Author + information
- Received August 19, 2019
- Revision received February 5, 2020
- Accepted February 14, 2020
- Published online October 5, 2020.
- Christos V. Bourantas, MD, PhDa,b,c,∗∗ (, )
- Thomas Zanchin, MDa,d,e,∗,
- Ryo Torii, PhDe,
- Patrick W. Serruys, MD, PhDf,
- Alexios Karagiannis, PhDg,
- Anantharaman Ramasamy, MBChBa,c,
- Hannah Safi, PhDb,
- Ahmet Umit Coskun, PhDh,
- Gerhard Koning, MSci,
- Yoshinobu Onuma, MD, PhDj,
- Christian Zanchin, MDd,
- Rob Krams, MD, PhDk,
- Anthony Mathur, MD, PhDa,c,
- Andreas Baumbach, MDa,c,
- Gary Mintz, MDl,
- Stephan Windecker, MDd,
- Alexandra Lansky, MDb,m,
- Akiko Maehara, MDl,
- Peter H. Stone, MDn,
- Lorenz Raber, MD, PhDd and
- Gregg W. Stone, MDm
- aDepartment of Cardiology, Barts Heart Centre, Barts Health NHS, London, United Kingdom
- bInstitute of Cardiovascular Sciences, University College London, London, United Kingdom
- cCentre for Cardiovascular Medicine and Device Innovation, Queen Mary University London, London, United Kingdom
- dDepartment of Cardiology, Bern University Hospital, Bern, Switzerland
- eDepartment of Mechanical Engineering, University College London, London, United Kingdom
- fFaculty of Medicine, National Heart & Lung Institute, Imperial College London, United Kingdom
- gCTU Bern, Institute of Social and Preventive Medicine, Bern University, Bern, Switzerland
- hMechanical and Industrial Engineering, Northeastern University, Boston, Massachusetts
- iMedis medical imaging systems bv, Leiden, the Netherlands
- jDepartment of Interventional Cardiology, Thoraxcenter, Erasmus Medical Center, Rotterdam, the Netherlands
- kDepartment of Molecular Bioengineering Engineering and Material Sciences, Queen Mary University London, London, United Kingdom
- lDepartment of Cardiology, Columbia University Medical Center and the Cardiovascular Research Foundation, New York, New York
- mDivision of Cardiovascular Medicine, Department of Internal Medicine, Yale School of Medicine, New Haven, Connecticut
- nCardiovascular Division, Brigham & Women’s Hospital, Harvard Medical School, Boston, Massachusetts
- ↵∗Address for correspondence:
Dr. Christos V. Bourantas, Barts Heart Centre, West Smithfield, London EC1A 7BE, United Kingdom.
Objectives This study examined the value of endothelial shear stress (ESS) estimated in 3-dimensional quantitative coronary angiography (3D-QCA) models in detecting plaques that are likely to progress and cause events.
Background Cumulative evidence has shown that plaque characteristics and ESS derived from intravascular ultrasound (IVUS)−based reconstructions enable prediction of lesions that will cause cardiovascular events. However, the prognostic value of ESS estimated by 3D-QCA in nonflow limiting lesions is yet unclear.
Methods This study analyzed baseline virtual histology (VH)-IVUS and angiographic data from 28 lipid-rich lesions (i.e., fibroatheromas) that caused major adverse cardiovascular events or required revascularization (MACE-R) at 5-year follow-up and 119 lipid-rich plaques from a control group that remained quiescent. The segments studied by VH-IVUS at baseline were reconstructed using 3D-QCA software. In the obtained geometries, blood flow simulation was performed, and the pressure gradient across the lipid-rich plaque and the mean ESS values in 3-mm segments were estimated. The additive value of these hemodynamic indexes in predicting MACE-R beyond plaque characteristics was examined.
Results MACE-R lesions were longer, had smaller minimum lumen area, increased plaque burden (PB), were exposed to higher ESS, and exhibited a higher pressure gradient. In multivariable analysis, PB (hazard ratio: 1.08; p = 0.004) and the maximum 3-mm ESS value (hazard ratio: 1.11; p = 0.001) were independent predictors of MACE-R. Lesions exposed to high ESS (>4.95 Pa) with a high-risk anatomy (minimal lumen area <4 mm2 and PB >70%) had a higher MACE-R rate (53.8%) than those with a low-risk anatomy exposed to high ESS (31.6%) or those exposed to low ESS who had high- (20.0%) or low-risk anatomy (7.1%; p < 0.001).
Conclusions In the present study, 3D-QCA-derived local hemodynamic variables provided useful prognostic information, and, in combination with lesion anatomy, enabled more accurate identification of MACE-R lesions.
- Received August 19, 2019.
- Revision received February 5, 2020.
- Accepted February 14, 2020.
- 2020 American College of Cardiology Foundation
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