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Coronary artery disease
Original research article
Implications of the local haemodynamic forces on the phenotype of coronary plaques
  1. Christos V Bourantas1,2,3,
  2. Thomas Zanchin1,4,5,
  3. Antonis Sakellarios6,
  4. Alexios Karagiannis7,
  5. Anantharaman Ramasamy1,
  6. Kyohei Yamaji8,
  7. Masanori Taniwaki8,
  8. Dik Heg7,
  9. Aris Moschovitis8,
  10. Dimitrios Fotiadis6,
  11. Lampros Mihalis9,
  12. Andreas Baumbach1,10,
  13. Ryo Torii5,
  14. Patrick Serruys11,
  15. Hector M Garcia-Garcia12,
  16. Stephan Windecker4,
  17. Lorenz Räber8
  1. 1 Department of Cardiology, Barts Heart Centre, Barts Health NHS Trust, London, UK
  2. 2 Institute of Cardiovascular Sciences, University College London, London, UK
  3. 3 School of Medicine and Dentistry, Queen Mary University London, London, UK
  4. 4 Department of Cardiology, Swiss Cardiovascular Center, Bern University Hospital, Bern, Switzerland
  5. 5 Department of Mechanical Engineering, University College London, London, UK
  6. 6 Department of Materials Science and Engineering, University of Ioannina, Ioannina, Greece
  7. 7 Clinical Trial Unit, Institute of Social and Preventive Medicine, Bern, Switzerland
  8. 8 Department of Cardiology, Bern University Hospital, Bern, Switzerland
  9. 9 Department of Cardiology, University of Ioannina, Ioannina, Greece
  10. 10 School of Medicine and Dentistry, Queen Mary University London, London, London, UK
  11. 11 International Centre for Circulatory Health, Imperial College London Institute of Clinical Sciences, London, UK
  12. 12 Section of Interventional Cardiology, MedStar Washington Hospital Center, Washington, Columbia, USA
  1. Correspondence to Dr Lorenz Räber, Department of Cardiology, Bern University Hospital, Bern, 3010, Switzerland; lorenz.raeber{at}insel.ch

Abstract

Aim To examine the effect of endothelial shear stress (ESS) on the dynamic changes in plaque phenotype.

Methods Patients with myocardial infarction that had intravascular ultrasound-virtual histology (IVUS-VH) and optical coherence tomography (OCT) at baseline and 13-month follow-up were studied. The IVUS-VH data were used to reconstruct the nonculprit vessels, and in the obtained models the ESS was estimated in 3 mm segments. Plaque morphology was derived in each segment from IVUS-VH and OCT. Disease progression was defined as the presence of ≥2 out of the following criteria: reduction in lumen area, increase in plaque burden and change of plaque morphology to a more vulnerable phenotype. Linear mixed effects models were used to assess the effect of ESS in different phenotypes.

Results Sixty-eight vessels were included in the analysis. Low ESS was associated with plaque progression in all phenotypes. The effect of ESS on plaque burden (p for interaction=0.467) and phenotype (p for interaction=0.188) was similar in all plaque types, whereas the effect of ESS on the changes in lumen dimensions was more prominent in disease-free (β=0.70, p<0.001) than fibrotic/fibrocalcific (β=0.28, p<0.001) or lipid-rich plaques (β=0.15, p=0.015). Standalone IVUS-VH misclassified plaque morphology in one-third of the cases leading to erroneous estimations about the effect of ESS on plaque evolution in different phenotypes.

Conclusions The effect of ESS on plaque progression is similar in all phenotypes and cannot be accurately assessed by standalone IVUS-VH which often misclassifies plaque morphology. Therefore, multimodality imaging should be considered to examine the implications of ESS on plaque evolution.

Clinical trial registration NCT00962416; Post-results.

  • coronary artery disease

https://doi.org/10.1136/heartjnl-2018-314086

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    Footnotes

    • CVB and TZ contributed equally.

    • Contributors CVB and LR: designed and planned the study; CVB and TZ: interpreted the data and drafted the manuscript. CVB, AS and AK: analysed the data. The other authors: revised it critically for important intellectual content and gave final approval of the version to be published.

    • Funding The IBIS4 trial was supported by the Swiss National Science Foundation and St. Jude Medical. Anantharaman Ramasamy was funded by research funds of Whipps Cross University Hospital, London. Thomas Zanchin is supported by the Swiss National Science Foundation grant number 323530-171146.

    • Competing interests LR reports research grants by Abbott, Sanofi and Regeneron.

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