ABSTRACT
OBJECTIVES: Driveline infections continue to be a significant complication following left ventricular assist device (LVAD) implantation. Driveline exit-site care is crucial for the prevention of infections; however, there are no uniform guidelines. The goal of this study was to provide an overview of the currently published driveline exit-site care protocols in patients with LVAD. METHODS: A systematic literature review was performed. Studies before 15 December 2020 were included if the number of driveline infections was a primary outcome and the driveline exit-site care protocol was explained. RESULTS: Eleven articles were included in the systematic review, including 1602 patients with LVADs. The median of the frequency of driveline infections in the articles was 13.8% with a range of 0-52.6%. There was a marked variability in the methods of care of driveline exit sites, without a standardized driveline dressing technique in patients with LVADs. The frequency of driveline infections was 6-7.5% in studies using a dressing kit that included chlorhexidine, a silver-based dressing and an anchoring device. Furthermore, there was variability in the anchoring devices and the frequency of dressing changes, which varied from daily to weekly. No specific anchoring device or change frequency was found to be superior. CONCLUSIONS: Based on this systematic review, driveline exit care protocols that included chlorhexidine, a silver-based dressing, the use of an anchoring device and dressing kits might be best in reducing driveline infection rates. However, prospective studies with larger cohorts are needed to establish the optimal protocol for driveline exit-site care.
Subject(s)
Heart Failure , Heart-Assist Devices , Prosthesis-Related Infections , Clinical Protocols , Heart Failure/therapy , Heart Ventricles , Heart-Assist Devices/adverse effects , Humans , Prospective Studies , Prosthesis-Related Infections/epidemiology , Prosthesis-Related Infections/prevention & controlABSTRACT
Molecular mimicry of Campylobacter jejuni lipooligosaccharides (LOS) by gangliosides in peripheral nerve tissue probably triggers the Guillain-Barré syndrome due to the induction of cross-reactive antibodies. PCR-restriction fragment length polymorphism analysis of C. jejuni genes involved in the biosynthesis of LOS demonstrated that specific genes were associated with the expression of ganglioside mimics and the development of neuropathy.
Subject(s)
Antibodies, Bacterial/immunology , Campylobacter jejuni/genetics , Guillain-Barre Syndrome/immunology , Lipopolysaccharides/biosynthesis , Polymerase Chain Reaction/methods , Polymorphism, Restriction Fragment Length , Biomarkers , Cross Reactions , Gene Expression Regulation, Bacterial , Humans , Lipopolysaccharides/immunology , Molecular MimicryABSTRACT
Tuberous sclerosis is an autosomal dominant human disorder caused by inactivating mutations to either the TSC1 or TSC2 tumour suppressor gene. Hamartin and tuberin, the TSC1 and TSC2 gene products, interact and the tuberin-hamartin complex inhibits cell growth by antagonising signal transduction to downstream effectors of the mammalian target of rapamycin (mTOR) through the small GTPase rheb. Previously, we showed that pathogenic tuberin amino-acid substitutions disrupt the tuberin-hamartin complex. Here, we investigate how these mutations affect the role of tuberin in the control of signal transduction through mTOR. Our data indicate that specific amino-acid substitutions have distinct effects on tuberin function.
