{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,4,15]],"date-time":"2026-04-15T14:11:14Z","timestamp":1776262274493,"version":"3.50.1"},"reference-count":37,"publisher":"BMJ","issue":"10","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Heart"],"accepted":{"date-parts":[[2010,6,30]]},"published-print":{"date-parts":[[2011,5,15]]},"abstract":"<jats:sec>\n                  <jats:title>Objective<\/jats:title>\n                  <jats:p>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.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Methods<\/jats:title>\n                  <jats:p>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 \u2018non-calcified\u2019 versus calcified) and (5) the presence of vascular remodeling in areas of non-calcified plaque.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Results<\/jats:title>\n                  <jats:p>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 \u226514\u2005pg\/ml (range 14.0\u201334.4). Weak, albeit significant, correlations were found between hsTnT and calcium scoring (r=0.45, p&lt;0.001), while a stronger correlation was found between hsTnT and the total non-calcified plaque burden (r=0.79, p&lt;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\u00b15.2 vs 8.3\u00b12.6 and 8.8\u00b13.0\u2005pg\/ml, respectively, p&lt;0.001). Furthermore, those with remodeled non-calcified plaque (n=8) showed even higher hsTnT values of 26.3\u00b16.5\u2005pg\/ml than all other groups (p&lt;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).<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Conclusions<\/jats:title>\n                  <jats:p>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 \u2018vulnerable\u2019 coronary lesions even in presumably stable CAD.<\/jats:p>\n               <\/jats:sec>","DOI":"10.1136\/hrt.2010.193201","type":"journal-article","created":{"date-parts":[[2010,9,30]],"date-time":"2010-09-30T22:28:45Z","timestamp":1285885725000},"page":"823-831","source":"Crossref","is-referenced-by-count":157,"title":["Determinants of troponin release in patients with stable coronary artery disease: insights from CT angiography characteristics of atherosclerotic 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