Post-operative Outcomes and Survivorship for Shoulder Arthroplasty following Glenohumeral Tumor Resection.

A paucity of data exists for post-operative complications and survivorship in patients undergoing resection arthroplasty procedures for treatment of glenohumeral tumors. This study investigates patient and tumor characteristics, 90-day and long-term post-operative complications, and overall survivorship following glenohumeral tumor resection arthroplasty procedures. This single-center retrospective review identified 13 patients, with mean age of 51.6 ± 15.7 years, mean body mass index of 26.5 ± 6.4 kg/m2, and mean Charlson Comorbidity Index of 4.9 ± 2.4, who underwent shoulder arthroplasty procedures for glenohumeral tumors, most commonly for chondrosarcoma (n = 5) and metastatic disease (n = 3). Nine patients (69.2%) underwent revision surgeries at a median of 677 days, most commonly for prosthesis instability, dislocation (n=4) or aseptic loosening (n = 3). Seven patients (53.8%) were deceased at a median of 593.6 days. Resection arthroplasty in the treatment of glenohumeral tumors demonstrates low rates of complications during the global period but are fraught with long-term complications. This data provides pertinent information to pre-operatively counsel patients on post-operative expectations. (Journal of Surgical Orthopaedic Advances 31(4):248-251, 2022).

Genetic ablation of serotonin receptor 2B improves aortic valve hemodynamics of Notch1 heterozygous mice in a high-cholesterol diet model.

Calcific aortic valve disease (CAVD) is a deadly disease that is rising in prevalence due to population aging. While the disease is complex and poorly understood, one well-documented driver of valvulopathy is serotonin agonism. Both serotonin overexpression, as seen with carcinoid tumors and drug-related agonism, such as with Fenfluramine use, are linked with various diseases of the valves. Thus, the objective of this study was to determine if genetic ablation or pharmacological antagonism of the 5-HT2B serotonin receptor (gene: Htr2b) could improve the hemodynamic and histological progression of calcific aortic valve disease. Htr2b mutant mice were crossed with Notch1+/- mice, an established small animal model of CAVD, to determine if genetic ablation affects CAVD progression. To assess the effect of pharmacological inhibition on CAVD progression, Notch1+/- mice were treated with the 5-HT2B receptor antagonist SB204741. Mice were analyzed using echocardiography, histology, immunofluorescence, and real-time quantitative polymerase chain reaction. Htr2b mutant mice showed lower aortic valve peak velocity and mean pressure gradient-classical hemodynamic indicators of aortic valve stenosis-without concurrent left ventricle change. 5-HT2B receptor antagonism, however, did not affect hemodynamic progression. Leaflet thickness, collagen density, and CAVD-associated transcriptional markers were not significantly different in any group. This study reveals that genetic ablation of Htr2b attenuates hemodynamic development of CAVD in the Notch1+/- mice, but pharmacological antagonism may require high doses or long-term treatment to slow progression.