The Annals of thoracic surgery
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With increasing clinical experience, it has become clear that two distinct forms of neurological injury occur after operations on the thoracic aorta that require temporary exclusion of the cerebral circulation. Traditionally, evaluation of neurological outcome was limited to reporting the incidence of postoperative stroke related to ischemic infarcts due to particulate embolization. More recently, the symptom complex defined as "temporary neurological dysfunction" (TND) was recognized as a functional manifestation of subtle and presumably transient brain injury, but whether this early postoperative syndrome is associated with long-term deficits of cognitive and intellectual functions has not been established. ⋯ The incidence and severity of clinically apparent temporary neurological dysfunction correlates significantly with poor performance on neuropsychological tests 1 week postoperatively. Such poor performance predicts continued deficits in memory and motor function at 6 weeks. Thus, TND may not be a benign self-limited condition as previously supposed, but rather a clinical marker for insidious but significant neurological injury associated with measurable long-term deficits in cerebral function. A concerted effort to reduce the incidence of this complication is therefore necessary.
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This series consists of a 12-year experience with a policy of identifying and replacing the aortic segment containing the primary intimal tear for repair of acute aortic dissection. ⋯ Systematic resection of the primary tear yielded similar hospital mortality, 5-year survival, and aorta-related event-free survival rates for subtypes of acute type A dissection. Excellent results were obtained with a selective approach to type B dissection.
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N1 disease represents a heterogeneous group of non-small cell lung carcinoma with varying 5-year survival rates. Specific types of N1 lymph node involvement need to be further investigated and their prognostic significance clarified. ⋯ N1 disease is a compound of two subgroups: one located inside the lobes is related to N0, and the other (extralobar or hilar) behaves like an early stage of N2 disease. This offers further information for clinical, therapeutic, and research purposes.
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There is evidence that lung ischemia reperfusion injury is a result of the activation of components of the inflammatory cascade. However, the role of neutrophils in lung reperfusion injury continues to be a source of controversy. ⋯ Leukocyte depletion of the blood reperfusate protects against microvascular permeability and significantly improves pulmonary graft function. The neutrophil plays a major role in amplifying lung injury later during reperfusion, and this lung ischemia reperfusion injury may be reversed through the interruption of the inflammatory cascade and the interference with neutrophil infiltration.
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Randomized Controlled Trial Clinical Trial
A prospective randomized trial of Duraflo II heparin-coated circuits in cardiac reoperations.
Heparin-coated circuits in cardiopulmonary bypass have been shown to decrease the systemic inflammatory responses associated with cardiopulmonary bypass. Previous clinical studies on low-risk patients who had coronary artery bypass grafting (CABG) and received full-dose systemic heparin did not have clearly improved clinical outcomes. We hypothesized that the beneficial effects of heparin-coated circuits might be seen in patients who had cardiac reoperations. ⋯ We conclude that the use of heparin-coated circuits was safe and imparted protection from reoperations for bleeding and major bleeding episodes. Material-independent blood activation (eg, blood-air interface and cardiotomy suction) blunted the total effect of the heparin-coated surface.