Key result
Remodeled non-calcified plaque was associated with significantly higher hsTnT levels compared to normal vessels (26.3 vs 8.3 pg/ml, p<0.001), allowing identification with high accuracy (AUC 0.90).
Why the study?
Do high sensitive troponin T levels correlate with specific CTA characteristics of atherosclerotic plaque in patients with stable coronary artery disease?
Cross-Sectional (n=124)
Do high sensitive troponin T levels correlate with specific CTA characteristics of atherosclerotic plaque in patients with stable coronary artery disease?
High-sensitivity troponin T levels correlate strongly with non-calcified plaque burden and vascular remodeling on CTA, suggesting it may serve as a biomarker for vulnerable coronary lesions in stable CAD.
hsTnT may flag vulnerable plaque on CTA in stable CAD; leaves open whether it refines prognosis or therapy decisions.
OBJECTIVE: To understand the determinants of troponin release in patients with stable coronary artery disease (CAD) by comparing high sensitive troponin T (hsTnT) levels with computed tomography angiography (CTA) characteristics of atherosclerotic plaque. METHODS: hsTnT was determined in 124 consecutive patients with stable angina, who underwent clinically indicated 256-slice CTA for suspected CAD. CTA was used to assess (1) coronary calcification; (2) stenosis severity; (3) non-calcified plaque volume; (4) plaque composition (soft or mixed, described as 'non-calcified' versus calcified) and (5) the presence of vascular remodeling in areas of non-calcified plaque. RESULTS: All CT scans were performed without adverse events, and diagnostic image quality was achieved in 1830/1848 available coronary segments (99.0%). In 29/124 patients, hsTnT was ≥14 pg/ml (range 14.0-34.4). Weak, albeit significant, correlations were found between hsTnT and calcium scoring (r=0.45, p<0.001), while a stronger correlation was found between hsTnT and the total non-calcified plaque burden (r=0.79, p<0.001). Patients with non-calcified plaque (n=44) yielded significantly higher hsTnT values than those with normal vessels (n=46) or those with only calcified lesions (n=26), (12.6 ± 5.2 vs 8.3 ± 2.6 and 8.8 ± 3.0 pg/ml, respectively, p<0.001). Furthermore, those with remodeled non-calcified plaque (n=8) showed even higher hsTnT values of 26.3 ± 6.5 pg/ml than all other groups (p<0.001). This allowed the identification of patients with remodeled non-calcified plaque by hsTnT with high accuracy (area under the curve=0.90, SE=0.07, 95% CI 0.84 to 0.95). CONCLUSIONS: Chronic clinically silent rupture of non-calcified plaque with subsequent microembolisation may be a potential source of troponin elevation. In light of recent imaging studies, in which patients with positively remodeled non-calcified plaque were shown to be at high risk for developing acute coronary syndromes, hsTnT may serve as a biomarker for such 'vulnerable' coronary lesions even in presumably stable CAD.
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Korosoglou et al. (2010) conducted a cross-sectional in stable coronary artery disease (n=124). Remodeled non-calcified plaque vs. Normal vessels or only calcified lesions was evaluated on High sensitive troponin T (hsTnT) levels (AUC 0.90, 95% CI 0.84 to 0.95, p=<0.001). Remodeled non-calcified plaque was associated with significantly higher hsTnT levels compared to normal vessels (26.3 vs 8.3 pg/ml, p<0.001), allowing identification with high accuracy (AUC 0.90).
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