Journal of cardiovascular computed tomography · 2023
Low-attenuation coronary plaque burden and troponin release in chronic coronary syndrome: A mediation analysis.
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Vecsey-Nagy Milán, Kolossváry Márton, Varga-Szemes Akos, Boussoussou Melinda, Vattay Borbála, Nagy Martin, Juhász Dénes, Merkely Béla, Radovits Tamás, Szilveszter Bálint
Аннотация
BACKGROUND: Coronary 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).
METHODS: A 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.
RESULTS: In 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).
CONCLUSION: Although 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.
METHODS: A 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.
RESULTS: In 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).
CONCLUSION: Although 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.