Determinants of troponin release in patients with stable coronary artery disease: insights from CT angiography characteristics of atherosclerotic plaque

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 consecu...

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Hauptverfasser: Korosoglou, Grigorios (VerfasserIn) , Lehrke, Stephanie (VerfasserIn) , Mueller, Dirk (VerfasserIn) , Hosch, Waldemar P. (VerfasserIn) , Kauczor, Hans-Ulrich (VerfasserIn) , Humpert, Per Magnus (VerfasserIn) , Giannitsis, Evangelos (VerfasserIn) , Katus, Hugo (VerfasserIn)
Dokumenttyp: Article (Journal)
Sprache:Englisch
Veröffentlicht: April 21, 2011
In: Heart
Year: 2011, Jahrgang: 97, Heft: 10, Pages: 823-831
ISSN:1468-201X
DOI:10.1136/hrt.2010.193201
Online-Zugang:Verlag, lizenzpflichtig, Volltext: https://doi.org/10.1136/hrt.2010.193201
Verlag, lizenzpflichtig, Volltext: https://heart.bmj.com/content/97/10/823
Volltext
Verfasserangaben:Grigorios Korosoglou, Stephanie Lehrke, Dirk Mueller, Waldemar Hosch, Hans-Ulrich Kauczor, Per M. Humpert, Evangelos Giannitsis, Hugo A. Katus

MARC

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520 |a 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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650 4 |a High sensitive troponin T, atherosclerotic plaque 
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