We report a case of a 21-year-old young man with underlying congenital heart disease who developed Bartonella henselae endocarditis of the right ventricular outflow tract (RVOT) conduit of his Melody transcatheter (percutaneous) pulmonary valve (TPV), with an initial presentation of glomerulonephritis with a dominant C3 pattern, with renal failure and circulating cryoglobulins. There are few reports of a glomerulonephritis with a dominant C3 pattern presenting as a manifestation of B. henselae endocarditis. While most cases of B. henselae endocarditis affect the aortic valve, in this case the valve damage was to the RVOT of the Melody TPV, a percutaneous transcatheter valve delivery system that had previously replaced his pulmonary homograft, which had become dysfunctional as a result of prior Streptococcus viridans endocarditis. The pulmonary homograft had been in place since childhood as a result of a Ross procedure to repair his congenital aortic stenosis. The patient's renal failure significantly improved after surgical resection of the infected RVOT and institution of appropriate antibiotic therapy.

Immature granulocyte counts in newborns appeared to be higher than reported for other age groups. Use of adult and child norms for IG% would not be appropriate for newborns being evaluated for early-onset sepsis.

A primary concern in the utilization of implantable neural interfaces for the treatment of medical diseases is to follow the Hippocratic dictum: First, do no harm. If we are to avoid harm to the Vagus nerve in our use of stimulatory electrodes in the treatment of heart failure, we must understand the structural and functional elements that comprise peripheral nerves, their susceptibility to various types of injury that might be expected to occur secondary to functional electrical stimulation and how to separate the various components of the response of peripheral nervous system elements to stresses that may occur in the complex interactions that take place between electrode and nerve. To this end, we review the functional histology of peripheral nerve, followed by a consideration of salient types of nerve injuries, which have been elucidated through the combination of careful observations of human disease and well-constructed experimental models. We then examine the extant literature on stimulation-induced nerve injury in light of recent developments in the understanding of electropermeabilization of biological membranes. Finally, we briefly discuss our experience using the CardioFit™ electrode on the canine Vagus nerve.

Background - Acute myocarditis (AM) is a well-known cause of sudden death and heart failure, often caused by prevalent viruses. We previously showed that some pediatric AM correlates with putatively damaging variants in genes related to cardiomyocyte structure and function. We sought to evaluate whether deleterious cardiomyopathic variants were enriched among fatal pediatric AM cases in New York City compared to ancestry-matched controls. Methods - Twenty-four children (aged 3 weeks to 20 years) with death due to AM were identified through autopsy records; histologies were reviewed to confirm that all cases met Dallas criteria for AM and targeted panel sequencing of 57 cardiomyopathic genes was performed. Controls without cardiovascular disease were identified from a pediatric database and matched by genetic ancestry to cases using principal components from exome sequencing. Rates of putative deleterious genetic variation (DV) were compared between cases and controls. Where available, AM tissues underwent viral analysis by PCR. Results - DV were identified in 4 of 24 AM cases (16.7%), compared to 2 of 96 age and ancestry-matched controls (2.1%, P=0.014). Viral etiologies were proven for 6 of 8 AM cases (75%), including the one DV+ case where tissue was available for testing. DV+ cases were more likely to be female, have no evidence of chronic inflammation, and associate with sudden cardiac death than DV- cases. Conclusions - Deleterious variants in genes related to cardiomyocyte integrity are more common in children with fatal AM than controls, likely conferring susceptibility. Additionally, genetically-mediated AM may progress more rapidly and be more severe.