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Background: Aortic root management in type A acute aortic dissection is controversial. This study compared outcomes of root replacement (RR) interventions versus more conservative root (CR) management., Methods: Of 1,995 type A acute aortic dissection patients enrolled in the International Registry of Acute Aortic Dissection, 699 (35%) underwent RR interventions and 1,296 (65%) underwent CR management. Independent predictors of hospital and 3-year survival were identified using multivariable logistic and Cox regression models., Results: Compared with CR patients, RR patients were younger (56.9 versus 62.3 years; p = 0.023) and more likely to present with larger root diameter (4.7 cm versus 4.0 cm; p < 0.001), Marfan syndrome (8.7% versus 2.5%; p < 0.001), aortic insufficiency (64.0% versus 50.3%; p < 0.001), and hypotension, shock, or tamponade (33.0% versus 26.5%; p = 0.003). Root replacement management did not increase hospital mortality (propensity score-adjusted odds ratio, 1.14; p = 0.674). On Kaplan-Meier analysis, 3-year survival (RR, 92.5% ± 1.7% versus CR, 91.6% ± 1.3%; log-rank p = 0.623) and freedom from aortic root reintervention (RR, 99.2% ± 0.1% versus CR, 99.3% ± 0.1%; log-rank p = 0.770) were similar. Only 2 patients (1 per group) underwent follow-up root reintervention. Propensity score-adjusted Cox regression excluded a relationship between root treatment and follow-up survival (hazard ratio, 1.5; 95% confidence interval, 0.502 to 5.010; p = 0.432)., Conclusions: In type A acute aortic dissection patients more-extensive RR interventions are not associated with increased hospital mortality. This supports such an approach in young patients and patients with connective tissue diseases and bicuspid aortic valves. Excellent midterm survival and freedom from root reintervention in both groups suggest stable behavior of the nonreplaced aortic sinuses at 3 years. Thus, pending studies with longer follow-up, the use of aggressive RR techniques can be determined by patient-specific and dissection-related factors., (Copyright © 2014 The Society of Thoracic Surgeons. Published by Elsevier Inc. All rights reserved.)

Background: The impact of different cannulation strategies on outcomes of aortic arch surgery remains controversial. This retrospective study sought to evaluate central cannulation (ascending aorta, right axillary, and innominate artery) compared with femoral artery cannulation for aortic arch surgery, and to identify among preoperative and intraoperative variables the independent predictors of death and permanent neurologic dysfunction (PND) in aortic arch surgery., Methods: All patients were operated through a median sternotomy using antegrade selective cerebral perfusion with moderate hypothermia as a method of brain protection. Treatment bias was addressed by use of propensity-score matching and multivariate regression analysis. Logistic regression models were used to identify the independent predictors of hospital mortality and PND., Results: Of the 473 patients undergoing aortic arch surgery, 273 (57.7%) underwent femoral cannulation (FC), and 200 (42.3%) underwent central cannulation (CC). The CC and FC cannulation were associated with similar risk of in-hospital death (absolute risk reduction [ARR]: 0.7%; p = 0.880) and PND (ARR:-2.6%, p = 0.361) in the overall cohort and after adjusting for propensity-based matching (ARR for hospital mortality: 2.2%, p = 0.589; ARR for PND: 3.4%, p = 0.271). Female gender (odds ratio [OR]:2.1, p = 0.030), type A acute dissection or intramural hematoma (OR: 2.2; p = 0.041), and CPB time (OR: 1.010/minute, p = 0.015) were independent predictors of in-hospital death. Female gender (OR: 2.4; p = 0.033), type A acute dissection or intramural hematoma (OR: 4.2; p = 0.005), and diabetes (OR: 6.6, p = 0.007) were independent predictors of PND., Conclusions: During aortic arch surgery, CC and FC are associated with a similar risk of postoperative death and PND. Type A acute aortic dissection and cardiopulmonary bypass time remain strong risk factors for mortality and PND., (Copyright © 2013 The Society of Thoracic Surgeons. Published by Elsevier Inc. All rights reserved.)

Background: An accurate prognosis prediction represents a key element in chronic heart failure (CHF) management. Seattle Heart Failure Model (SHFM) prognostic power, a validated risk score for predicting mortality in CHF, is improved by adding B-type natriuretic peptide (BNP). We evaluated in a prospective study the incremental value of several biomarkers, linked to different biological domains, on death risk prediction of BNP-added SHFM., Methods: Troponin I (cTnI), norepinephrine, plasma renin activity, aldosterone, high sensitivity-C reactive protein (hs-CRP), tumor necrosis factor-α (TNF-α), interleukin 6 (IL-6), interleukin 2 soluble receptor, leptin, prealbumin, free malondialdehyde, and 15-F2t-isoprostane were measured in plasma from 142 consecutive ambulatory, non-diabetic stable CHF (mean NYHA-class 2.6) patients (mean age 75±8years). Calibration, discrimination, and risk reclassification of BNP-added SHFM were evaluated after individual biomarker addition., Results: Individual addition of biomarkers to BNP-added SHFM did not improve death prediction, except for prealbumin (HR 0.49 CI: (0.31-0.76) p=0.002) and cTnI (HR 2.03 CI: (1.20-3.45) p=0.009). In fact, with respect to BNP-added SHFM (Harrell's C-statistic 0.702), prealbumin emerged as a stronger predictor of death showing the highest improvement in model discrimination (+0.021, p=0.033) and only a trend was observed for cTn I (+0.023, p=0.063). These biomarkers showed also the best reclassification statistic (Integrated Discrimination Improvement-IDI) at 1-year (IDI: cTnI, p=0.002; prealbumin, p=0.020), 2-years (IDI: cTnI, p=0.018; prealbumin: p=0.006) and 3-years of follow-up (IDI: cTnI p=0.024; prealbumin: p=0.012)., Conclusions: Individual addition of prealbumin allows a more accurate prediction of mortality of BNP enriched SHFM in ambulatory elderly CHF suggesting its potential use in identifying those at high-risk that need nutritional surveillance., (Copyright © 2013 Elsevier Ireland Ltd. All rights reserved.)

Background: A growing body of evidence has shown that delayed management of traumatic injury of the thoracic aorta determines survival benefits as compared with immediate treatment. However, few data exist comparing outcomes after delayed open surgical or endovascular management. Accordingly, we reviewed our experience with delayed management, stratifying the data according to type of repair; open surgical versus endovascular., Methods: Since 1992, delayed aortic repair has represented our first-line management for all blunt traumatic thoracic aortic injury (BTTAI) patients, except for those who presented with or became unstable due to impending aortic rupture. These patients were converted to urgent primary aortic repair. Thus, between 1992 and 2010, a total of 77 BTTAI patients were managed according to this policy. There were 57 (74%) men having a mean age of 33.4 years. Thirty-one (41.3%) patients underwent open surgical repair (SR), 44 (58.6%) underwent endovascular repair (ER), and 2 died while awaiting aortic repair. At admission, the clinical and trauma characteristics were similar in both groups. The trauma-to-repair time span (in days) was 200 (Q1-Q3: 27 to 340) and 10 (Q1-Q3: 2 to 79) for SR and ER patients, respectively (p = 0.001). Due to unpaired hemodynamic or imaging signs of impending aortic rupture, 15 patients required urgent repair, which was endovascular in 11 (25%) cases and surgical in 4 (12.9%)., Results: Overall, hospital mortality was 3.9% (n = 3), being 0% in SR patients and 2.3% (n = 1) in ER patients (p = 0.398). No new postoperative paraplegia occurred; a cerebellar stroke occurred in 1 (2.3%) ER patient receiving intentional coverage of the left subclavian artery. During follow-up (96.1% complete at 95 ± 70 months), no late deaths occurred. At 15 years, the estimates of survival and freedom from secondary aortic procedures were 96% and 100%, respectively., Conclusions: Delayed management of traumatic aortic injury was associated with satisfactory short- and long-term results without significant differences between open surgical and endovascular repair. However, the reduced invasiveness of endovascular repair can optimize operative timing allowing prompt aortic repair in unstable patients, earlier repair in stable patients, and, when indicated, easier concomitant non-aortic surgery., (Copyright © 2013 The Society of Thoracic Surgeons. Published by Elsevier Inc. All rights reserved.)

In redo aortic surgery, an important issue of brain and myocardial protection is raised in patients presenting with large aneurysm (or pseudoaneurysm) adherent to the sternum and severe aortic valve regurgitation. We present our technique involving antegrade brain perfusion before resternotomy and left ventricle venting through the apex using a small anterolateral left thoracotomy., (Copyright © 2013 The Society of Thoracic Surgeons. Published by Elsevier Inc. All rights reserved.)

An integrated approach based on ambient and biological monitoring, the latter including both biomarkers of exposure and susceptibility, was applied to characterize benzene exposure in a group of 37 taxi drivers of the city of Parma (Italy). Airborne benzene concentrations were assessed by 24 h personal sampling and work-shift sampling inside the taxicab using passive samplers (Radiello). Benzene metabolites, trans,trans-muconic acid (t,t-MA) and S-phenylmercapturic acid (S-PMA), and urinary cotinine as biomarker of smoking habits were measured by isotopic dilution liquid chromatography tandem mass spectrometry in both pre-shift (PS) and end-of-shift (EOS) samples. Urinary benzene (U-B) levels were determined by solid-phase microextraction gas chromatography-mass spectrometry in EOS samples. Relevant polymorphisms of microsomal epoxide hydrolase, NAD(P)H:quinone oxidoreductase, glutathione S-transferases M1-1 (GSTM1), T1-1, and A1 were characterized by PCR-based methods. Mean airborne benzene concentration was 5.85 +/- 1.65 microg/m3, as assessed by 24 h personal sampling integrating for work-shift, indoor or general environment activities. Significantly, higher benzene concentrations were detected in the taxicab during the work-shift (7.71 +/- 1.95 microg/m3, p < 0.005). Smokers eliminated significantly higher concentrations of U-B and S-PMA than non-smokers in EOS samples [geometric mean (geometric S.D.): 2.58 (4.23) versus 0.44 (1.79) microg/l for U-B; 3.79 (1.50) versus 2.14 (1.87) microg/gcreat. for S-PMA, p < 0.002]. Within smokers, S-PMA concentrations significantly increased at the end of the work-shift compared to pre-shift values (p < 0.05). t,t-MA showed a similar behaviour, although differences were not significant. In the narrow range examined, no correlation was observed between air benzene concentration and urinary biomarkers. All benzene biomarkers but EOS t,t-MA were correlated with U-cotinine (p < 0.05). GSTM1 polymorphism significantly modulated S-PMA excretion, as subjects bearing the GSTM1pos genotype [3.61 (1.15) microg/gcreat.] excreted significantly higher S-PMA concentrations than GSTM1null subjects [2.19 (1.18) microg/gcreat., p < 0.05].

This study was aimed at evaluating whether controlled short-term exposure to ozone (O(3)) induces changes in biomarkers of lung inflammation and oxidative stress in exhaled breath condensate (EBC) and blood of healthy subjects. Twenty-two volunteers were exposed to 0.1 ppm of O(3) for 2 h while performing moderate intermittent exercise. EBC and blood were collected before, immediately after and 18 h after exposure. Changes in biomarkers were measured both in EBC and blood, without significant alterations of lung function tests. Changes in EBC, but not in blood, were mainly accounted for by a subgroup of 'susceptible' individuals bearing the wild genotype for NAD(P)H:quinone oxidoreductase (NQO1) and the null genotype for glutathione-S-transferase M1 (GSTM1). Thus, a single 2-h exposure to 0.1 ppm of O(3) induces changes in biomarkers of inflammation and oxidative stress. Polymorphic NQO1 and GSTM1 act as modifier of the lung response to O(3).

In this paper we report a study on the mechanism of the enantiomeric separation of unmodified D,L-amino acids in RP-HPLC by copper(II) complexes of two tetradentate diaminodiamido ligands, (S,S)-N,N'-bis(phenylalanyl)ethanediamine (PheNN-2) and (S,S)-N,N'-bis(methylphenylalanyl)ethanediamine (Me2PheNN-2), added to the eluent. The aim is to investigate whether and how a copper(II) complex with no free equatorial positions can perform chiral discrimination of bidentate analytes such as unmodified amino acids. The problem is approached in a systematic way by: (a) varying the different chromatographic parameters (pH, selector concentration, eluent polarity); (b) performing chiral separation with the selector adsorbed on the stationary phase; (c) studying the ternary complex formation of these ligands with D- and L-amino acids in solution by glass electrode potentiometry and electrospray ionization MS. All the experimental data are consistent with a mechanism of chiral recognition, based on ligand exchange, which involves as selectors the species [Cu2L2H(-2)]2+ and [CuLH(-2)] and proceeds by displacement of two binding sites from the equatorial positions, giving rise to the ternary species [CuLA]+ and [CuLH(-1) A]. The most important factor responsible for chiral discrimination seems to be the affinity of the diastereomeric ternary complexes for the stationary phase since no enantioselectivity is observed in solution.