Mis-sizing of stent promotes intimal hyperplasia: impact of endothelial shear and intramural stress

• Published in: American journal of physiology. Heart and circulatory physiology 2011-12, Vol.301 (6), p.H2254-H2263
• Main Authors: Chen, Henry Y, Sinha, Anjan K, Choy, Jenny S, Zheng, Hai, Sturek, Michael, Bigelow, Brian, Bhatt, Deepak L, Kassab, Ghassan S
• Format: Article
• Language: English
• Subjects: Angioplasty, Balloon, Coronary - adverse effects; Angioplasty, Balloon, Coronary - instrumentation; Animals; Biomechanical Phenomena; Cell Proliferation; Computer Simulation; Coronary Circulation; Coronary Restenosis - diagnostic imaging; Coronary Restenosis - etiology; Coronary Restenosis - pathology; Coronary Restenosis - physiopathology; Coronary vessels; Coronary Vessels - diagnostic imaging; Coronary Vessels - pathology; Coronary Vessels - physiopathology; Endothelium, Vascular - diagnostic imaging; Endothelium, Vascular - pathology; Endothelium, Vascular - physiopathology; Hyperplasia; Linear Models; Male; Metals; Models, Animal; Models, Cardiovascular; Prosthesis Design; Regression analysis; Shear stress; Stents; Stents - adverse effects; Stress, Mechanical; Swine; Ultrasonography, Interventional; Vascular Biology and Microcirculation
• ISSN: 0363-6135; 1522-1539
• DOI: 10.1152/ajpheart.00240.2011

Stent can cause flow disturbances on the endothelium and compliance mismatch and increased stress on the vessel wall. These effects can cause low wall shear stress (WSS), high wall shear stress gradient (WSSG), oscillatory shear index (OSI), and circumferential wall stress (CWS), which may promote neointimal hyperplasia (IH). The hypothesis is that stent-induced abnormal fluid and solid mechanics contribute to IH. To vary the range of WSS, WSSG, OSI, and CWS, we intentionally mismatched the size of stents to that of the vessel lumen. Stents were implanted in coronary arteries of 10 swine. Intravascular ultrasound (IVUS) was used to size the coronary arteries and stents. After 4 wk of stent implantation, IVUS was performed again to determine the extent of IH. In conjunction, computational models of actual stents, the artery, and non-Newtonian blood were created in a computer simulation to yield the distribution of WSS, WSSG, OSI, and CWS in the stented vessel wall. An inverse relation (R(2) = 0.59, P < 0.005) between WSS and IH was found based on a linear regression analysis. Linear relations between WSSG, OSI, and IH were observed (R(2) = 0.48 and 0.50, respectively, P < 0.005). A linear relation (R(2) = 0.58, P < 0.005) between CWS and IH was also found. More statistically significant linear relations between the ratio of CWS to WSS (CWS/WSS), the products CWS × WSSG and CWS × OSI, and IH were observed (R(2) = 0.67, 0.54, and 0.56, respectively, P < 0.005), suggesting that both fluid and solid mechanics influence the extent of IH. Stents create endothelial flow disturbances and intramural wall stress concentrations, which correlate with the extent of IH formation, and these effects were exaggerated with mismatch of stent/vessel size. These findings reveal the importance of reliable vessel and stent sizing to improve the mechanics on the vessel wall and minimize IH.