Why the study?
Coronary low-attenuation plaque burden strongly predicts myocardial infarction in stable chest pain, but its relationship with circulating hs-cTnT and the underlying etiology remained to be determined.
Is low-attenuation coronary plaque burden associated with hs-cTnT release in patients with stable chest pain, and is this mediated by ischemia or inflammation?
Is low-attenuation coronary plaque burden associated with hs-cTnT release in patients with stable chest pain, and is this mediated by ischemia or inflammation?
Low-attenuation plaque burden is independently associated with hs-cTnT levels in stable chest pain patients, but this relationship does not appear to be mediated by ischemia or inflammation.
LAP burden links to hs-cTnT independently of ischemia or inflammation in stable chest pain; hypothesis-generating and requires prospective confirmation before clinical relevance.
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.
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Vecsey-Nagy et al. (2023) studied this question.
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