Long-Term Alterations in Large-Caliber Arterial Prostheses Used for Aortic Repair Areck A. Ucuzian and Howard P. Greisler Large-caliber prostheses used for aortic replacement initiate blood–material interfacial processes that begin almost immediately upon establishment of circulatory flow. These processes lead to prosthetic encapsulation and structural alteration, occasionally a degree of degradation of synthetic polymers, and ultimately these events contribute to the long-term development of thrombosis, intimal hyperplasia, tissue incorporation, and dilatation of aortic prostheses. Early Host Responses to Implanted Materials Protein Deposition Almost immediately after circulatory flow is established, protein adsorbs to the biomaterial surface and provides the initial scaffold upon which host coagulation and healing responses will build. Initially, the most abundant and mobile proteins such as albumin, immunoglobulin G (IgG), low-density lipoprotein (LDL) cholesterol, high-density lipoprotein (HDL) cholesterol, fibrinogen, and others are adsorbed to the prosthetic surfaces. Over the next several minutes to hours, protein adsorption continues on the biomaterial surface as determined by the Vroman effect. This is characterized by the dynamic interchange between proteins initially adsorbed on the biomaterial surface and proteins with higher affinity whose binding properties depend on their intrinsic three-dimensional conformational and electrochemical properties, as well as the structural irregularity and electrochemical activity of the biomaterial itself. Platelet Deposition and Coagulation The tendency of biomaterials to adhere platelets and promote their aggregation and activation before fibrin coagulum forms is a critical component to the host’s response to prosthetic material. Clearly, thrombus formation not only leads to acute graft failures but also serves as a scaffold for mesenchymal and inflammatory cell infiltration before the formation of atherosclerotic plaques and intimal hyperplastic lesions. Platelet adherence occurs by way of binding of the platelet surface glycoprotein (GP) receptor complexes to exposed subendothelial extracellular matrix (ECM) proteins like collagen or to von Willebrand factor (vWF) bound to collagen. The interaction between these glycoproteins and vWF bound to the exposed subendothelium or to endothelial cell (EC) surfaces activates platelets and causes the release of α-granule products, and it increases the local concentrations of serotonin, epinephrine, and adenosine diphosphate (ADP), among others. This degranulation serves to propagate platelet aggregation and activation. The formation of the prothrombinase complex on activated platelets mediated by the extrinsic coagulation pathway facilitates thrombin formation and subsequent fibrin generation. Inflammation Implanted prosthetics activate complement primarily through the classical and alternative pathways, and the degree of complement activation appears to depend on the type of biomaterial used. The activation of complement can have significant downstream effects by propagating inflammation, inducing anaphylactoid reactions, and potentially promoting graft thrombosis. In response to complement activation, generated C5a, chemokines like leukotriene B4 (LTB4), platelet-activating factor (PAF), and deposited fibrin coagulum, neutrophils are recruited early in inflammation and produce products of oxygen metabolism and proteases that contribute to tissue injury and prosthetic degradation. If an endothelium is present, neutrophil integrin receptors and sulfated sialyl-Lewis receptors bind to endothelial cell intercellular adhesion molecules (ICAMs) and P- and E-selectins. Subsequent to neutrophil infiltration, macrophages, which either are resident in the tissues or are derived from circulating monocytes, also comprise part of the early response to implanted vascular grafts. Monocytes are recruited to implanted grafts by numerous chemokines and macrophage-recruiting mediators from various sources including the regenerating endothelium, platelets, and other macrophages, as well by the fibrin coagulum and complement products. These activated macrophages produce inflammatory mediators like interleukin 1 (IL-1), tumor necrosis factor (TNF), and others, which propagate the host response of wound healing and the reaction to foreign materials and which promote the development and remodeling of pseudointimal hyperplastic regions on the surface of grafts. The formation of foreign body giant cells by macrophages, which cover the surface of polytetrafluoroethylene (ePTFE) and polyethylene terephthalate (PET), is part of a larger chronic inflammatory state that attenuates the healing and re-endothelialization of the biomaterial. Mesenchymal Cell Infiltration The infiltration of smooth muscle cells (SMCs) and fibroblasts onto the luminal surface of implanted prosthetic grafts is an early event in the development of the later consequence of intimal hyperplasia. These cells migrate from the arterial media and adventitia to the luminal surface of the implanted prosthesis (or the disrupted luminal surface of vein grafts or arteries following therapeutic interventions) primarily, in the case of synthetic prostheses, at the prosthesis–host anastomotic junction. There the SMCs proliferate over the next several weeks to months. Continued synthetic behavior by SMCs contributes to the deposition of extracellular matrix proteins such as collagens and further propagation and remodeling of the perianastomotic pseudointimal lesion. Beyond 1 to 2 cm from either anastomosis of synthetic prostheses, the luminal surface becomes covered primarily by compacted organized fibrin coagulum, devoid of mesenchymal cells. Platelet deposition onto this surface remains chronically elevated, but platelet desquamation generally results in minimal late progression of pseudointimal thickness in the mid-portion of these implants. Only gold members can continue reading. 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Long-Term Alterations in Large-Caliber Arterial Prostheses Used for Aortic Repair Areck A. Ucuzian and Howard P. Greisler Large-caliber prostheses used for aortic replacement initiate blood–material interfacial processes that begin almost immediately upon establishment of circulatory flow. These processes lead to prosthetic encapsulation and structural alteration, occasionally a degree of degradation of synthetic polymers, and ultimately these events contribute to the long-term development of thrombosis, intimal hyperplasia, tissue incorporation, and dilatation of aortic prostheses. Early Host Responses to Implanted Materials Protein Deposition Almost immediately after circulatory flow is established, protein adsorbs to the biomaterial surface and provides the initial scaffold upon which host coagulation and healing responses will build. Initially, the most abundant and mobile proteins such as albumin, immunoglobulin G (IgG), low-density lipoprotein (LDL) cholesterol, high-density lipoprotein (HDL) cholesterol, fibrinogen, and others are adsorbed to the prosthetic surfaces. Over the next several minutes to hours, protein adsorption continues on the biomaterial surface as determined by the Vroman effect. This is characterized by the dynamic interchange between proteins initially adsorbed on the biomaterial surface and proteins with higher affinity whose binding properties depend on their intrinsic three-dimensional conformational and electrochemical properties, as well as the structural irregularity and electrochemical activity of the biomaterial itself. Platelet Deposition and Coagulation The tendency of biomaterials to adhere platelets and promote their aggregation and activation before fibrin coagulum forms is a critical component to the host’s response to prosthetic material. Clearly, thrombus formation not only leads to acute graft failures but also serves as a scaffold for mesenchymal and inflammatory cell infiltration before the formation of atherosclerotic plaques and intimal hyperplastic lesions. Platelet adherence occurs by way of binding of the platelet surface glycoprotein (GP) receptor complexes to exposed subendothelial extracellular matrix (ECM) proteins like collagen or to von Willebrand factor (vWF) bound to collagen. The interaction between these glycoproteins and vWF bound to the exposed subendothelium or to endothelial cell (EC) surfaces activates platelets and causes the release of α-granule products, and it increases the local concentrations of serotonin, epinephrine, and adenosine diphosphate (ADP), among others. This degranulation serves to propagate platelet aggregation and activation. The formation of the prothrombinase complex on activated platelets mediated by the extrinsic coagulation pathway facilitates thrombin formation and subsequent fibrin generation. Inflammation Implanted prosthetics activate complement primarily through the classical and alternative pathways, and the degree of complement activation appears to depend on the type of biomaterial used. The activation of complement can have significant downstream effects by propagating inflammation, inducing anaphylactoid reactions, and potentially promoting graft thrombosis. In response to complement activation, generated C5a, chemokines like leukotriene B4 (LTB4), platelet-activating factor (PAF), and deposited fibrin coagulum, neutrophils are recruited early in inflammation and produce products of oxygen metabolism and proteases that contribute to tissue injury and prosthetic degradation. If an endothelium is present, neutrophil integrin receptors and sulfated sialyl-Lewis receptors bind to endothelial cell intercellular adhesion molecules (ICAMs) and P- and E-selectins. Subsequent to neutrophil infiltration, macrophages, which either are resident in the tissues or are derived from circulating monocytes, also comprise part of the early response to implanted vascular grafts. Monocytes are recruited to implanted grafts by numerous chemokines and macrophage-recruiting mediators from various sources including the regenerating endothelium, platelets, and other macrophages, as well by the fibrin coagulum and complement products. These activated macrophages produce inflammatory mediators like interleukin 1 (IL-1), tumor necrosis factor (TNF), and others, which propagate the host response of wound healing and the reaction to foreign materials and which promote the development and remodeling of pseudointimal hyperplastic regions on the surface of grafts. The formation of foreign body giant cells by macrophages, which cover the surface of polytetrafluoroethylene (ePTFE) and polyethylene terephthalate (PET), is part of a larger chronic inflammatory state that attenuates the healing and re-endothelialization of the biomaterial. Mesenchymal Cell Infiltration The infiltration of smooth muscle cells (SMCs) and fibroblasts onto the luminal surface of implanted prosthetic grafts is an early event in the development of the later consequence of intimal hyperplasia. These cells migrate from the arterial media and adventitia to the luminal surface of the implanted prosthesis (or the disrupted luminal surface of vein grafts or arteries following therapeutic interventions) primarily, in the case of synthetic prostheses, at the prosthesis–host anastomotic junction. There the SMCs proliferate over the next several weeks to months. Continued synthetic behavior by SMCs contributes to the deposition of extracellular matrix proteins such as collagens and further propagation and remodeling of the perianastomotic pseudointimal lesion. Beyond 1 to 2 cm from either anastomosis of synthetic prostheses, the luminal surface becomes covered primarily by compacted organized fibrin coagulum, devoid of mesenchymal cells. Platelet deposition onto this surface remains chronically elevated, but platelet desquamation generally results in minimal late progression of pseudointimal thickness in the mid-portion of these implants. Only gold members can continue reading. Log In or Register to continue Share this:Click to share on Twitter (Opens in new window)Click to share on Facebook (Opens in new window) Related Related posts: Technical Aspects of Percutaneous Carotid Angioplasty and Stenting for Arteriosclerotic Disease Management of Acute Limb Ischemia Complicating Aortic Reconstruction Treatment of Dyslipidemia and Hypertriglyceridemia Intraoperative Assessment of the Technical Adequacy of Carotid Endarterectomy Stay updated, free articles. Join our Telegram channel Join Tags: Current Therapy in Vascular and Endovascular Surgery Aug 25, 2016 | Posted by admin in CARDIOLOGY | Comments Off on Long-Term Alterations in Large-Caliber Arterial Prostheses Used for Aortic Repair Full access? Get Clinical Tree
