Christos V Bourantas1,2, Anantharaman Ramasamy1, Alexios Karagiannis3, Antonis Sakellarios3, Thomas Zanchin4, Kyohei Yamaji4, Yasushi Ueki4, Xiaohui Shen5, Dimitrios I Fotiadis6, Lampros K Michalis7, Anthony Mathur1, Patrick W Serruys8, Hector M Garcia-Garcia9, Kostantinos Koskinas4, Ryo Torii5, Stephan Windecker4, Lorenz Räber4. 1. Department of Cardiology, Barts Heart Centre, Barts Health NHS Trust, London, UK. 2. Institute of Cardiovascular Sciences, University College London, London, UK. 3. CTU Bern, Institute of Social and Preventive Medicine, Bern University, Bern, Switzerland. 4. Department of Cardiology, Bern University Hospital, Bern, Switzerland. 5. Department of Mechanical Engineering, University College London, London, UK. 6. Department of Materials Science and Engineering, University of Ioannina, Ioannina, Greece. 7. 2nd Department of Cardiology, Medical School, University of Ioannina, Ioannina, Greece. 8. International Centre for Circulatory Health, NHLI, Imperial College London, London, UK. 9. Section of Interventional Cardiology, MedStar Washington Hospital Center, Washington, DC, USA.
Abstract
AIMS: To examine the efficacy of angiography derived endothelial shear stress (ESS) in predicting atherosclerotic disease progression. METHODS AND RESULTS: Thirty-five patients admitted with ST-elevation myocardial infarction that had three-vessel intravascular ultrasound (IVUS) immediately after revascularization and at 13 months follow-up were included. Three dimensional (3D) reconstruction of the non-culprit vessels were performed using (i) quantitative coronary angiography (QCA) and (ii) methodology involving fusion of IVUS and biplane angiography. In both models, blood flow simulation was performed and the minimum predominant ESS was estimated in 3 mm segments. Baseline plaque characteristics and ESS were used to identify predictors of atherosclerotic disease progression defied as plaque area increase and lumen reduction at follow-up. Fifty-four vessels were included in the final analysis. A moderate correlation was noted between ESS estimated in the 3D QCA and the IVUS-derived models (r = 0.588, P < 0.001); 3D QCA accurately identified segments exposed to low (<1 Pa) ESS in the IVUS-based reconstructions (AUC: 0.793, P < 0.001). Low 3D QCA-derived ESS (<1.75 Pa) was associated with an increase in plaque area, burden, and necrotic core at follow-up. In multivariate analysis, low ESS estimated either in 3D QCA [odds ratio (OR): 2.07, 95% confidence interval (CI): 1.17-3.67; P = 0.012) or in IVUS (<1 Pa; OR: 2.23, 95% CI: 1.23-4.03; P = 0.008) models, and plaque burden were independent predictors of atherosclerotic disease progression; 3D QCA and IVUS-derived models had a similar accuracy in predicting disease progression (AUC: 0.826 vs. 0.827, P = 0.907). CONCLUSIONS: 3D QCA-derived ESS can predict disease progression. Further research is required to examine its value in detecting vulnerable plaques. Published on behalf of the European Society of Cardiology. All rights reserved.
AIMS: To examine the efficacy of angiography derived endothelial shear stress (ESS) in predicting atherosclerotic disease progression. METHODS AND RESULTS: Thirty-five patients admitted with ST-elevation myocardial infarction that had three-vessel intravascular ultrasound (IVUS) immediately after revascularization and at 13 months follow-up were included. Three dimensional (3D) reconstruction of the non-culprit vessels were performed using (i) quantitative coronary angiography (QCA) and (ii) methodology involving fusion of IVUS and biplane angiography. In both models, blood flow simulation was performed and the minimum predominant ESS was estimated in 3 mm segments. Baseline plaque characteristics and ESS were used to identify predictors of atherosclerotic disease progression defied as plaque area increase and lumen reduction at follow-up. Fifty-four vessels were included in the final analysis. A moderate correlation was noted between ESS estimated in the 3D QCA and the IVUS-derived models (r = 0.588, P < 0.001); 3D QCA accurately identified segments exposed to low (<1 Pa) ESS in the IVUS-based reconstructions (AUC: 0.793, P < 0.001). Low 3D QCA-derived ESS (<1.75 Pa) was associated with an increase in plaque area, burden, and necrotic core at follow-up. In multivariate analysis, low ESS estimated either in 3D QCA [odds ratio (OR): 2.07, 95% confidence interval (CI): 1.17-3.67; P = 0.012) or in IVUS (<1 Pa; OR: 2.23, 95% CI: 1.23-4.03; P = 0.008) models, and plaque burden were independent predictors of atherosclerotic disease progression; 3D QCA and IVUS-derived models had a similar accuracy in predicting disease progression (AUC: 0.826 vs. 0.827, P = 0.907). CONCLUSIONS: 3D QCA-derived ESS can predict disease progression. Further research is required to examine its value in detecting vulnerable plaques. Published on behalf of the European Society of Cardiology. All rights reserved.
Authors: Frank Gijsen; Yuki Katagiri; Peter Barlis; Christos Bourantas; Carlos Collet; Umit Coskun; Joost Daemen; Jouke Dijkstra; Elazer Edelman; Paul Evans; Kim van der Heiden; Rod Hose; Bon-Kwon Koo; Rob Krams; Alison Marsden; Francesco Migliavacca; Yoshinobu Onuma; Andrew Ooi; Eric Poon; Habib Samady; Peter Stone; Kuniaki Takahashi; Dalin Tang; Vikas Thondapu; Erhan Tenekecioglu; Lucas Timmins; Ryo Torii; Jolanda Wentzel; Patrick Serruys Journal: Eur Heart J Date: 2019-11-01 Impact factor: 29.983