Neo-intimal development on textured biomaterial surfaces during clinical use of an implantable left ventricular assist device

Graham, Timothy R.; Dasse, Kurt A.; Coumbe, A.; Salih, Vehid; Marrinan, M. T.; Frazier, O.H.; Lewis, C. T.

doi:10.1016/1010-7940(90)90002-h

Cited by 65 publications

(26 citation statements)

References 9 publications

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“…Surface modifications have shown great potential for improving the hemocompatibility of biomedical materials and devices [26]. Several authors have discussed the biocompatibility and hemocompatibility of pure titanium [27–30]; therefore, titanium is a promising biocompatible material for biomedical devices, either in the orthopedic or in the cardiovascular field [27]. …”

Section: Discussionmentioning

confidence: 99%

A Novel Platelet Concentrate: Titanium-Prepared Platelet-Rich Fibrin

Tunalı

Özdemir

Küçükodacı

et al. 2014

BioMed Research International

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We developed a new product called titanium-prepared platelet-rich fibrin (T-PRF). The T-PRF method is based on the hypothesis that titanium may be more effective in activating platelets than the silica activators used with glass tubes in Chouckroun's leukocyte- and platelet-rich fibrin (L-PRF) method. In this study, we aimed to define the structural characteristics of T-PRF and compare it with L-PRF. Blood samples were collected from 10 healthy male volunteers. The blood samples were drawn using a syringe. Nine milliliters was transferred to a dry glass tube, and 9 mL was transferred to a titanium tube. Half of each clot (i.e., the blood that was clotted using T-PRF or L-PRF) was processed with a scanning electron microscope (SEM). The other half of each clot was processed for fluorescence microscopy analysis and light microscopy analysis. The T-PRF samples seemed to have a highly organized network with continuous integrity compared to the other L-PRF samples. Histomorphometric analysis showed that T-PRF fibrin network covers larger area than L-PRF fibrin network; also fibrin seemed thicker in the T-PRF samples. This is the first human study to define T-PRF as an autogenous leukocyte- and platelet-rich fibrin product. The platelet activation by titanium seems to offer some high characteristics to T-PRF.

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Section: Discussionmentioning

confidence: 99%

A Novel Platelet Concentrate: Titanium-Prepared Platelet-Rich Fibrin

Tunalı

Özdemir

Küçükodacı

et al. 2014

BioMed Research International

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“…These observations probably reflect changes in the composition of the neointimal lining on the surface of textured cardiac assist devices [8,9,26,27]. Over time, the neointima becomes increasingly covered with cellular components, and the amount of ECM that is exposed to the bloodstream is reduced [8,41]. This change in the cellular surface may account for the reduced bacterial adherence to the VAD membrane.…”

Section: Discussionmentioning

confidence: 99%

The Role ofStaphylococcus aureusAdhesins in the Pathogenesis of Ventricular Assist Device–Related Infections

Arrecubieta

Asai

Bayern³

et al. 2006

J INFECT DIS

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Ventricular assist devices (VADs) are an important form of therapy for end-stage congestive heart failure. However, infection of the VAD, which is often caused by Staphylococcus aureus, poses a major threat to survival. Using a novel in vitro binding assay with VAD membranes and a heterologous lactococcal system of expression, we identify 3 S. aureus proteins-clumping factor A (ClfA) and fibronectin binding proteins A and B (FnBPA and FnBPB) as the main factors involved in adherence to VAD polyurethane membranes. Adherence is greatly diminished by long implantation times, reflecting a change in topological features of the VAD membrane, and is primarily mediated by the FnBPA domains in the staphylococcal proteins. We also compare the adherence of S. aureus mutant strains and show that other staphylococcal components appear to be involved in adherence to VAD membranes. Finally, we demonstrate that ClfA, FnBPA, and FnBPB mediate bacterial infection of implanted murine intra-aortic polyurethane patches.The ventricular assist device (VAD) is an important form of therapy for patients with congestive heart failure. Originally introduced as a bridge to cardiac transplantation, it is increasingly also used for "destination therapy" [1]. A serious limitation to the long-term use of VADs has been the high incidence of device-related infections, which occur in 28%-48% of patients [2][3][4][5]. These infections, which are often caused by Staphylococcus aureus, pose a major threat to survival, because eradication of the infection usually requires removal of the device [2,6,7].Although the clinical features of VAD-related infections caused by S. aureus are well described, little is known about their pathogenetic processes [2,[5][6][7]. The microenvironment of the VAD surface is dynamic, with constant remodeling of the neointimal surface, beginning with platelet deposition and formation of a fibrin scaffold after which a variety of cell types attach and proliferate [8,9]. As a result of this process, the bacterialneointimal surface interactions change over time. Despite the increasing biological relevance of these interactions, the complex interplay of bacterial adhesins and the prosthetic neointimal surface has received limited attention. In particular, the contribution of proteins belonging to the family of microbial surface components recognizing adhesive matrix molecules (MSCRAMMs), which have been demonstrated to play a role in other S. aureus inDownloaded from https://academic.oup.

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“…52 Published by Woodhead Publishing Limited, 2012 Heparin coatings are applied, preferably, through immobilization by covalent bonding, but the chemistry involved is rather complex.…”

Section: Heparin Coatingsmentioning

confidence: 99%