Ryo Torii1, Rodrigue Stettler2, Lorenz Räber3, Yao-Jun Zhang4, Antonis Karanasos5, Jouke Dijkstra6, Kush Patel2, Tom Crake2, Steve Hamshere2, Hector M Garcia-Garcia5, Erhan Tenekecioglu5, Muhiddin Ozkor2, Andreas Baumbach7, Stephan Windecker3, Patrick W Serruys8, Evelyn Regar9, Anthony Mathur7, Christos V Bourantas10. 1. Department of Mechanical Engineering, University College London, London, United Kingdom. 2. Barts Heart Centre, Barts Health NHS, London, United Kingdom. 3. Bern University Hospital, Bern, Switzerland. 4. Xuzhou Third People's Hospital, Jiangsu University, Xuzhou, China; Nanjing First Hospital, Nanjing Medical University, Nanjing, China. 5. Thoraxcenter, Erasmus Medical Centre, Rotterdam, the Netherlands. 6. Leiden University Medical Centre, Leiden, the Netherlands. 7. Barts Heart Centre, Barts Health NHS, London, United Kingdom; Queen Mary University London, London, United Kingdom. 8. Thoraxcenter, Erasmus Medical Centre, Rotterdam, the Netherlands; Faculty of Medicine, National Heart & Lung Institute, Imperial College London, United Kingdom. 9. Department of Cardiovascular Surgery, University Hospital Zürich, Zürich, Switzerland. 10. Barts Heart Centre, Barts Health NHS, London, United Kingdom; Queen Mary University London, London, United Kingdom; Institute of Cardiovascular Sciences, University College London, London, United Kingdom. Electronic address: Christos.Bourantas@bartshealth.nhs.uk.
Abstract
OBJECTIVE: To examine the implications of endothelial shear stress (ESS) distribution in the formation of neoatherosclerotic lesions. METHODS: Thirty six patients with neoatherosclerotic lesions on optical coherence tomography (OCT) were included in this study. The OCT data were used to reconstruct coronary anatomy. Blood flow simulation was performed in the models reconstructed from the stent borders which it was assumed that represented the lumen surface at baseline, immediate after stent implantation, and the estimated ESS was associated with the neointima burden, neoatherosclerotic burden and neointima characteristics. In segments with neointima rupture blood flow simulation was also performed in the model representing the lumen surface before rupture and the ESS was estimated at the ruptured site. RESULTS: An inverse association was noted between baseline ESS and the incidence and the burden of neoatherosclerotic (β = -0.60, P < 0.001, and β = -4.05, P < 0.001, respectively) and lipid-rich neoatherosclerotic tissue (β = -0.54, P < 0.001, and β = -3.60, P < 0.001, respectively). Segments exposed to low ESS (<1 Pa) were more likely to exhibit macrophages accumulation (28.2% vs 10.9%, P < 0.001), thrombus (11.0% vs 2.6%, P < 0.001) and evidence of neointima discontinuities (8.1% vs 0.9%, P < 0.001) compared to those exposed to normal or high ESS. In segments with neointima rupture the ESS was high at the rupture site compared to the average ESS over the culprit lesion (4.00 ± 3.65 Pa vs 3.14 ± 2.90 Pa, P < 0.001). CONCLUSIONS: Local EES is associated with neoatherosclerotic lesion characteristics, which suggests involvement of ESS in the formation of vulnerable plaques in stented segments.
OBJECTIVE: To examine the implications of endothelial shear stress (ESS) distribution in the formation of neoatherosclerotic lesions. METHODS: Thirty six patients with neoatherosclerotic lesions on optical coherence tomography (OCT) were included in this study. The OCT data were used to reconstruct coronary anatomy. Blood flow simulation was performed in the models reconstructed from the stent borders which it was assumed that represented the lumen surface at baseline, immediate after stent implantation, and the estimated ESS was associated with the neointima burden, neoatherosclerotic burden and neointima characteristics. In segments with neointima rupture blood flow simulation was also performed in the model representing the lumen surface before rupture and the ESS was estimated at the ruptured site. RESULTS: An inverse association was noted between baseline ESS and the incidence and the burden of neoatherosclerotic (β = -0.60, P < 0.001, and β = -4.05, P < 0.001, respectively) and lipid-rich neoatherosclerotic tissue (β = -0.54, P < 0.001, and β = -3.60, P < 0.001, respectively). Segments exposed to low ESS (<1 Pa) were more likely to exhibit macrophages accumulation (28.2% vs 10.9%, P < 0.001), thrombus (11.0% vs 2.6%, P < 0.001) and evidence of neointima discontinuities (8.1% vs 0.9%, P < 0.001) compared to those exposed to normal or high ESS. In segments with neointima rupture the ESS was high at the rupture site compared to the average ESS over the culprit lesion (4.00 ± 3.65 Pa vs 3.14 ± 2.90 Pa, P < 0.001). CONCLUSIONS: Local EES is associated with neoatherosclerotic lesion characteristics, which suggests involvement of ESS in the formation of vulnerable plaques in stented segments.
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