Utility of preoperative Holter monitoring in children undergoing extracardiac conduit Fontan operation.

BACKGROUND: In patients undergoing extracardiac conduit Fontan (ECF) who require postoperative pacing, epicardial leads are usually required because of anatomical constraints. If indicated, these could be conveniently placed at the time of ECF. We have routinely performed ambulatory 24-hour Holter monitoring before ECF to determine the presence or absence of preoperative sinus node dysfunction, in an attempt to avoid repeat sternotomy at a later time. METHODS: We performed a retrospective study of all patients undergoing ECF from January 2000 to December 2015. RESULTS: Two hundred sixteen patients met inclusion criteria. Patients were separated into two groups, those with preoperative Holter monitoring (PHM, n = 150) and those without (No-PHM, n = 66). Ten patients (4.6%) underwent permanent pacemaker implantation at the time of ECF (eight patients [5.3%] in PHM vs two patients [3.0%] in No-PHM, P = 0.46). There were seven (3.2%) patients who underwent pacemaker implantation after ECF requiring repeat sternotomy (four patients [2.7%] in PHM vs three patients [4.5%] in No-PHM, P = 0.47). Fourteen (6.5%) patients underwent permanent epicardial lead placement without a pulse generator at the time of ECF. None from this group underwent pacemaker implantation to date (median follow-up of 5.7 years). The overall incidence of pacemaker implantation was 9.3% (20 patients). CONCLUSIONS: In our series, arrhythmia disturbances requiring pacing after ECF occurred in just over 9% of patients. While PHM in those patients may help predict which patients might require postoperative pacing, this approach did not result in a significant decrease in those patients requiring repeat sternotomy for pacemaker implantation.

Identifying the Long-Term Role of Inducible Nitric Oxide Synthase after Contusive Spinal Cord Injury Using a Transgenic Mouse Model.

Inducible nitric oxide synthase (iNOS) is a potent mediator of oxidative stress during neuroinflammation triggered by neurotrauma or neurodegeneration. We previously demonstrated that acute iNOS inhibition attenuated iNOS levels and promoted neuroprotection and functional recovery after spinal cord injury (SCI). The present study investigated the effects of chronic iNOS ablation after SCI using inos-null mice. iNOS-/- knockout and wild-type (WT) control mice underwent a moderate thoracic (T8) contusive SCI. Locomotor function was assessed weekly, using the Basso Mouse Scale (BMS), and at the endpoint (six weeks), by footprint analysis. At the endpoint, the volume of preserved white and gray matter, as well as the number of dorsal column axons and perilesional blood vessels rostral to the injury, were quantified. At weeks two and three after SCI, iNOS-/- mice exhibited a significant locomotor improvement compared to WT controls, although a sustained improvement was not observed during later weeks. At the endpoint, iNOS-/- mice showed significantly less preserved white and gray matter, as well as fewer dorsal column axons and perilesional blood vessels, compared to WT controls. While short-term antagonism of iNOS provides histological and functional benefits, its long-term ablation after SCI may be deleterious, blocking protective or reparative processes important for angiogenesis and tissue preservation.