Low-attenuation coronary plaque burden and troponin release in chronic coronary syndrome: A mediation analysis

Abstract

BackgroundCoronary low-attenuation plaque (LAP) burden is a strong predictor of myocardial infarction in patients with stable chest pain. We aimed to assess the relationship between LAP burden and circulating levels of high-sensitivity cardiac troponin T (hs-cTnT), and to explore the potential underlying etiology in patients undergoing clinically indicated coronary CT angiography (CCTA). MethodsA comprehensive metabolic and lipid panel, as well as C-reactive protein (CRP) and hs-cTnT tests were obtained from consecutive patients with stable chest pain at the time of CCTA. Qualitative and quantitative coronary plaque analysis, CT-derived fractional flow reserve (FFR) calculation, and pericoronary adipose tissue (PCAT) attenuation measurement around the right coronary artery were performed on CCTA images. Linear regression analyses were performed to identify independent associations with hs-cTnT concentration and mediation analysis was used to assess whether ischemia or markers of inflammation mediate hs-cTnT elevation. ResultsIn total, 114 patients (56.3 ​± ​10.6 years, 44.7 ​% female) were enrolled. In multivariable analysis, age (β ​= ​0.04 [95%CI: 0.02; 0.06], p ​< ​0.001), female sex (β ​= ​−0.77 [95%CI: −1.20; 0.33], p ​< ​0.001), and LAP burden (β ​= ​0.03 [95%CI: 0.001; 0.06], p ​= ​0.04) were independently associated with hs-cTnT levels. Mediation analysis, on the other hand, did not identify a significant mediating effect of lesion-specific ischemia based on CT-FFR, circulating CRP levels, or PCAT values between LAP burden and hs-cTnT levels (all p ​> ​0.05). ConclusionAlthough ischemia and inflammation have previously been proposed to mediate the association between LAP burden and hs-cTnT levels, our results did not confirm the role of these pathophysiological pathways in patients with stable chest pain.