Author + information
- Michael Michail, MBBS, BSc∗,
- Ryo Torii, MSc, PhD†,
- Tom Crake, MD∗,
- Muhiddin Ozkor, MD, BSc∗,
- Hector M. Garcia-Garcia, MD, PhD‡,
- Erhan Tenekecioglu, MD‡,
- Yoshinobu Onuma, MD, PhD‡,
- Anthony Mathur, MD, PhD§,
- Patrick W. Serruys, MD, PhD‡,‖ and
- Christos V. Bourantas, MD, PhD∗,¶∗ ()
- ∗The Heart Hospital, University College London Hospitals NHS Foundation Trust, London, United Kingdom
- †Department of Mechanical Engineering, University College London, London, United Kingdom
- ‡Department of Interventional Cardiology, Erasmus University Medical Centre, Thoraxcenter, Rotterdam, the Netherlands
- §Department of Cardiology, Barts Heart Center, Bart’s Health NHS Trust, London, United Kingdom
- ‖Faculty of Medicine, National Heart & Lung Institute, Imperial College London, United Kingdom
- ¶Department of Cardiovascular Sciences, University College London, United Kingdom
- ↵∗Reprint requests and correspondence:
Dr. Christos V. Bourantas, Department of Cardiology, The Heart Hospital, 16-18 Westmoreland Street, London W1G 8PH, United Kingdom.
A 51-year-old male was admitted with non–ST-segment elevation myocardial infarction. Coronary angiography demonstrated a hazy lesion in the stented (Promus Element 3.5 × 32 mm and 3.5 × 20 mm, Boston Scientific, Natick, Massachusetts) left anterior descending artery (Figure 1A). Optical coherence tomography was performed that showed focal neoatherosclerosis in the proximal stent and plaque rupture (asterisk) (Figure 1, panels 1 and 2). Blood flow simulation was performed in the reconstructed stent and lumen surface (Figures 1B, 1C, and 1E). An inverse, weak association was noted between endothelial shear stress (ESS) in the stent surface and neointima thickness (Figure 1D). The ESS in the stent surface was lower in the segment with neoatherosclerosis compared with the segments with fibrotic neointima (Figure 1F). In contrast to current hypotheses, segments covered by neointima had higher ESS compared with those without (Figure 1H). Additionally, plaque rupture occurred not in the throat (Figure 1F, 1, and 1′) or upstream, but in the downstream of the neoatherosclerotic lesion where low ESS (average ESS: 0.9 Pa) and flow recirculation were noted (Figure 1G, 2, and 2′). In drug-eluting stents, other local mechanisms besides ESS may determine neoatherosclerotic lesion formation and its evolution.
Dr. Onuma has served as a member of the advisory board for Abbott Vascular. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.
- American College of Cardiology Foundation