNF-α, and IFN-γ. Methods: REGARDS recruited 30,239 Black and White adults aged ≥45 years from the 48 contiguous states in 2003-07. The Biomarkers as Mediators of Racial Disparities in Risk Factors (BioMedioR) substudy included 4,400 sex-race stratified REGARDS participants who also attendd a visit in 2013-16. We excluded those in BioMedioR with prevalent hypertension: 140/90 mm Hg threshold or self-reported antihypertensive medication use. Serum ELISAs assessed cytokines. Modified Poisson regression estimated relative risk (RR) of incident hypertension by detectable threshold (IL-1β; >0.06 pg/mL) or cytokine tertiles (tertile thresholds [33 rd & 66 th %iles] in pg/mL: IL-6, 0.56 & 0.94; TNF-α, 1.30 & 1.69; IFN-γ, 4.01 & 6.56). IL-1β was stratified on race because of a statistically significant interaction. Results: Among the 1,877 participants at risk for incident hypertension (mean [SD] age 62 [8] years, 36% Black race, 51% women), incident hypertension occurred in 31% of White adults and 45% of Black adults. With full adjustment ( Figure ), higher TNF-α and IFN-γ in everyone, and detectable IL-1β in White but not Black adults, were associated with greater incident hypertension risk. There was no association of higher IL-6 with incident hypertension. Conclusions: Among Black and White adults without prevalent hypertension, higher TNF-α, and IFN-γ, and detectable IL-1β (among White but not Black adults), were associated with greater risk of incident hypertension. Future basic and clinical research should study these inflammatory pathways toward developing hypertension prevention strategies.