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Determinants of troponin release in patients with stable coronary artery disease: insights from CT angiography characteristics of atherosclerotic plaque
  1. Grigorios Korosoglou1,
  2. Stephanie Lehrke1,
  3. Dirk Mueller2,
  4. Waldemar Hosch3,
  5. Hans-Ulrich Kauczor3,
  6. Per M Humpert4,
  7. Evangelos Giannitsis1,
  8. Hugo A Katus1
  1. 1University of Heidelberg, Department of Cardiology, Heidelberg, Germany
  2. 2Philips GmbH Healthcare Division, Hamburg, Germany
  3. 3University of Heidelberg, Department of Radiology, Heidelberg, Germany
  4. 4University of Heidelberg, Department of Medicine I and Clinical Chemistry, Heidelberg, Germany
  1. Correspondence to Dr Grigorios Korosoglou, University of Heidelberg, Department of Cardiology, Im Neuenheimer Feld 410, Heidelberg, 69120, Germany; gkorosoglou{at}hotmail.com

Abstract

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.

  • High sensitive troponin T, atherosclerotic plaque
  • plaque composition, vascular remodeling
  • cardiac CT
  • CT scanning
  • atherosclerosis

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Footnotes

  • Competing interests None.

  • Patient consent Obtained.

  • Ethics approval This study was conducted with the approval of the local ethics committee, University of Heidelberg.

  • Provenance and peer review Not commissioned; externally peer reviewed.

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