Kidney transplantation in ESRD patients with advanced systolic heart failure results in an increase in LVEF, improves functional status of CHF, and increases survival. To abrogate the adverse effects of prolonged dialysis on myocardial function, ESRD patients should be counseled for kidney transplantation as soon as the diagnosis of systolic heart failure is established.

The shear-induced intracellular signal transduction pathway in vascular endothelial cells involves tyrosine phosphorylation and activation of mitogen-activated protein (MAP) kinase, which may be responsible for the sustained release of nitric oxide. MAP kinase is known to be activated by reactive oxygen species (ROS), such as H2O2, in several cell types. ROS production in ligand-stimulated nonphagocytic cells appears to require the participation of a Ras-related small GTP-binding protein, Rac1. We hypothesized that Rac1 might serve as a mediator for the effect of shear stress on MAP kinase activation. Exposure of bovine aortic endothelial cells to laminar shear stress of 20 dyn/cm2 for 5–30 min stimulated total cellular and cytosolic tyrosine phosphorylation as well as tyrosine phosphorylation of MAP kinase. Treating endothelial cells with the antioxidants N-acetylcysteine and pyrrolidine dithiocarbamate inhibited in a dose-dependent manner the shear-stimulated increase in total cytosolic and, specifically, MAP kinase tyrosine phosphorylation. Hence, the onset of shear stress caused an enhanced generation of intracellular ROS, as evidenced by an oxidized protein detection kit, which were required for the shear-induced total cellular and MAP kinase tyrosine phosphorylation. Total cellular and MAP kinase tyrosine phosphorylation was completely blocked in sheared bovine aortic endothelial cells expressing a dominant negative Rac1 gene product (N17rac1). We concluded that the GTPase Rac1 mediates the shear-induced tyrosine phosphorylation of MAP kinase via regulation of the flow-dependent redox changes in endothelial cells in physiological and pathological circumstances.

Our series demonstrates the simple and safe technique of transfemoral lead snaring to assist lead extraction and maintain vascular access in the setting of venous occlusion, when the distal lead tip pulls free of the myocardium before an extraction sheath is passed beyond the point of venous obstruction.

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Background: Cardiac implantable electronic device infections are associated with substantial morbidity and mortality. There are varied recommendations in the literature about treatment of the wound after extraction of all hardware, but only conservative, time-consuming approaches such as open packing and negative-pressure therapy along with a long interval before reimplanting any hardware have generally been recommended for the treatment. 1 – 4 Methods: A retrospective review was performed of 42 patients treated at Jersey Shore University Medical Center for implantable cardioverter defibrillator and permanent pacemaker infections between July 2010 and April 2018 with an aggressive, multidisciplinary approach utilizing an invasive cardiologist and a plastic surgeon. Clinical and demographic data were collected, and a descriptive analysis was conducted. Results: A total of 42 patients, with a median age of 76 years, were selected for our treatment of pacemaker pocket infection. Patients underwent removal of all hardware followed by debridement and flap closure of the wound soon after extraction. Reimplantation was performed when indicated typically within a week after initial extraction and typically on the contralateral side. There were no reports of reinfection and no mortality in all 42 patients treated. Conclusion: We found that the aggressive removal of all hardware and excisional debridement of the entire capsule followed by flap coverage and closure of the wound allowed for a shortened interval to reimplantation with no ipsilateral or contralateral infections during the follow-up period.