Electrical abnormalities with St. Jude/Abbott pacing leads: A systematic review and meta-analysis.

BACKGROUND: Although there is a paucity of contemporary data on pacemaker lead survival rates, small studies suggest that some leads may have higher malfunction rates than do others. OBJECTIVE: The purpose of this study was to determine the malfunction rates of current pacemaker leads. METHODS: A meta-analysis including studies that examined the non-implant-related lead malfunction rates of current commercially available active fixation pacemaker leads was performed. An electronic search of MEDLINE/PubMed, Scopus, and Embase was performed. DerSimonian and Laird random effects models were used. RESULTS: Eight studies with a total of 14,579 leads were included. Abbott accounted for 10,838 (74%), Medtronic 2510 (17%), Boston Scientific 849 (6%), and MicroPort 382 (3%) leads. The weighted mean follow-up period was 3.6 years. Lead abnormalities occurred in 5.0% of all leads, 6.1% of Abbott leads, 1.1% of Medtronic, 1.4% of Boston Scientific, and 5.5% of MicroPort. The most common lead abnormality was lead noise with normal impedance. Abbott leads were associated with an increased risk of abnormalities (relative risk [RR] 7.81; 95% confidence interval [CI] 3.21-19.04), reprogramming (RR 7.95; 95% CI 3.55-17.82), and lead revision or extraction (RR 8.91; 95% CI 3.36-23.60). Abbott leads connected to an Abbott generator had the highest abnormality rate (8.0%) followed by Abbott leads connected to a non-Abbott generator (4.7%) and non-Abbott leads connected to an Abbott generator (0.4%). CONCLUSIONS: Abbott leads are associated with an increased risk of abnormalities compared with leads of other manufacturers, primarily manifesting as lead noise with normal impedance, and are associated with an increased risk of lead reprogramming and lead revision or extraction.

Endoscopic Endonasal Reconstruction of High-Flow Cerebrospinal Fluid Leak with Fascia Lata "Button" Graft and Nasoseptal Flap: Surgical Technique and Case Series.

Background The endoscopic endonasal approach (EEA) has become increasingly used for resection of skull base tumors in the sellar and suprasellar regions. A nasoseptal flap (NSF) is routinely used for anterior skull base reconstruction; however, there are numerous additional allografts and autografts being used in conjunction with the NSF. The role of perioperative cerebrospinal fluid (CSF) diversion is also unclear. Objective This study was aimed to analyze success of high-flow CSF leak repair during EEA procedures without use of CSF diversion through lumbar drainage. Methods A retrospective chart review of patients who had intraoperative high-flow CSF leak during EEA procedures at our institution between January 2013 and December 2017 was performed. CSF leaks were repaired with use of a fascia lata button graft and nasoseptal flap, without use of perioperative lumbar drains. Results A total of 38 patients were identified (10 male, 28 female). Patient BMIs ranged from 19.7 to 49 kg/m 2 (median = 31 kg/m 2 ), with 18 patients meeting criteria for obesity (BMI > 30 kg/m 2 ) and 12 patients overweight (25 kg/m 2 < BMI < 29.9 kg/m 2 ). There was no incidence of postoperative CSF leak. Conclusion In our experience, the nasoseptal flap used in conjunction with the fascia lata button graft is a safe, effective and robust combination for cranial base reconstruction with high-flow intraoperative CSF leaks, without need for lumbar drains.

Inhibition of p16INK4A to Rejuvenate Aging Human Cardiac Progenitor Cells via the Upregulation of Anti-oxidant and NFκB Signal Pathways.

Autologous human cardiac stem/progenitor cell (hCPC) therapy is a promising treatment that has come into use in recent years for patients with cardiomyopathy. Though innovative in theory, a major hindrance to the practical application of this treatment is that the hCPCs of elderly patients, who are most susceptible to myocardial disease, are senescent and prone to cell death. Rejuvenating hCPCs from elderly patients may help overcome this obstacle, and can be accomplished by reversing entry into the cellular stage of senescence. p16INK4A, a cyclin dependent kinase inhibitor, is an important player in the regulation of cell senescence. In this study, we investigated whether knockdown of p16INK4A will rejuvenate aging hCPCs to a youthful phenotype. Our data indicated that upregulation of p16INK4A is associated with hCPC senescence. Both cell proliferation and survival capacity were significantly increased in hCPCs infected with lentivirus expressing p16INK4A shRNA when compared to control hCPCs. The knockdown of p16INK4A also induced antioxidant properties as indicated by a 50% decrease in ROS generation at basal cell metabolism, and a 25% decrease in ROS generation after exposure to oxidative stress. Genes associated with cell senescence (p21CIP1), anti-apoptosis (BCL2 and MCL1), anti-oxidant (CYGB, PRDX1 and SRXN1), and NFκB signal pathway (p65, IKBKB, HMOX1, etc.), were significantly upregulated after the p16INK4A knockdown. Knocking down the NFĸB-p65 expression also significantly diminished the cytoprotective effect caused by the p16INK4A knockdown. Our results suggest that genetic knockdown of p16INK4A may play a significant role in inducing antioxidant effects and extending lifespan of aging hCPCs. This genetic modification may enhance the effectiveness of autologous hCPC therapy for repair of infarcted myocardium.