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Association of soluble tumour necrosis factor-related apoptosis-inducing ligand levels with coronary plaque burden and composition
  1. Spyridon Deftereos1,
  2. Georgios Giannopoulos1,
  3. Charalampos Kossyvakis1,
  4. Andreas Kaoukis1,
  5. Konstantinos Raisakis1,
  6. Vasiliki Panagopoulou1,
  7. Antigoni Miliou2,
  8. Andreas Theodorakis1,
  9. Metaxia Driva1,
  10. Vlasios Pyrgakis1,
  11. Christodoulos Stefanadis2,
  12. Michael W Cleman3
  1. 1Department of Cardiology and Cardiac Catheterization Laboratory, Athens General Hospital ‘G Gennimatas’, Athens, Greece
  2. 21st Cardiology Department, University of Athens Medical School, Athens, Greece
  3. 3Cardiac Catheterization Laboratory, Yale–New Haven Hospital, Yale School of Medicine, New Haven, Connecticut, USA
  1. Correspondence to Dr Georgios Giannopoulos, Cardiology Department, Athens General Hospital ‘G Gennimatas’, 154 Mesogeion Avenue, 11527 Athens, Greece; ggiann{at}med.uoa.gr

Abstract

Background Evidence shows that the soluble tumour necrosis factor-related apoptosis-inducing ligand (sTRAIL) may play a protective role against atherosclerosis. This study sought to investigate the potential association of sTRAIL levels with intravascular ultrasound (IVUS) and virtual histology characteristics of coronary plaques.

Methods Patients with stable angina or positive for ischaemia non-invasive test were submitted to left cardiac catheterisation. Coronary blood samples were collected and sTRAIL was measured. Coronary arteries with at least one 50% or greater stenosis were studied with IVUS.

Results 56 coronary arteries were studied with significant coronary artery disease. Plaque volume per unit of arterial length was 63±5 mm3/cm in arteries at the lower quartile of sTRAIL concentration versus 30±4 mm3/cm at the upper quartile (p<0.001; 95% CI of the difference 19.7 to 46.3 mm3/cm). The necrotic core and fibrofatty content of atheromatous plaques were inversely associated with sTRAIL (p<0.001). Thin-cap fibroatheromas (TCFA) were discovered in 16 of the 56 arterial segments. The mean sTRAIL concentration in these segments was 56.8±7.5 pg/ml versus 99.9±5.7 pg/ml in those without TCFA (p<0.001; 95% CI of the difference 22.7 to 63.5 pg/ml). The association of sTRAIL with the presence of TCFA remained significant in the logistic multivariate analysis (p=0.009).

Conclusion According to the findings of the present study, in addition to coronary artery disease burden, the sTRAIL concentration is also related to the composition of atheromatous plaques. A significant association is demonstrated between low sTRAIL levels and the presence of TCFA, the IVUS–virtual histology prototype of the vulnerable plaque.

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Footnotes

  • Competing interests None.

  • Patient consent Obtained.

  • Ethics approval The protocol was approved by the competent institutional review board and was implemented according to the Declaration of Helsinki.

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

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