Hemodynamic conditions in a failing peripheral artery bypass graft

• Published in: Journal of vascular surgery Vol. 56; no. 2; pp. 403 - 409
• Main Authors: McGah, Patrick M., MS, Leotta, Daniel F., PhD, Beach, Kirk W., PhD, MD, Zierler, R. Eugene, MD, Riley, James J., PhD, Aliseda, Alberto, PhD
• Format: Journal Article
• Language: English
• Published: New York, NY Mosby, Inc 01-08-2012; Elsevier
• Subjects: Biological and medical sciences; Blood and lymphatic vessels; Cardiology. Vascular system; Dilatation, Pathologic; Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous; Graft Occlusion, Vascular - physiopathology; Hemodynamics; Humans; Hyperplasia; Medical sciences; Retrospective Studies; Saphenous Vein - pathology; Saphenous Vein - transplantation; Stress, Mechanical; Surgery; Surgery (general aspects). Transplantations, organ and tissue grafts. Graft diseases; Transplantation, Autologous; Tunica Intima - pathology; Vascular surgery: aorta, extremities, vena cava. Surgery of the lymphatic vessels; Cardiovascular disease; Hemodynamics; Bypass; Surgery
• DOI: 10.1016/j.jvs.2012.01.045
• EISSN: 1097-6809
• ISSN: 0741-5214

Objective The mechanisms of restenosis in autogenous vein bypass grafts placed for peripheral artery disease are not completely understood. We investigated the role of hemodynamic stress in a case study of a revised bypass graft that failed due to restenosis. Methods The morphology of the lumen was reconstructed from a custom three-dimensional ultrasound system. Scans were taken at 1, 6, and 16 months after a patch angioplasty procedure. Computational hemodynamic simulations of the patient-specific model provided the blood flow features and the hemodynamic stresses on the vessel wall at the three times studied. Results The vessel was initially free of any detectable lesions, but a 60% diameter-reducing stenosis developed during the 16-month study interval. As determined from the simulations, chaotic and recirculating flow occurred downstream of the stenosis due to the sudden widening of the lumen at the patch location. Curvature and a sudden increase in the lumen cross-sectional area induced these flow features that are hypothesized to be conducive to intimal hyperplasia. Favorable agreement was found between simulation results and in vivo Doppler ultrasound velocity measurements. Conclusions Transitional and chaotic flow occurs at the site of the revision, inducing a complex pattern of wall shear as computed with the hemodynamic simulations. This supports the hypothesis that the hemodynamic stresses in the revised segment, produced by the coupling of vessel geometry and chaotic flow, led to the intimal hyperplasia and restenosis of the graft.