Objectives Medicaid and Uninsured populations are a significant focus of current healthcare reform. We hypothesized that outcomes following major surgical operations in the United States is dependent on primary payer status. Methods From 2003 to 2007, 893,658 major surgical operations were evaluated using the Nationwide Inpatient Sample (NIS) database: lung resection, esophagectomy, colectomy, pancreatectomy, gastrectomy, abdominal aortic aneurysm repair, hip replacement, and coronary artery bypass. Patients were stratified by primary payer status: Medicare (n = 491,829), Medicaid (n = 40,259), Private Insurance (n = 337,535), and Uninsured (n = 24,035). Multivariate regression models were applied to assess outcomes. Results Unadjusted mortality for Medicare (4.4%; odds ratio [OR], 3.51), Medicaid (3.7%; OR, 2.86), and Uninsured (3.2%; OR, 2.51) patient groups were higher compared to Private Insurance groups (1.3%, P < 0.001). Mortality was lowest for Private Insurance patients independent of operation. After controlling for age, gender, income, geographic region, operation, and 30 comorbid conditions, Medicaid payer status was associated with the longest length of stay and highest total costs (P < 0.001). Medicaid (P < 0.001) and Uninsured (P < 0.001) payer status independently conferred the highest adjusted risks of mortality. Conclusions Medicaid and Uninsured payer status confers increased risk-adjusted mortality. Medicaid was further associated with the greatest adjusted length of stay and total costs despite risk factors or operation. These differences serve as an important proxy for larger socioeconomic and health system-related issues that could be targeted to improve surgical outcomes for US Patients.

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Implementation of a blood use initiative significantly improves postoperative morbidity, mortality, and resource utilization. Limiting intraoperative and postoperative blood product transfusion decreases adverse postoperative events and reduces health care costs. Blood conservation efforts are bolstered by collaboration and guideline development.

Rationale: We recently implicated a role for CD4 1 T cells and demonstrated elevated IL-17A expression in lung ischemia-reperfusion (IR) injury. However, identification of the specific subset of CD4 1 T cells and their mechanistic role in IR injury remains unknown. Objectives: We tested the hypothesis that invariant natural killer T (iNKT) cells mediate lung IR injury via IL-17A signaling. Methods: Mice underwent lung IR via left hilar ligation. Pulmonary function was measured using an isolated lung system. Lung injury was assessed by measuring edema (wet/dry weight) and vascular permeability (Evans blue dye). Inflammation was assessed by measuring proinflammatory cytokines in lungs, and neutrophil infiltration was measured by immunohistochemistry and myeloperoxidase levels. Measurements and Main Results: Pulmonary dysfunction (increased airway resistance and pulmonary artery pressure and decreased pulmonary compliance), injury (edema, vascular permeability), and inflammation (elevated IL-17A; IL-6; tumor necrosis factor-a; monocyte chemotactic protein-1; keratinocyte-derived chemokine; regulated upon activation, normal T-cell expressed and secreted; and neutrophil infiltration) after IR were attenuated in IL-17A 2/2 and Rag-1 2/2 mice. Anti-IL-17A antibody attenuated lung dysfunction in wildtype mice after IR. Reconstitution of Rag-1 2/2 mice with wild-type, but not IL-17A 2/2 , CD4 1 T cells restored lung dysfunction, injury, and inflammation after IR. Lung dysfunction, injury, IL-17A expression, and neutrophil infiltration were attenuated in Ja18 2/2 mice after IR, all of which were restored by reconstitution with wild-type, but not IL-17A 2/2 , iNKT cells. Flow cytometry and enzyme-linked immunosorbent spot assay confirmed IL-17A production by iNKT cells after IR.Conclusions: These results demonstrate that CD4 1 iNKT cells play a pivotal role in initiating lung injury, inflammation, and neutrophil recruitment after IR via an IL-17A-dependent mechanism.

Background Patients with long-standing persistent (LSP) atrial fibrillation (AF) who have previously undergone catheter ablation represent a challenging patient population. Repeat catheter ablation in these patients is arduous and associated with a high failure rate, whereas surgical ablation can be complicated by multiple flutters. We sought to determine if minimally-invasive surgical ablation, followed by catheter ablation of all inducible flutters, would improve success rates over repeat catheter ablation alone. Methods Fifteen patients (Sequential) with persistent or LSP AF who failed at least one catheter ablation and one anti-arrhythmic drug (AAD) underwent surgical ablation, followed by planned endocardial evaluation and catheter mapping with ablation during the same hospitalization. Sequential patients were matched to 30 patients who had previously failed at least one catheter ablation and underwent a repeat catheter ablation (catheter-alone). The primary end point was event-free survival of any documented AF recurrence or AAD use. Results All patients underwent uncomplicated surgical ablation and electrophysiology procedure. Five Sequential patients had seven inducible flutters that were mapped and ablated. After a mean follow-up of 20.7 ± 4.5 months, 13/15 (86.7%) Sequential patients, but only 16/30 (53.3%) catheter-alone patients, were free of any atrial arrhythmia and off of AAD (p = 0.04). On AAD, 14/15 (93.3%) Sequential patients were free of any atrial arrhythmia recurrence, compared to 17/30 (56.7%) catheter-alone patients (p = 0.01). Conclusions For patients with atrial fibrillation who have failed catheter ablation, Sequential minimally invasive epicardial surgical ablation, followed by endocardial catheter-based ablation, has a higher early success rate than repeat catheter ablation alone.