Bovine pericardium is widely used in surgery and is commonly used for a patch after arteriotomy during cardiovascular surgery. Bovine pericardial patches have several advantages compared to prosthetic patches, including superior biocompatability, easy handling, less suture line bleeding and possibly reduced rates of infection. These advantages of bovine pericardium have led to its common use during carotid endarterectomy. However, long-term clinical results reported after carotid endarterectomy have suggested several issues that may be related to the patch including restenosis, pseudoaneurysm formation, infection, fibrosis, calcification and thrombosis. These complications may diminish the long-term efficacy of carotid endarterectomy and suggest potential areas for improvement of surgical patches. Understanding the mechanisms by which bovine pericardium heals after patch angioplasty may lead to next generation tissue engineered patches.Bovine pericardium (BP) has come into common clinical use during the past 20 years, especially when used as a patch for arterial closure during vascular and cardiac surgery. Bovine pericardial patches possess many technical merits that have led to their widespread adoption in the operating room, including easy handling, less suture bleeding and the ability to immediately perform arterial duplex examination at the site of angioplasty. However, long-term results of this biomaterial are poorly documented and need cautious interpretation as to whether its long term performance is related to the material itself or to the operation in which it is used. For example, it is unclear whether restenosis after carotid endarterectomy is directly related to the patch itself or whether restenosis is an inevitable consequence of the arterial procedure. In addition, there are sporadic reports of unusual complications with BP patches, including patch rupture and cartilaginous metaplasia. Although these reports are Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. unusual, careful examination of these potential areas of improvement may lead to future generations of BP patches with superior performance. NIH Public AccessThe native structure of bovine pericardium has three layers: 1) the serosa, the inner thin layer consisting of mesothelial cells; 2) the fibrosa, the thicker layer formed by diversely oriented, wavy bundles of collagen and elastin; and 3) the epipericardial connective tissue layer, the outer layer that is partly continuous with the pericardiosternal ligaments. Commercially available patches are processed to be acellular, preventing transpl...
For patients with coronary artery disease or limb ischemia, placement of a vein graft as a conduit for a bypass is an important and generally durable strategy among the options for arterial reconstructive surgery. Vein grafts adapt to the arterial environment; limited formation of intimal hyperplasia in the vein graft wall is thought to be an important component of successful vein graft adaptation. However, it is also known that abnormal, or uncontrolled, adaptation may lead to abnormal vessel wall remodeling with excessive neointimal hyperplasia, and ultimately vein graft failure and clinical complications. Therefore, understanding the venous-specific pathophysiological and molecular mechanisms of vein graft adaptation are important for clinical vein graft management. Of particular importance, it is currently unknown whether several specific distinct molecular differences in venous mechanisms of adaptation exist that are distinct from arterial post-injury responses; in particular, the participation of the venous marker Eph-B4 and the vascular protective molecule Nogo-B may be involved in mechanisms of vessel remodeling specific to the vein. In this review, we describe 1) venous biology from embryonic development to the mature quiescent state; 2) sequential pathologies of vein graft neointima formation; and 3) novel candidates for strategies of vein graft management. We believe that the scientific inquiry of venous-specific adaptation mechanisms will ultimately provide improvements in vein graft outcomes.
In 1990, Dalman and Taylor published a compilation of reported data they identified as related to infrainguinal revascularization procedures in peripheral vascular surgery during the decade of the 1980s. The intervening 20 years has seen revolutionary advances in the field of Peripheral Vascular Surgery, especially in the adoption of endovascular techniques, and an explosion of data related to emerging technologies in the field of infrainguinal revascularization. The tables in this manuscript reflect the evolution of our surgical knowledge during the turn of the 21st century. The superior patency of autologous saphenous vein in all positions is reaffirmed.
Carotid angioplasty is associated with adverse events in elderly patients; it is unclear whether this is related to an altered inflammatory axis. The carotid arteries of young (6 months) or aged (22-24 months) Fischer 344 rats were balloon injured. Aged rats had reduced lumen area (0.18 ± 0.03 vs 0.24 ± 0.01 mm(2), p = .02) and increased neointimal thickening (0.15 ± 0.04 vs 0.08 ± 0.03 mm(2), p = .006). Aged rats had increased circulating monocytes (96 ± 21 vs. 54 ± 7; p = .002) as well as increased numbers of monocytes at the post-angioplasty site. Aged rats had sustained monocyte chemotactic protein-1 expression after angioplasty but young rats did not. Aged arteries also exhibited defective vasorelaxation and abnormal eNOS localization. Aged (≥80 years) human patients with high-grade carotid stenosis had increased number of monocytes (9.1% ± 0.4%) compared with younger (65-80 years) patients (8.1% ± 0.3%, p = .013). Aged rats develop neointimal hyperplasia after carotid angioplasty with increased numbers of monocytes, and elderly humans with carotid stenosis have increased numbers of circulating monocytes. These preliminary results may suggest a role for monocytes in the response to carotid angioplasty.
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