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

Objective We aimed to evaluate the association between inflammatory markers and coronary plaque features on coronary computed tomography angiography (CCTA) among asymptomatic individuals. Methods Baseline 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. Results We 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 3rd tertile 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. Conclusion Elevated 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. ### Competing Interest Statement The authors have declared no competing interest. ### Clinical Trial N/A ### Funding Statement No external funding was obtained for this work. ### Author Declarations I confirm all relevant ethical guidelines have been followed, and any necessary IRB and/or ethics committee approvals have been obtained. Yes The details of the IRB/oversight body that provided approval or exemption for the research described are given below: The protocol for the study was approved by the IRB at Baptist Health South Florida. I confirm that all necessary patient/participant consent has been obtained and the appropriate institutional forms have been archived, and that any patient/participant/sample identifiers included were not known to anyone (e.g., hospital staff, patients or participants themselves) outside the research group so cannot be used to identify individuals. Yes I understand that all clinical trials and any other prospective interventional studies must be registered with an ICMJE-approved registry, such as ClinicalTrials.gov. I confirm that any such study reported in the manuscript has been registered and the trial registration ID is provided (note: if posting a prospective study registered retrospectively, please provide a statement in the trial ID field explaining why the study was not registered in advance). Yes I have followed all appropriate research reporting guidelines, such as any relevant EQUATOR Network research reporting checklist(s) and other pertinent material, if applicable. Yes Data included in the manuscript will be made available upon request.