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Objective: Bicuspid aortic valve disease is heterogeneous with respect to valve morphology and aortopathy risk. This study searched for early imaging predictors of aortopathy in patients with a bicuspid aortic valve with right-left coronary cusp fusion, the most common morphotype., Methods: Time-resolved magnetic resonance imaging was performed in 36 subjects with nonstenotic, nonregurgitant bicuspid aortic valves and nondilated aortas and in 10 healthy controls with tricuspid aortic valves. Sinus dimensions (diameter, width, and height), ascending tract diameters, and wall strain were measured for each sinus/leaflet unit and corresponding ascending tract area to account for asymmetries. A novel parameter, "cusp opening angle," measured the degree of valve leaflet alignment to outflow axis in systole, quantifying cusp motility. Phase-contrast magnetic resonance imaging and computational fluid dynamic models assessed flow patterns. Aortic growth rate was estimated over a follow-up period ranging from 9 to 84 months., Results: The expected restriction of bicuspid aortic valve opening (conjoint cusp opening angle, 62°±5° vs 76°±3° for nonfused leaflet and 75°±3° for tricuspid aortic valve cusps; P<.001) was confirmed, and the introduced parameter reproducibly quantified this phenomenon. Phase-contrast magnetic resonance imaging demonstrated systolic flow deflection toward the right, affecting the right anterolateral ascending wall. Computational models confirmed that restricted cusp motion alone is sufficient to cause the observed flow pattern. Ascending tract wall strain was not circumferentially homogeneous in bicuspid aortic valves. In multivariable analyses, the conjoint cusp opening angle independently predicted ascending aorta diameters and growth rate (P<.001)., Conclusions: In the bicuspid aortic valve commonly defined as normofunctional by echocardiographic criteria, restricted systolic conjoint cusp motion causes flow deflection. The novel measurement introduced can quantify restricted cusp opening, possibly assuming prognostic importance., (Copyright © 2012 The American Association for Thoracic Surgery. Published by Mosby, Inc. All rights reserved.)

Objective: Congenital bicuspid aortic valves frequently cause aortic stenosis or regurgitation. Improved understanding of valve and root biomechanics is needed to achieve advancements in surgical repair techniques. By using imaging-derived data, finite element models were developed to quantify aortic valve and root biomechanical alterations associated with bicuspid geometry., Methods: A dynamic 3-dimensional finite element model of the aortic root with a bicuspid aortic valve (type 1 right/left) was developed. The model's geometry was based on measurements from 2-dimensional magnetic resonance images acquired in 8 normotensive and otherwise healthy subjects with echocardiographically normal function of their bicuspid aortic valves. Numeric results were compared with those obtained from our previous model representing the normal root with a tricuspid aortic valve. The effects of raphe thickening on valve kinematics and stresses were also evaluated., Results: During systole, the bicuspid valve opened asymmetrically compared with the normal valve, resulting in an elliptic shape of its orifice. During diastole, the conjoint cusp occluded a larger proportion of the valve orifice and leaflet bending was altered, although competence was preserved. The bicuspid model presented higher stresses compared with the tricuspid model, particularly in the central basal region of the conjoint cusp (+800%). The presence of a raphe partially reduced stress in this region but increased stress in the other cusp., Conclusions: Aortic valve function is altered in clinically normally functioning bicuspid aortic valves. Bicuspid geometry per se entails abnormal leaflet stress. The stress location suggests that leaflet stress may play a role in tissue remodeling at the raphe region and in early leaflet degeneration., (Copyright © 2010 The American Association for Thoracic Surgery. Published by Mosby, Inc. All rights reserved.)

Objective: Leukocytes in allogeneic blood transfusions cause several immunomodulatory events. This before-and-after cohort study evaluated clinical outcomes after adoption of prestorage leukoreduction program for blood transfusions, with particular focus on acute kidney injury., Methods: One thousand thirty-four consecutive patients who underwent on-pump coronary artery bypass grafting between January 2004 and December 2007 were included. Propensity score analysis for transfusion was performed in the whole population; patients who were actually transfused were then divided according to leukoreduction. From these 2 groups, 147 pairs matched for propensity score were considered to evaluate with bivariate and multivariable analyses the effects of leukoreduction, with all-cause in-hospital mortality and morbidity as main outcomes., Results: Unadjusted in-hospital mortalities were 6.6% for the entire cohort and 44.2% for those with acute kidney injury. In the matched population, after introduction of leukoreduction, mortality rates decreased to 5.4% (vs 11.4%) and acute kidney injury (RIFLE [Risk, Injury, Failure, Loss of function, End-stage renal disease] class R or greater) dropped from 51.7% to 41.5% (relative risk -20%, P < .045). No difference emerged regarding other major complications. At multivariable analysis, intra-aortic balloon pump, RIFLE score, and propensity score for transfusion proved independent predictors of in-hospital mortality. Intra-aortic balloon pump and nonleukodepleted transfusion emerged as independent predictors of acute kidney injury. Multivariable analysis on the overall cohort of transfused patients confirmed that nonleukodepleted transfusion was an independent predictor of acute kidney injury., Conclusions: Leukoreduction of allogeneic blood products is associated with decreased acute kidney injury and mortality in highly transfused patients., (2010 The American Association for Thoracic Surgery. Published by Mosby, Inc. All rights reserved.)

Objective: Extubation failure is a serious complication after cardiac surgery. The role of noninvasive positive-pressure ventilation for acute respiratory failure in patients undergoing cardiac surgery is unknown. This study aimed to assess the safety of implementing noninvasive positive-pressure ventilation in this setting and its impact on lung function and operative outcomes., Methods: In a 6-month pilot prospective survey, the study population comprised 43 patients (32 were male with a mean age of 65.73 +/- 9 years; 3 heart transplantations, 18 coronary artery bypass grafts, 5 aortic dissections, and 17 valvular procedures; 34 active smokers, 25 with medically treated chronic obstructive pulmonary disease, 21 emergency/urgency procedures) who required noninvasive positive-pressure ventilation for acute respiratory failure after initial weaning from a respirator. The cause of acute respiratory failure (classified as post-cardiopulmonary bypass lung injury in 48.8% [21 patients], cardiogenic edema in 30.2% [13 patients], and pneumonia in 21% [9 patients]), length of noninvasive positive-pressure ventilation support, respiratory ratios (arterial oxygen tension/fraction of inspired oxygen assessed immediately before noninvasive positive-pressure ventilation, and every 6 hours after institution of pressure ventilation), and need for reintubation along with a set of predefined safety parameters were recorded., Results: The mean length of noninvasive positive-pressure ventilation support was 33.8 +/- 24.04 hours. Plotting respiratory ratios with length of noninvasive positive-pressure ventilation supports a significant improvement was already evident within the first 6-hour frame (133.6 +/- 39.5 vs 205 +/- 65.7; P < .001) for all causes. Noninvasive positive-pressure ventilation prevented intubation in 74.4% of the patients, with satisfactory recovery for post-cardiopulmonary bypass lung injury and cardiogenic dysfunction (90.5% and 69.2%, respectively) and poor results (55% reintubated) in those treated for pneumonia. Noninvasive positive-pressure ventilation safety approached 97.7%., Conclusion: In appropriate candidates, noninvasive positive-pressure ventilation exerts favorable effects on lung function, preventing reintubation. The cost-effectiveness of its systematic use in this setting should be assessed.

Objective: The present study examined temporal and spatial patterns of extracellular matrix and smooth muscle cell changes in the ascending aorta with bicuspid and tricuspid aortic valve stenosis., Methods: Wall specimens were retrieved from both the greater and the lesser curvature ("convexity" and "concavity") of 14 nonaneurysmal and 12 aneurysmal aortas (aortic ratios 1.2 and 1.5, respectively) and from 3 heart donors (normal). Immunochemistry was performed for detection of apoptotic (terminal deoxynucleotidyl transferase-mediated dUTP nick end labelling [TUNEL]-positive) and proliferating (Ki-67-positive) smooth muscle cells and for semiquantification of matrix proteins (collagens, fibronectin, tenascin, laminin). Co-immunoprecipitation assessed the extent of Bcl-2-modifying factor binding to Bcl-2, indicating a matrix-derived cytoskeleton-mediated proapoptotic signaling. Polymerase chain reaction allowed for quantification of messenger RNA expression for Bcl-2., Results: In both bicuspid and tricuspid aneurysms, fibrillar collagens were reduced, whereas fibronectin and tenascin were increased compared with those in normal conditions. These matrix alterations were already evident in bicuspid nonaneurysmal aortas at the convexity, with significant elevation of apoptotic indexes (P = .02 bicuspid vs normal; P = .48 tricuspid vs normal). Apoptotic indexes correlated with aortic dimensions only in tricuspid aortas (P = .01). No significant increase in Ki-67 was found. Higher levels of Bcl-2-modifying factor-Bcl-2 binding were found in bicuspid nonaneurysmal aorta versus tricuspid (P = .03) and normal aortas (P = .01). Bcl-2 messenger RNA expression was reduced in the bicuspid aorta versus normal (P = .08)., Conclusions: Smooth muscle cell apoptosis with bicuspid aortic valve stenosis occurred before overt aortic dilation, mainly at the convexity, where wall stress is expectedly higher. In this setting, a matrix-dependent proapoptotic signaling was evidenced by increased Bcl-2-modifying factor-Bcl-2 binding. Stress-dependent bicuspid aortic valve matrix changes may trigger early apoptosis by inducing cytoskeletal rearrangement.