Salvage Coronary Artery Bypass Predicts Increased Mortality During Aortic Root Operation.

BACKGROUND: Aortic root replacement (ROOT) has been an established therapy, yet the impact of adding coronary artery bypass grafting (CABG) to ROOT (CABG-R) is unknown. The purpose of this research was to investigate the impact of CABG on the outcomes of ROOT. METHODS: A retrospective review from 2004 to 2016 of patients undergoing nonemergent ROOT surgical procedure was performed. Cohorts were established based on the presence or absence of added CABG. A propensity-score weighted comparison of outcomes was then conducted. RESULTS: A total of 867 patients met inclusion criteria and were analyzed (711 ROOT [72.0%], 156 CABG-R [18.0%]). CABG-R patients were older and had higher proportions of previous valve operation, hypertension, endocarditis, immunosuppressive therapy, renal insufficiency, and redo operation (all p < 0.01). Indications for CABG included anatomy (n = 48, 30.8%), coronary artery disease (80, 51.3%), and ventricular failure (28, 17.9%). The permanent stroke rate was not significantly increased with the addition of CABG-R (p = 0.06). Thirty-day mortality was 5.5% for the entire cohort but was substantially higher in patients who underwent concomitant CABG (3.4% ROOT, 15.4% CABG-R). Mortality rates were highest among patients with acute ventricular failure and CABG (28.8%) compared with patients who underwent CABG for coronary artery disease (6.3%) or patients for anatomy (22.9%; p = 0.003). CONCLUSIONS: CABG-R results in increased postoperative morbidity or mortality compared with isolated ROOT. Outcomes, however, are influenced by the specific clinical indication. CABG for coronary artery disease was associated with similar outcomes compared with isolated ROOT. Patients undergoing unplanned CABG for acute ventricular failure had the worst outcomes, thus underscoring the importance of technical success during coronary reimplantation.

The protective effect of the blood brain barrier from systemic cytokines in an animal femur fracture model.

BACKGROUND: Previous studies of head trauma have shown profound release of cytokines in the brain. These changes were not expressed in peripheral tissues. The intent of this study was to take an animal model of femur fracture, monitor the expression of biochemical markers in the periphery, and compare this to their expression in the brain. METHODS: Rats were subjected to a weight-drop, femur fracture model, and then killed at various times. Samples of muscle, liver, serum, and brain were analyzed for concentrations of cytokines, and compared with controls. RESULTS: Statistically significant (p < 0.05) results from the study were found in the liver. Interleukin (IL)-2, IL-10, IL-11, and other acute phase reactants were elevated at 24 hours after injury, compared with in controls. Analysis of these cytokines in the brain showed no significant increase when compared with those of controls. Further analysis also demonstrated an increase in plasma C-reactive protein and leptin in the fracture group. These results differ from our previous brain trauma study, which demonstrated no increased expression of cytokines in liver or plasma. CONCLUSIONS: This animal model of peripheral injury demonstrates that there is a significant rise in acute phase reactants in liver tissue and plasma within 24 hours after injury, without a corresponding rise in cytokine concentration in the brain. These results suggest that although the brain is potentially exposed to the biochemical response to injury, the brain parenchyma itself is protected from up-regulation of proinflammatory cytokines. Interestingly, this is the opposite effect seen in our isolated brain injury study.