Systemic Inflammation and CT-Derived Coronary Plaque Characteristics Among Asymptomatic US Adults: The Miami Heart Study

Abstract

AbstractObjectiveWe aimed to evaluate the association between inflammatory markers and coronary plaque features on coronary computed tomography angiography (CCTA) among asymptomatic individuals.MethodsBaseline data from Miami Heart Study — an ongoing prospective community-based study of a primary prevention cohort from the Greater Miami Area without prior known CAD — were used for this cross-sectional analysis. Independent variables included high-sensitivity C-reactive protein (hsCRP; <2 vs ≥ 2mg/L) and Interleukin-6 (IL–6; in tertiles). The outcomes of interest were CCTA-based plaque findings: any plaque, CAC>0, CAC>100, maximal stenosis >50%, and high-risk plaque. Multivariable logistic regression models were constructed to evaluate the association between inflammatory markers and coronary plaque features.ResultsWe evaluated 2,342 participants (50.4% men; mean age 53.4±6.7 years, 47% Hispanic, 43% non-Hispanic White, 8.3% diabetes, 56% hypertension, 22% on statin therapy). After adjusting for age, sex, and race/ethnicity, hsCRP ≥2 mg/L was associated with increased odds of having any plaque on CCTA [odds ratio (OR), 1.31 (95% confidence interval [CI], 1.09–1.58)] and stenosis ≥ 50% [OR, 1.69 (95% CI, 1.18–2.41)]. participants with IL–6 levels in 3rdtertile were associated with higher odds of detecting any plaque [OR, 1.59 (95% CI, (1.27–1.99)], CAC >0 [OR, 1.34 (95% CI, 1.06–1.69)], ≥50% stenosis [OR, 2.41 (95% CI, 1.56–3.81)], and any high-risk plaque [OR, 2.41 (95% CI, 1.56–3.81)] Further adjustment for LDL, diabetes, hypertension, obesity, and tobacco use yielded nonsignificant associations.ConclusionElevated levels of hsCRP and IL–6 are associated with the presence of coronary plaque and stenosis on CCTA when adjusted for demographics. However, these associations became nonsignificant after adjusting for additional cardiovascular risk factors. Our findings suggest a role of systemic inflammation as a mediator of the effect of cardiovascular risk factors on coronary plaque burden.