Biodegradation of polyether polyurethane inner insulation in bipolar pacemaker leads

Wiggins, Michael J.; Wilkoff, Bruce L.; Anderson, J. M.; Hiltner, A.

doi:10.1002/1097-4636(2001)58:3<302::aid-jbm1021>3.3.co;2-p

Cited by 45 publications

(82 citation statements)

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“…18 Monocytes, macrophages, and neutrophils are indicated as crucial cells in the biodegradation of polyurethane outer (environmental stress cracking) and inner insulation (metal ion oxidation) in bipolar pacemaker leads. 19,20 We observed failure of the outer silicone insulation of transcutaneously removed endocardial leads. 16,21 Scanning electron microscope (SEM) analysis revealed uncharacteristic silicone degradation.…”

Section: Clinical Perspective On P 286mentioning

confidence: 95%

Biodegradation of the Outer Silicone Insulation of Endocardial Leads

Kołodzińska

Kutarski

Kozłowska

et al. 2013

Circ: Arrhythmia and Electrophysiology

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Background-Silicone catheter insulation, larynx prostheses undergo biodegradation. The aims of the study were to verify the conviction that outer silicone lead insulation is biostable and inert in addition to determining the role of macrophages (M) and Staphylococcus aureus (S aureus) strains in the silicone lead insulation degradation. Methods and Results-Leads removed from 8 patients because of infective and noninfective indications were analyzed with stereomicroscope and classified according to Banacha abrasion classification, and additional analysis using scanning electron microscope was performed. The examination revealed excavations of different shape and depth in the abraded areas. Fresh silicone-insulated lead was cut into fragments. The fragments were cultured with RAW 264.7 macrophage cell line for 9 weeks. Additional lead fragments were placed with S aureus strains: ATCC 25923, ATCC 29213, and K9328H. Lead fragments were also cocultured with the bacterial strains and RAW M. In scanning electron microscope analysis, diminution in silicone was observed. All S aureus strains provoked insulation damage after 9 weeks. The lowest level of degradation of insulation concerned ATCC 25923. Silicone lead fragments in cocultures presented a further gone level of silicone biodegradation. Conclusions-S aureus, macrophages separately, and S aureus and macrophages cocultures initiate the biodegradation of silicone insulation. Differences in the level of biodegradation between strains of S aureus were observed, with the most aggressive reaction toward silicone visible in the cocultures. In vivo silicone biodegradation is initiated by tearing among surfaces of the lead insulation, macrophages may be the crucial cells for the process that may be aggravated by pathogen colonization. (Circ Arrhythm Electrophysiol. 2013;6:279-286.)Key Words: cardiovasular implantable electronic device infection ◼ endocardial lead abrasion ◼ endocardial lead damage ◼ infective endocarditis ◼ silicone biodegradation

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Section: Clinical Perspective On P 286mentioning

confidence: 95%

Biodegradation of the Outer Silicone Insulation of Endocardial Leads

Kołodzińska

Kutarski

Kozłowska

et al. 2013

Circ: Arrhythmia and Electrophysiology

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“…sarcoidosis, rheumatoid arthritis, and various neoplasias, or the presence of foreign bodies (Chambers 1982, Anderson 2000. So-called foreign body-type giant cells (FBGC) form extensively on implanted biomedical devices, covering up to 25% of implant surface area, and mediate biomaterial degradation (Zhao 1991, Wiggins 2001 leading to implant failure and retrieval (Anderson 1988). Although multinucleated giant cells were documented well over a century ago in lesions of tuberculosis (Langhans 1868) and have long been regarded as hallmark histiological features of chronic inflammation, little is known about the signals that drive their formation, the molecular mechanism(s) by which macrophage fusion occurs, or their physiological significance at sites of chronic inflammation.…”

Section: Introductionmentioning

confidence: 99%

Foreign body-type multinucleated giant cell formation requires protein kinase C β, δ, and ζ

McNally

MacEwan

Anderson

2008

Experimental and Molecular Pathology

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Multinucleated giant cells are a classic cellular feature of chronic inflammation, although the mechanism of macrophage fusion leading to their formation is not well understood. Here, we investigate the participation of protein kinase C (PKC) in the interleukin (IL)-4-induced fusion of human monocyte-derived macrophages and foreign body giant cell (FBGC) formation in vitro. The PKC inhibitors H-7 and calphostin C attenuated macrophage fusion, whereas H-8, which is more selective for PKA and PKG, did not. Macrophage fusion was also prevented by the phospholipase C inhibitor, Et-18-OCH 3 , the PKC isoform inhibitors GO6983 or rottlerin and by peptide inhibitors for PKC (20-28), PKCβ, or PKCζ but not by HBDDE or peptide inhibitors for PKCε or PKA. In cultures of fusing macrophages/FBGC, we detected only PKCα, β, δ, and ζ by immunoprecipitation and immunoblotting, and we also observed strong expression of these isoforms by immunocytochemistry. Our collective results suggest that the γ, ε, η, μ, θ, or ι PKC isoforms are not required in the mechanism of IL-4-induced macrophage fusion; whether PKCα is required is unclear. However, new evidence is provided that FBGC formation is supported by PKCβ, PKCδ, and PKCζ in combined diacylglycerol-dependent (PKCβ and PKCδ) and -independent (PKCζ) signaling pathways.

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“…The main reason for interest in PUs is because of their excellent physical properties, such as elasticity, abrasion resistance, durability, chemical stability and easy processability [87]. These properties enable the use of PUs in several biomedical applications [86], including pacemaker lead insulation [88,89], breast implants [90,91], heart valves [92,93], vascular prostheses [94,95], bioadhesives [96,97] and vehicles for controlled delivery of active compounds [98,99].…”

Section: Polyurethanementioning

confidence: 99%