Impact of Chronic Obstructive Pulmonary Disease on Postoperative Complications Following Simultaneous Bilateral Total Knee Arthroplasty.

For patients who qualify, simultaneous bilateral total knee arthroplasty (TKA) is a viable option for the treatment of bilateral symptoms. However, the incidence of chronic obstructive pulmonary disease (COPD) has been steadily rising over the past few decades and may impact those who qualify as candidates for bilateral TKA. As such, the aim of this study was to determine the impact of COPD on postoperative outcomes in patients who receive simultaneous bilateral TKA. A retrospective cohort study was conducted utilizing data provided through the American College of Surgeons National Surgical Quality Improvement Program. All patients who had undergone simultaneous bilateral TKA between 2007 and 2016 were identified and further stratified into groups based upon the COPD status. Incidence of adverse events after TKA in the acute postoperative period was evaluated with univariate and multivariate analyses. COPD was found to be an independent risk factor for the development of major (odds ratio [OR]: 2.5; p = 0.015), renal (OR: 5.1; p = 0.02), and thromboembolic complications (OR: 2.5; p = 0.027). In addition, patients with COPD were at increased risk for having an extended hospital length of stay (LOS; p < 0.001) and development of urinary tract infections (p < 0.001). Patients with COPD are at higher risk for development of overall major complications, as well as renal and thromboembolic complications after simultaneous bilateral TKA. Interestingly, patients were not at increased risk for the development of pulmonary or wound complications. When considering a staged versus simultaneous bilateral TKA, surgeons should be aware of the impact COPD status has on the postoperative complication rate.

CCN3 Regulates Macrophage Foam Cell Formation and Atherosclerosis.

Recent studies implicate the Cyr61, CTGF, Nov (CCN) matricellular signaling protein family as emerging players in vascular biology, with NOV (alias CCN3) as an important regulator of vascular homeostasis. Herein, we examined the role of CCN3 in the pathogenesis of atherosclerosis. In response to a 15-week high-fat diet feeding, CCN3-deficient mice on the atherosclerosis-prone Apoe-/- background developed increased aortic lipid-rich plaques compared to control Apoe-/- mice, a result that was observed in the absence of alterations in plasma lipid content. To address the cellular contributor(s) responsible for the atherosclerotic phenotype, we performed bone marrow transplantation experiments. Transplantation of Apoe; Ccn3 double-knockout bone marrow into Apoe-/- mice resulted in an increase of atherosclerotic plaque burden, whereas transplantation of Apoe-/- marrow to Apoe; Ccn3 double-knockout mice caused a reduction of atherosclerosis. These results indicate that CCN3 deficiency, specifically in the bone marrow, plays a major role in the development of atherosclerosis. Mechanistically, cell-based studies in isolated peritoneal macrophages demonstrated that CCN3 deficiency leads to an increase of lipid uptake and foam cell formation, an effect potentially attributed to the increased expression of scavenger receptors CD36 and SRA1, key factors involved in lipoprotein uptake. These results suggest that bone marrow-derived CCN3 is an essential regulator of atherosclerosis and point to a novel role of CCN3 in modulating lipid accumulation within macrophages.