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Original research article
Evaluation of human coronary vasodilator function predicts future coronary atheroma progression
  1. Samuel L Sidharta1,2,3,
  2. Timothy J Baillie1,
  3. Stuart Howell4,
  4. Stephen J Nicholls1,2,3,
  5. Natalie Montarello3,
  6. Satoshi Honda2,
  7. Daisuke Shishikura2,
  8. Sinny Delacroix1,
  9. Susan Kim2,
  10. John F Beltrame1,
  11. Peter J Psaltis1,2,3,
  12. Stephen G Worthley1,
  13. Matthew I Worthley1,2,3
  1. 1Discipline of Medicine, University of Adelaide, Adelaide, South Australia, Australia
  2. 2Vascular Research Centre, Heart Health Theme, South Australian Health and Medical Research Institute, Adelaide, South Australia, Australia
  3. 3Central Adelaide Local Health Network, Royal Adelaide Hospital, Adelaide, South Australia, Australia
  4. 4Data, Design and Statistics Service, Adelaide Health Technology Assessment (AHTA), School of Public Health, The University of Adelaide, Adelaide, South Australia, Australia
  1. Correspondence to Dr Samuel L Sidharta, Royal Adelaide Hospital, Adelaide, SA 5000, Australia; samuel.sidharta{at}


Objective Coronary vasodilator function and atherosclerotic plaque progression have both been shown to be associated with adverse cardiovascular events. However, the relationship between these factors and the lipid burden of coronary plaque remains unknown. These experiments focus on investigating the relationship between impaired coronary vasodilator function (endothelium dependent (salbutamol) and endothelium independent (glyceryl trinitrate)) and the natural history of atheroma plaque progression and lipid burden using dual modality intravascular ultrasound (IVUS) and near-infrared spectroscopy (NIRS) imaging.

Methods 33 patients with stable chest pain or acute coronary syndrome underwent serial assessment of coronary vasodilator function and intracoronary plaque IVUS and NIRS imaging. Coronary segmental macrovascular response (% change segmental lumen volume (ΔSLV)), plaque burden (per cent atheroma volume (PAV)), lipid core (lipid-rich plaque (LRP) and lipid core burden index (LCBI)) were measured at baseline and after an interval of 12–18 months (n=520 segments).

Results Lipid-negative coronary segments which develop into LRP over the study time period demonstrated impaired endothelial-dependent function (−0.24±2.96 vs 5.60±1.47%, P=0.04) and endothelial-independent function (13.91±4.45 vs 21.19±3.19%, P=0.036), at baseline. By multivariate analysis, endothelial-dependent function predicted ∆LCBI (β coefficient: −3.03, 95% CI (−5.81 to −0.25), P=0.033) whereas endothelial-independent function predicted ∆PAV (β coefficient: 0.07, 95% CI (0.04 to 0.10), P<0.0001).

Conclusions Epicardial coronary vasodilator function is a determinant of future atheroma progression and composition irrespective of the nature of clinical presentation.

Trial registration number ACTRN12612000594820, Post-results.

  • coronary artery disease
  • advanced cardiac imaging
  • vascular biology

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  • Contributors SLS, MIW: study design, patient recruitment, analysis. SLS: preparation of manuscript. TJB, NM, SH, DS, SD, PJP: correction and critical review of manuscript. SH, SK: statistical analysis, correction and critical review of manuscript. SJN, JFB, SGW, MIW: supervision, correction and critical review of manuscript. SLS, TJB, NM: data collection.

  • Funding SLS is individually supported by Royal Adelaide Hospital AR Clarkson Scholarship and University of Adelaide Australian Postgraduate Awards. Equipment funding for this study was supported by National Heart Foundation Tom Simpson Trust Award. MIW is an SA Health Early to Mid-Career Practitioner Fellow.

  • Competing interests None declared.

  • Patient consent Not required.

  • Ethics approval Royal Adelaide Hospital Research Ethics Committee.

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

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