ObjectivesAn increasing number of octogenarians are referred to undergo mitral valve surgery for degenerative disease, and percutaneous approaches are being increasingly used in this subgroup of patients. We sought to determine the survival and its predictors after Mitral Valve Surgery in Octogenarians (MiSO) in a multicenter UK study of high-volume specialized centers.MethodsPooled data from 3 centers were collected retrospectively. To identify the predictors of short-term composite outcome of 30 days mortality, acute kidney injury, and cerebrovascular accident, a multivariable logistic regression model was developed. Multiple Cox regression analysis was performed for late mortality. Kaplan–Meier curves were generated for long-term survival in various subsets of patients. Receiver operating characteristic analysis was done to determine the predictive power of the logistic European System for Cardiac Operative Risk Evaluation.ResultsA total of 247 patients were included in the study. The median follow-up was 2.9 years (minimum 0, maximum 14 years). A total of 150 patients (60.7%) underwent mitral valve repair, and 97 patients (39.3%) underwent mitral valve replacement. Apart from redo cardiac surgery (mitral valve repair 6 [4%] vs mitral valve replacement 11 [11.3%], P = .04) and preoperative atrial fibrillation (mitral valve repair 79 [52.6%] vs mitral valve replacement 34 [35.1%], P < .01), there was no significant difference in terms of any other preoperative characteristics between the 2 groups. Patient operative risk, as estimated by logistic European System for Cardiac Operative Risk Evaluation, was lower in the mitral valve repair group (10.2 ± 11.8 vs 13.7 ± 15.2 in mitral valve replacement; P = .07). No difference was found between groups for duration of cardiopulmonary bypass and aortic crossclamp times. The 30-day mortality for the whole cohort was 13.8% (mitral valve repair 4.7% vs mitral valve replacement 18.6%; P < .01). No differences were found in terms of postoperative cerebrovascular accident (2% vs 3.1%; P = .9), acute kidney injury requiring dialysis (6.7% vs 13.4%; P = .12), and superficial or deep sternal wound infection (10% vs 16.5%, P = .17; 2% vs 3.1%, P = .67, respectively). The final multiple regression model for short-term composite outcome included previous cardiac surgery (odds ratio [OR], 4.47; 95% confidence interval [CI], 1.37-17.46; P = .02), intra-aortic balloon pump use (OR, 4.77; 95% CI, 1.67-15.79; P < .01), and mitral valve replacement (OR, 7.7; 95% CI, 4.04-14.9; P < .01). Overall survival for the entire cohort at 1, 5, and 10 years was 82.4%, 63.7%, and 45.5% (mitral valve repair vs mitral valve replacement: 89.9% vs 70.7% at 1 year, 69.6% vs 54% at 5 years, and 51.8% vs 35.5% at 10 years; P = .0005). Cox proportional hazard model results showed mitral valve replacement (hazard ratio, 1.88; 95% CI, 1.22-2.89; P < .01) and intra-aortic balloon pump use (hazard ratio, 2.54; 95% CI, 1.26-5.13; P < .01) to be independent predictor factors affecting long-term survival. Logisti...

Objective-The aim of this study was to explore the molecular mechanisms involved in late preconditioning-induced cell protection in endothelial cells. Methods and Results-Preconditioning (PC) was induced by exposing bovine aortic endothelial cells (BAECs) to 3 cycles of 15 minutes of hypoxia followed by 15 minutes of reoxygenation. A 12-hour period of hypoxia induced cell death in 60% of BAECs (48Ϯ5% apoptosis, 12Ϯ4% necrosis). Early and late PC decreased hypoxia-induced apoptotic (25Ϯ5% and 28Ϯ4%, respectively) and necrotic (6Ϯ3%, and 8Ϯ2%, respectively) cell death. Consistently, hypoxia-induced caspase-3 cleavage was reduced by PC. Pretreatment with H89 (protein kinase A [PKA] inhibitor), LY294002 (phosphatidyl-inositol-3-kinase [PI3K] inhibitor), and N-acetyl-cysteine (antioxidant) abrogated late PC-induced cell protection, whereas inhibition of protein kinase C by Go6983, and of nitric oxide synthesis by L-NAME,1400W and bovine eNOS siRNA did not. In addition, in early and late PC, PKA physically interacted with the phosphorylated form of Akt, suggesting that PKA is required for Akt phosphorylation. Expression of PKA and Akt dominant negative mutants inhibited ischemic late PC-induced protection, indicating that these kinases play a key role in late PC-mediated cell protection. Conclusions-Late ischemic PC protects BAECs against hypoxia through PKA-and PI3K-dependent activation of

OBJECTIVESTo investigate the in-hospital health outcome and 10-year survival in patients undergoing redo coronary surgery with (redo-CABG) or without (redo-OPCAB) cardiopulmonary bypass.METHODSA total of 349 redo coronary surgery patients were identified from our registry. Of these, 143 redo-OPCAB patients (40.97%) were compared with 206 redo-CABG patients. To minimize the bias, we also conducted propensity score matching. In Matched Analysis A, 111 redo-OPCAB patients with any type of primary cardiac operation were compared with 111 redo-CABG cases. In Matched Analysis B, 84 redo-OPCAB patients with isolated coronary surgery as their primary operation were compared with 84 redo-CABG patients. We assessed for all 3 analyses a composite of in-hospital mortality, acute kidney injury, stroke and severe low cardiac output requiring intra-aortic balloon pump. In addition, we assessed 1-, 5-, and 10-year survival.RESULTSIn the unmatched analysis, redo-CABG was associated with higher usage of intra-aortic balloon pump (10 vs 3%, P = 0.01) and composite compared with redo-OPCAB (25 vs 16%, P = 0.06) and similar 10-year survival (67.2 vs 68.5%, log-rank test: P = 0.78). Matched Analysis A showed similar rates of composite (15 vs 21%, P = 0.25) and 10-year survival (65.1 vs 60.8%, log-rank test: P = 0.5). Matched Analysis B showed reduction of the composite (19 vs 8%, P = 0.04), less in-hospital mortality (5 vs 0%, P = 0.13), 4.5 times less need for intra-aortic balloon pump (2 vs 11%, P = 0.02) favouring redo-OPCAB and a similar 10-year survival (71.6 vs 71.7%, log-rank test: P = 0.61).CONCLUSIONSRedo-OPCAB surgery is feasible, safe and effective with improved in-hospital outcome and similar 10-year survival compared to redo-CABG.

Background Ischemia and malperfusion are strong predictors of poor postoperative outcomes in type A acute aortic dissection (TAAAD). Serum lactate is an accurate surrogate point‐of‐care marker of malperfusion. The aim of this study is to investigate the correlation between lactate, in‐hospital outcomes, and 1‐year survival following TAAAD repair. Methods One hundred and thirty‐two patients underwent operative repair of TAAAD over a 4‐year period at our institution 128 patients had serum lactate measurements at three stages peri‐operatively‐preoperatively, at the end of cardiopulmonary bypass (post‐CPB) and 6 h postintensive care unit (ICU) admission. The primary outcomes were in‐hospital mortality and 1‐year survival. The secondary outcomes were the incidences of in‐hospital morbidities. Results Patients were divided into two groups: 88 (68.8%) with normal lactate and 40 (31.2%) with elevated lactate (>2.2 mmol/L). Lactate measured preoperatively (odds ratio 1.52, 95% confidence interval 1.17–2.07, p < .01), post‐CPB (1.34, 1.14–1.64, p < .01) and 6 h post‐ICU admission (1.29, 1.08–1.55, p < .01) was an independent predictor of in‐hospital mortality. Following adjustment for the Penn Classification, lactate continued to have a significant correlation with in‐hospital mortality at all three timepoints. There was a higher incidence of complications in the elevated lactate group and especially hemofiltration (20% vs. 9.1%, p = .08). 1‐year survival was similar in both groups (p = .23). Conclusions There is a direct correlation between elevated serum lactate and postoperative mortality after TAAAD repair, which is independent of the Penn Classification status on admission.