Coronary Atherosclerosis, Cardiac Troponin, and Interleukin-6 in Patients With Chest Pain

The authors determined whether biomarkers of inflammation and myocardial injury—interleukin (IL)-6 and high-sensitivity troponin (hs-cTn)—were associated with the presence and extent of CAD and were independent predictors of major adverse cardiovascular events (MACE) in stable chest pain. Increased inflammation and myocardial injury can be observed in the absence of myocardial infarction or obstructive coronary artery disease (CAD). Using participants from the PROMISE trial, we measured hs-cTn I and IL-6 concentrations and analyzed computed tomography angiography images in the core laboratory for CAD characteristics: significant stenosis (≥70%), high-risk plaque (HRP), Coronary Artery Disease Reporting and Data System (CAD-RADS) categories, segment involvement score (SIS), and coronary artery calcium score. The primary endpoint was a composite MACE (death, myocardial infarction, or unstable angina). We included 1,796 participants (age 60.2 ± 8.0 years; 47.5% men, median follow-up 25 months). In multivariable linear regression adjusted for atherosclerotic cardiovascular disease (ASCVD) risk, hs-cTn was associated with HRP, stenosis, CAD-RADS, and SIS. IL-6 was only associated with stenosis and CAD-RADS. Hs-cTn above median (1.5 ng/L) was associated with MACE in univariable analysis (HR: 2.1 [95% CI: 1.3-3.6]; P = 0.006), but not in multivariable analysis adjusted for ASCVD and CAD. IL-6 above median (1.8 ng/L) was associated with MACE in multivariable analysis adjusted for ASCVD and HRP (HR: 1.9 [95% CI: 1.1-3.3]; P = 0.03), coronary artery calcium (HR: 1.9 [95% CI: 1.0-3.4]; P = 0.04), and SIS (HR: 1.8 [95% CI: 1.0-3.2]; P = 0.04), but not for stenosis or CAD-RADS. In participants with nonobstructive CAD (stenosis 1%-69%), the presence of both hs-cTn and IL-6 above median was strongly associated with MACE (HR: 2.5-2.7 after adjustment for CAD characteristics). Concentrations of hs-cTn and IL-6 were associated with CAD characteristics and MACE, indicating that myocardial injury and inflammation may each contribute to pathways in CAD pathophysiology. This association was most pronounced among participants with nonobstructive CAD representing an opportunity to tailor treatment in this at-risk group. (PROspective Multicenter Imaging Study for Evaluation of Chest Pain [PROMISE]; NCT01174550 )